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AS-IV enhances the antitumor effects of propofol in NSCLC cells by inhibiting autophagy

  • Jintao Liu , Long Chen EMAIL logo , Jialing Zhang , Xiaopan Luo , Yingyi Tan and Shaojie Qian
Published/Copyright: September 25, 2023
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Open Medicine
From the journal Open Medicine Volume 18 Issue 1

Abstract

Non-small cell lung cancer (NSCLC) is one of the most lethal malignant tumors. It has been shown that the general anesthetic agents, propofol and astragaloside IV (AS-IV) both exert antitumor effects in NSCLC. However, the effects of the combination of propofol with AS-IV in NSCLC remain unclear. Cell counting kit-8, and EdU and Transwell assays were performed to evaluate NSCLC cell viability, proliferation, and migration. Cell apoptosis and autophagy were observed by flow cytometric analysis and TUNEL and LC3 staining, respectively. AS-IV notably enhanced the anti-proliferative, pro-apoptotic, and anti-migratory properties of propofol in NSCLC cells. Moreover, AS-IV remarkably facilitated the anti-autophagy effect of propofol in NSCLC cells by downregulating LC3, Beclin 1, and ATG5. Significantly, the pro-apoptotic ability of the AS-IV/propofol combination in NSCLC cells was further enhanced by the autophagy inhibitor 3-MA, suggesting that autophagy plays a tumor-promoting role in NSCLC cells. Collectively, AS-IV could facilitate the antitumor abilities of propofol in NSCLC cells by inhibiting autophagy. These findings may be beneficial for future studies on the use of AS-IV and propofol for the treatment of NSCLC.

Keywords: non-small cell lung cancer; anesthetics; propofol; astragaloside IV; autophagy

1 Introduction

Non-small cell lung cancer (NSCLC) is one of the most common malignancies, representing 80% of total lung cancer cases [1]. The overall survival rate of NSCLC is poor due to delays in diagnosis and metastasis potential of this disease [2,3]. Recently, even with aggressive treatment protocols, including complete surgical resection, radiotherapy, immunotherapy, and chemotherapy, relapse was developed in the majority of NSCLC patients (25–70%) within 5 years [4–6]. Therefore, discovering novel efficient therapeutic approaches for NSCLC is urgently needed.

Local anesthetics are extensively applied in clinical cancer surgeries [7,8]. Recently, evidence has shown that anesthetics also exhibit antitumor properties in multiple cancers, including NSCLC [9–11]. Propofol, a general anesthetic agent administered during surgery, has been found to suppress the progression of NSCLC [12]. Zhang et al. found that propofol could decrease NSCLC cell proliferation, migration, and invasion [13]. Meanwhile, propofol was able to enhance the sensitivity of lung cancer cells to cisplatin in NSCLC [14].

It has been shown that traditional Chinese medicine combined with antitumor drugs could achieve favorable effects for cancer treatment [15,16]. Astragalus membranaceus, a type of traditional Chinese medicine, possesses anti-inflammatory, antioxidative, and antitumor effects [17,18,19]. Astragaloside IV (AS-IV) is a main active component isolated from Astragalus membranaceus [20]. Jia et al. found that AS-IV could reduce NSCLC cell proliferation and migration by inhibiting Akt/GSK-3β signaling [21]. In addition, AS-IV could improve the response of NSCLC cells to cisplatin by inhibiting autophagy [22]. However, the role of the combination of AS-IV and propofol in NSCLC remains unclear. Therefore, we aimed to explore the antitumor activities of AS-IV combined with propofol on NSCLC cells. In this study, we found that AS-IV could enhance the pro-apoptotic and anti-migratory activities of propofol in NSCLC cells. These findings may be beneficial for future studies on the use of AS-IV and propofol for the treatment of NSCLC.

2 Materials and methods

2.1 Cell culture

Normal lung epithelial cells (BEAS2B) and NSCLC cell lines A549 and NCI-H1299 were obtained from Procell Life Science & Technology Co., Ltd. A549 and NCI-H1299 cells were maintained in complete medium consisting of DMEM (Thermo Fisher Scientific), 0.1% penicillin‒streptomycin, and 10% fetal bovine serum (FBS, Thermo Fisher Scientific, category number: 26010-074) at 37°C in a humidified atmosphere of 5% CO2. Cells were maintained in a 75 cm2 culture flask for culture. Cells were subcultured every 3 days with a maximum of passages not exceeding 25. When the cells grew to 70% confluence, they were collected and used for subsequent experiments.

2.2 Cell counting kit-8 (CCK-8) assay

BEAS2B or NSCLC cells (1  ×  104 cells/well) were plated into 96‐well plates overnight. Next NSCLC cells were treated with AS-IV (0, 5, 10, 20, or 40 ng/mL) [21] and/or propofol (0, 2.5, 5, 10, or 20 μg/mL) [23] for 48 h. After that, each well was supplemented with CCK-8 reagent (10 µL; Beyotime), and the cells were then incubated for 2 h. Finally, the absorbance at 450 nm was measured with a microplate reader (DR-200Bs, Diatek). AS-IV and propofol were obtained from Sigma-Aldrich (PHL89377 and Y0000016, Sigma-Aldrich, St Louis, USA).

2.3 EdU staining assay

The proliferative capacity of A549 and NCI-H1299 cells was assessed by EdU staining assay. The EdU assay was conducted using the Cell-Light EdU DNA cell proliferation kit (RiboBio). Briefly, NSCLC cells were treated with EdU solution (50 µM) for 2 h. After fixation with 4% paraformaldehyde (PFA), cells were stained with Apollo reagent for 30 min in darkness. The nuclear DNA was then stained with Hoechst 33342. Finally, EdU-positive cells were observed under a fluorescence microscope (OLYMPUS).

2.4 Flow cytometric analysis

Flow cytometry analysis was used to evaluate the apoptosis of A549 and NCI-H1299 cells. The cells were collected, and the apoptotic cells were identified with an annexin V-FITC cell apoptosis detection kit (product No. C1063; Biotech Research Institute) according to the manufacturer’s protocol. In short, 1 × 106 cells were resuspended in 1 mL binding buffer, incubated with 5 µL of Annexin V-FITC for 15 min, and then incubated at 4°C with 5 µL of PI for 5 min in the dark. Fluorescence signals were collected by FACScan flow cytometry (Beckman Coulter, Inc. and then analyzed by FlowJo 8.7.1 software (FlowJo LLC).

2.5 TUNEL staining assay

The TUNEL assay was conducted using the In Situ Cell Death Detection Kit (Roche). Briefly, NSCLC cells were incubated with the TUNEL working solution for 1 h in darkness. The nuclear DNA was then stained with DAPI for 30 min. Finally, the apoptotic cells were captured under a fluorescence microscope.

2.6 Transwell migration assay

NSCLC cells (2  ×  104 cells) suspended in serum-free DMEM were added to the upper compartment of 24-well migration chambers (Corning). Meanwhile, the lower compartment was filled with 500 µL of DMEM containing 10% FBS as the attracting agent. Cells in the upper chamber migrating through the polycarbonate membrane into the lower chamber with high nutritional content were considered to have high migration ability. Next 0.1% crystal violet was used to stain the migrated cells on the undersurface of the lower chamber at 24 h. Finally, the migrated cells were captured with a microscope.

2.7 Immunofluorescence assay

About 2 × 104 NSCLC cells were inoculated into a 24-well plate and fixed at room temperature with 4% PFA for 20 min. PBS containing 1% Triton X-100 was then added to permeate for 20 min. The cells were then incubated with anti-LC3 (ab192890, 1:1,000, Abcam) specific rabbit monoclonal antibody at 4°C overnight. The goat anti-rabbit IgG H&L (Alexa Fluor® 647) secondary antibody (ab150079, 1:1,000, Abcam) was then incubated at room temperature in darkness for 2 h. The nuclei were stained with DAPI. Subsequently, the LC3-positive cells were observed using a fluorescence microscope.

2.8 Western blot assay

Total protein was extracted from the cells using RIPA lysis buffer. Total proteins were quantified by the BCA protein assay kit (ASPEN). Next proteins (20 μg/lane) were dissolved by 10% SDS-PAGE and then electrotransferred onto a PVDF membrane (Millipore). After that, the membrane was incubated with specific primary antibodies, including anti-Beclin 1 (ab207612, 1:2,000, Abcam), anti-ATG5 (ab108327, 1:1,000, Abcam), anti-ERK (ab184699, 1:10,000, Abcam), anti-p-ERK (ab201015, 1:1,000, Abcam), anti-Bcl-2 (ab32124, 1:1,000, Abcam), anti-cleaved caspase 3 (ab32042, 1:500, Abcam), and anti-β-actin (ab6276, 1:5,000, Abcam), at 4°C overnight. Following incubation with the corresponding secondary antibody Goat Anti-Rabbit IgG H&L (HRP) (ab7090, 1:5,000, Abcam), the protein blots were developed by ECL reagent. Band intensity was measured using ImageJ software (ImageJ, NIH).

2.9 Statistical analyses

All data were repeated at least three times independently. Data are shown as the mean value ± standard deviation and analyzed with Graphpad Prism 7.0. Statistical analysis was performed by one-way analysis of variance (ANOVA) followed by Tukey’s test. p values <0.05 were considered statistically significant.

3 Results

3.1 AS-IV enhanced the cytotoxic effect of propofol in NSCLC cells

To investigate the role of AS-IV and propofol in NSCLC cells, CCK-8 assay was conducted to determine the effects of AS-IV and propofol on the viability of BEAS2B, A549, and NCI-H1299 cells. As shown in Figure 1a, no significant change in BEAS2B cell viability was observed when the concentration of AS-IV was less than 20 ng/mL. As shown in Figure 1b and c, AS-IV (10, 20, or 40 ng/mL) notably inhibited the viability of NSCLC cells. The viability of both A549 and NCI-H1299 cells at 40 ng/mL AS-IV was reduced to below 60%. Figure 1d showed that compared with the control group, there was no statistical significance in cell viability of BEAS-2B cells treated with propofol when the concentration was 2.5, 5, 10 μg/mL. Compared with the control group, the cell viability decreased when the concentration of propofol was 20 μg/mL, which had statistical significance. Propofol (2.5, 5, 10, or 20 μg/mL) markedly reduced the viability of NSCLC cells (Figure 1e and f). Furthermore, 2.5 μg/mL propofol significantly decreased NSCLC cell viability and exhibited approximately 20% growth inhibition. The viability of both A549 and NCI-H1299 cells at 20 μg/mL propofol was reduced to below 50%, but it had no significant effect on the cell survival rate of BEAS2B. In particular, the combination of propofol (2.5 μg/mL) and AS-IV (5 ng/mL) markedly reduced NSCLC cell viability and exhibited approximately 50% growth inhibition (Figure 1g–i). Therefore, 2.5 μg/mL propofol and 5 ng/mL AS-IV were utilized in the following experiments. Collectively, AS-IV could enhance the cytotoxic effect of propofol in NSCLC cells.

Figure 1 AS-IV enhanced the cytotoxic effect of propofol in NSCLC cells. (a) BEAS2B, (b) A549, and (c) NCI-H1299 cells were treated with AS-IV (0, 5, 10, 20, or 40 ng/mL) for 48 h to evaluate cell viability using CCK-8 assay. (d) BEAS2B, (e) A549, and (f) NCI-H1299 cells were treated with propofol (0, 2.5, 5, 10, or 20 μg/mL) for 48 h. (g) BEAS2B, (h) A549, and (i) NCI-H1299 cells were treated with propofol (2.5 μg/mL) and AS-IV (0, 5, 10, or 20 ng/mL) for 48 h. The 2.5 μg/mL propofol and 5 ng/mL AS-IV were utilized in the following experiments. **p < 0.01 vs control group; ## p < 0.01 vs propofol (2.5 μg/mL) treatment group.
Figure 1

AS-IV enhanced the cytotoxic effect of propofol in NSCLC cells. (a) BEAS2B, (b) A549, and (c) NCI-H1299 cells were treated with AS-IV (0, 5, 10, 20, or 40 ng/mL) for 48 h to evaluate cell viability using CCK-8 assay. (d) BEAS2B, (e) A549, and (f) NCI-H1299 cells were treated with propofol (0, 2.5, 5, 10, or 20 μg/mL) for 48 h. (g) BEAS2B, (h) A549, and (i) NCI-H1299 cells were treated with propofol (2.5 μg/mL) and AS-IV (0, 5, 10, or 20 ng/mL) for 48 h. The 2.5 μg/mL propofol and 5 ng/mL AS-IV were utilized in the following experiments. **p < 0.01 vs control group; ## p < 0.01 vs propofol (2.5 μg/mL) treatment group.

3.2 AS-IV enhanced the anti-proliferative, pro-apoptotic, and anti-migratory properties of propofol in NSCLC cells

Next we explored the effects of AS-IV and propofol on the proliferation, apoptosis, and migration of NSCLC cells. As indicated in Figure 2a and b, propofol (2.5 μg/mL) significantly suppressed NSCLC cell proliferation. As expected, the combination of AS-IV with propofol further inhibited the proliferation of NSCLC cells (the proportion of Edu-positive cells was decreased by 2-fold) compared to that of cells in the propofol treatment alone group (Figure 2a and b). Additionally, propofol treatment obviously resulted in increased NSCLC cell apoptosis (Figure 3a and b). Interestingly, AS-IV further strengthened propofol-induced NSCLC cell apoptosis (cell apoptosis above 35%) (Figure 3a and b). Furthermore, propofol or AS-IV treatment led to a remarkable decrease in NSCLC cell migration (Figure 4a and b). Meanwhile, the combination of AS-IV and propofol further reduced the migratory ability of NSCLC cells (the number of migrating cells decreased by more than 3-fold) compared to the propofol treatment alone group (Figure 4a and b). Collectively, AS-IV enhanced the anti-proliferative, pro-apoptotic, and anti-migratory properties of propofol in NSCLC cells.

Figure 2 AS-IV enhanced the anti-proliferative property of propofol in NSCLC cells. A549 and NCI-H1299 cells were treated with AS-IV (5 ng/mL) and/or propofol (2.5 μg/mL) for 48 h. Cell proliferation was assessed by CCK-8 (a) and EdU (b) staining assays (200×). The combination of AS-IV with propofol further inhibited the proliferation of NSCLC cells compared to the propofol treatment alone. *p < 0.05, **p < 0.01 vs control group; ## p < 0.01 vs propofol (2.5 μg/mL) treatment group.
Figure 2

AS-IV enhanced the anti-proliferative property of propofol in NSCLC cells. A549 and NCI-H1299 cells were treated with AS-IV (5 ng/mL) and/or propofol (2.5 μg/mL) for 48 h. Cell proliferation was assessed by CCK-8 (a) and EdU (b) staining assays (200×). The combination of AS-IV with propofol further inhibited the proliferation of NSCLC cells compared to the propofol treatment alone. *p < 0.05, **p < 0.01 vs control group; ## p < 0.01 vs propofol (2.5 μg/mL) treatment group.

Figure 3 AS-IV enhanced the pro-apoptotic property of propofol in NSCLC cells. A549 and NCI-H1299 cells were treated with AS-IV (5 ng/mL) and/or propofol (2.5 μg/mL) for 48 h. Cell apoptosis was assessed by flow cytometric analysis (a) and TUNEL assay (b) (200×). AS-IV further strengthened propofol-induced NSCLC cell apoptosis. *p < 0.05, **p < 0.01.
Figure 3

AS-IV enhanced the pro-apoptotic property of propofol in NSCLC cells. A549 and NCI-H1299 cells were treated with AS-IV (5 ng/mL) and/or propofol (2.5 μg/mL) for 48 h. Cell apoptosis was assessed by flow cytometric analysis (a) and TUNEL assay (b) (200×). AS-IV further strengthened propofol-induced NSCLC cell apoptosis. *p < 0.05, **p < 0.01.

Figure 4 AS-IV enhanced the anti-migratory property of propofol in NSCLC cells. (a) A549 and (b) NCI-H1299 cells were treated with AS-IV (5 ng/mL) and/or propofol (2.5 μg/mL) for 48 h. Cell migration was assessed by Transwell assay (200×). The combination of AS-IV and propofol further reduced the migratory ability of NSCLC cells compared with propofol treatment alone. *p < 0.05, **p < 0.01.
Figure 4

AS-IV enhanced the anti-migratory property of propofol in NSCLC cells. (a) A549 and (b) NCI-H1299 cells were treated with AS-IV (5 ng/mL) and/or propofol (2.5 μg/mL) for 48 h. Cell migration was assessed by Transwell assay (200×). The combination of AS-IV and propofol further reduced the migratory ability of NSCLC cells compared with propofol treatment alone. *p < 0.05, **p < 0.01.

3.3 Combination of AS-IV and propofol suppressed NSCLC cell autophagy and ERK1/2 signaling

Autophagy is a highly conserved cellular proteolysis process that plays an important role in cancer development [24]. Thus, we next explored whether AS-IV and propofol could affect NSCLC cell autophagy. As shown in Figure 5a–f, AS-IV (5 ng/mL) group and propofol (2.5 μg/mL) group significantly reduced LC3, Beclin 1, ATG5, and p-ERK/ERK levels in NSCLC cells. Interestingly, the combination of AS-IV and propofol further down-regulated LC3, Beclin 1, ATG5, and p-ERK/ERK levels in NSCLC cells. In summary, the combination of AS-IV and propofol suppressed NSCLC cell autophagy.

Figure 5 The combination of AS-IV and propofol suppressed NSCLC cell autophagy. A549 cells were treated with AS-IV (5 ng/mL) and/or propofol (2.5 μg/mL) for 48 h. (a) LC3 levels in A549 cells were detected by IF staining assay (400×). (b)–(f) Western blot assay was applied to determine Beclin 1, ATG5, and p-ERK/ERK levels in A549 cells. IF, Immunofluorescence. **p < 0.01.
Figure 5

The combination of AS-IV and propofol suppressed NSCLC cell autophagy. A549 cells were treated with AS-IV (5 ng/mL) and/or propofol (2.5 μg/mL) for 48 h. (a) LC3 levels in A549 cells were detected by IF staining assay (400×). (b)–(f) Western blot assay was applied to determine Beclin 1, ATG5, and p-ERK/ERK levels in A549 cells. IF, Immunofluorescence. **p < 0.01.

3.4 AS-IV combined with propofol triggered NSCLC cell apoptosis by inhibiting autophagy

Since the AS-IV/propofol combination could induce NSCLC cell apoptosis and suppress cell autophagy, we then focused on the interaction between apoptosis and autophagy in NSCLC cells. The pro-apoptotic effect of the AS-IV/propofol combination on NSCLC cells was further enhanced by treatment with the autophagy inhibitor 3-MA, as shown by the decreased level of Bcl-2 and increased level of cleaved caspase 3 (Figure 6a–e). Collectively, the combination of AS-IV and propofol could trigger NSCLC cell apoptosis by inhibiting autophagy.

Figure 6 The combination of AS-IV and propofol triggered NSCLC cell apoptosis by inhibiting autophagy. A549 cells were pretreated with 5 mM 3-MA prior to 12 h and then treated with propofol or propofol plus AS-IV for 48 h. Cell apoptosis was assessed by flow cytometric analysis (a) and TUNEL assay (b) (×200×). (c)–(e) Western blot assay was applied to determine Bcl-2 and cleaved caspase 3 levels in A549 cells. Combination of AS-IV and propofol could trigger NSCLC cell apoptosis by inhibiting autophagy. *p < 0.05, **p < 0.01.
Figure 6

The combination of AS-IV and propofol triggered NSCLC cell apoptosis by inhibiting autophagy. A549 cells were pretreated with 5 mM 3-MA prior to 12 h and then treated with propofol or propofol plus AS-IV for 48 h. Cell apoptosis was assessed by flow cytometric analysis (a) and TUNEL assay (b) (×200×). (c)–(e) Western blot assay was applied to determine Bcl-2 and cleaved caspase 3 levels in A549 cells. Combination of AS-IV and propofol could trigger NSCLC cell apoptosis by inhibiting autophagy. *p < 0.05, **p < 0.01.

4 Discussion

Recently, Chinese traditional medicine has been used in the treatment of NSCLC [25,26]. AS-IV isolated from Astragalus membranaceus has been recognized to exert anticancer effects in NSCLC [21]. In this research, we found that AS-IV could enhance the antitumor effects of propofol in NSCLC cells by suppressing autophagy.

Propofol, an anesthesia drug, has been proven to act as an antitumor agent in multiple cancers [27,28]. For example, propofol inhibits the development of bladder cancer [29] and colon cancer [30] by regulating miR-145-5p or JAK2/STAT3 signaling pathway. Propofol increases miR-486-5p levels in NSCLC cells and xenograft tumor tissues in a N6-methyladenosine (m6A) dependent manner, thereby inactivating the Ras associated protein 1 (RAP1)-NF-kappaB (NF-κB) axis to increase cisplatin sensitivity in NSCLC [23]. Propofol inhibits the development of NSCLC by inhibiting the circ-RHOT1/miR-326/Prognostic Significance of Forkhead Box M1 (FOXM1) [13] axis and miR-21/PTEN/AKT [12] axis. In addition, propofol could trigger NSCLC cell apoptosis by inactivating ERK1/2 signaling and upregulating p53-upregulated modulator of apoptosis [31]. These results demonstrate that propofol can function as a tumor suppressor in cancer through miRNA, JAK2/STAT3, RAP1/NF-κB, PTEN/AKT, and ERK1/2 signaling pathways. On the basis of these previous studies, our results showed that propofol treatment resulted in a significant decrease in NSCLC cell proliferation and migration and an increase in cell apoptosis. These results further confirmed the antitumor effects of propofol in NSCLC.

Recently, combination therapy has attracted increasing attention in cancer treatment due to the advantages of reduced toxicity, synergistic antitumor effects, and diminished acquired resistance [32,33,34]. Propofol regulates Wnt/β-Catenin, HIF-1 signaling pathway, circ-ERBB2/miR-7-5p/FOXM1 axis, inhibits NSCLC cell proliferation, invasion, and glycolysis, and accelerates cell apoptosis [14,35,36]. AS-IV inhibits AMPK signaling pathway, Akt/GSK-3β/β-Catenin, endoplasmic reticulum stress signaling pathway, and autophagy signaling pathway and evidence in previous studies also proved AS-IV inhibits the proliferation of NSCLC and promotes apoptosis [21,22,37]. This study found that the combination of propofol and AS-IV could further inhibit ERK1/2 signaling in NSCLC cells. Therefore, the combined action of propofol and AS-IV can synergistically act on multiple signal pathways, thereby inducing apoptosis in lung cancer cells. The combination of propofol and sevoflurane remarkably suppressed the migration and invasion of lung adenocarcinoma cells compared to single drugs [38]. The combination of propofol and paclitaxel obviously induced apoptosis in prostatic cancer cells compared to paclitaxel alone [39]. In addition, AS-IV and curcumin synergistically inhibited tumor growth in hepatocellular carcinoma [40]. These results predict that the therapeutic effect of the combination may be more significant than that of the single medication. Whether AS-IV would produce synergistic effects with propofol in NSCLC has not been reported. While the present study conducted a preliminary exploratory study of this blank, in this study, we found that AS-IV could strengthen the antitumor effects of propofol in NSCLC cells. Meanwhile, the combination of AS-IV and propofol exhibited broad antitumor activity compared to single drug treatment.

Autophagy is a self-degradative system that can exert tumor-promoting or antitumor effects in different contexts [41,42]. Propofol could enhance tumor sensitivity to cisplatin in gastric cancer by inhibiting autophagy [43]. In addition, AS-IV was able to induce vulvar squamous cell carcinoma cell apoptosis and autophagy by regulating TGF-β/Smad signaling [44]. Moreover, AS-IV was found to sensitize NSCLC cells to cisplatin treatment by inhibiting autophagy [22]. In this study, AS-IV significantly suppressed NSCLC cell autophagy, and propofol slightly suppressed NSCLC cell autophagy. As expected, the combination of AS-IV and propofol further inhibited NSCLC cell autophagy compared to single drug treatment by inhibiting LC3, Beclin1, and ATG5. In addition, inhibition of autophagy by 3-MA further increased the effect of combination-induced NSCLC cell apoptosis. These results showed that autophagy played a tumor-promoting effect in NSCLC cells. Collectively, combined AS-IV with propofol was able to trigger NSCLC cell apoptosis by inhibiting autophagy.

However, there are some limitations to this study. In this study, the effects of AS-IV and propofol via autophagy on the proliferation, migration, and apoptosis of NSCLC cells were investigated only at the cellular level in vitro and were not further verified at the in vivo level. In the future, it is necessary to construct an animal model of subcutaneous tumor of NSCLC to further study the anti-tumor effect of AS-IV combined with propofol. The lack of clinical trial data is also one of the limitations of this study. In addition, in this study, coadministration of AS-IV and propofol inhibited autophagy in lung cancer cells by further downregulating the level of the autophagy protein Beclin1, but the specific molecular mechanism still needs further investigation. In addition to that, we only explored the antitumor effects of propofol in NSCLC cells, future studies are suggested to explore the combined effect of other anesthetics, such as sevoflurane and dexmedetomidine, with AS-IV in NSCLC cells. These limitations need to be carefully addressed before this study can be translated into clinical practice.

5 Conclusion

In conclusion, AS-IV enhanced the antitumor effects of propofol in NSCLC cells by inhibiting autophagy. These findings might pave the way for the application of AS-IV and propofol in NSCLC in the future.

  1. Funding information: This study is supported by the Health Bureau of Zhejiang province (no. 2018KY221, 2022KY501).

  2. Author contributions: Jintao Liu made major contributions to the conception, design, and manuscript drafting of this study. Jialing Zhang, Xiaopan Luo, Yingyi Tan, and Shaojie Qian were responsible for data acquisition, data analysis, data interpretation, and manuscript revision. Long Chen made substantial contributions to the conception and design of the study and revised the manuscript. All authors agreed to be accountable for all aspects of the work. All authors read and approved the final manuscript.

  3. Conflict of interest: The authors declare that they have no competing interest.

  4. Data availability statement: The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.

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Received: 2023-05-23
Revised: 2023-07-25
Accepted: 2023-08-17
Published Online: 2023-09-25

© 2023 the author(s), published by De Gruyter

This work is licensed under the Creative Commons Attribution 4.0 International License.

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  202. Metabolomic analysis of serum short-chain fatty acid concentrations in a mouse of MPTP-induced Parkinson’s disease after dietary supplementation with branched-chain amino acids
  203. Cimifugin inhibits adipogenesis and TNF-α-induced insulin resistance in 3T3-L1 cells
  204. Predictors of gastrointestinal complaints in patients on metformin therapy
  205. Prescribing patterns in patients with chronic obstructive pulmonary disease and atrial fibrillation
  206. A retrospective analysis of the effect of latent tuberculosis infection on clinical pregnancy outcomes of in vitro fertilization–fresh embryo transferred in infertile women
  207. Appropriateness and clinical outcomes of short sustained low-efficiency dialysis: A national experience
  208. miR-29 regulates metabolism by inhibiting JNK-1 expression in non-obese patients with type 2 diabetes mellitus and NAFLD
  209. Clinical features and management of lymphoepithelial cyst
  210. Serum VEGF, high-sensitivity CRP, and cystatin-C assist in the diagnosis of type 2 diabetic retinopathy complicated with hyperuricemia
  211. ENPP1 ameliorates vascular calcification via inhibiting the osteogenic transformation of VSMCs and generating PPi
  212. Significance of monitoring the levels of thyroid hormone antibodies and glucose and lipid metabolism antibodies in patients suffer from type 2 diabetes
  213. The causal relationship between immune cells and different kidney diseases: A Mendelian randomization study
  214. Interleukin 33, soluble suppression of tumorigenicity 2, interleukin 27, and galectin 3 as predictors for outcome in patients admitted to intensive care units
  215. Identification of diagnostic immune-related gene biomarkers for predicting heart failure after acute myocardial infarction
  216. Long-term administration of probiotics prevents gastrointestinal mucosal barrier dysfunction in septic mice partly by upregulating the 5-HT degradation pathway
  217. miR-192 inhibits the activation of hepatic stellate cells by targeting Rictor
  218. Diagnostic and prognostic value of MR-pro ADM, procalcitonin, and copeptin in sepsis
  219. Review Articles
  220. Prenatal diagnosis of fetal defects and its implications on the delivery mode
  221. Electromagnetic fields exposure on fetal and childhood abnormalities: Systematic review and meta-analysis
  222. Characteristics of antibiotic resistance mechanisms and genes of Klebsiella pneumoniae
  223. Saddle pulmonary embolism in the setting of COVID-19 infection: A systematic review of case reports and case series
  224. Vitamin C and epigenetics: A short physiological overview
  225. Ebselen: A promising therapy protecting cardiomyocytes from excess iron in iron-overloaded thalassemia patients
  226. Aspirin versus LMWH for VTE prophylaxis after orthopedic surgery
  227. Mechanism of rhubarb in the treatment of hyperlipidemia: A recent review
  228. Surgical management and outcomes of traumatic global brachial plexus injury: A concise review and our center approach
  229. The progress of autoimmune hepatitis research and future challenges
  230. METTL16 in human diseases: What should we do next?
  231. New insights into the prevention of ureteral stents encrustation
  232. VISTA as a prospective immune checkpoint in gynecological malignant tumors: A review of the literature
  233. Case Reports
  234. Mycobacterium xenopi infection of the kidney and lymph nodes: A case report
  235. Genetic mutation of SLC6A20 (c.1072T > C) in a family with nephrolithiasis: A case report
  236. Chronic hepatitis B complicated with secondary hemochromatosis was cured clinically: A case report
  237. Liver abscess complicated with multiple organ invasive infection caused by hematogenous disseminated hypervirulent Klebsiella pneumoniae: A case report
  238. Urokinase-based lock solutions for catheter salvage: A case of an upcoming kidney transplant recipient
  239. Two case reports of maturity-onset diabetes of the young type 3 caused by the hepatocyte nuclear factor 1α gene mutation
  240. Immune checkpoint inhibitor-related pancreatitis: What is known and what is not
  241. Does total hip arthroplasty result in intercostal nerve injury? A case report and literature review
  242. Clinicopathological characteristics and diagnosis of hepatic sinusoidal obstruction syndrome caused by Tusanqi – Case report and literature review
  243. Synchronous triple primary gastrointestinal malignant tumors treated with laparoscopic surgery: A case report
  244. CT-guided percutaneous microwave ablation combined with bone cement injection for the treatment of transverse metastases: A case report
  245. Malignant hyperthermia: Report on a successful rescue of a case with the highest temperature of 44.2°C
  246. Anesthetic management of fetal pulmonary valvuloplasty: A case report
  247. Rapid Communication
  248. Impact of COVID-19 lockdown on glycemic levels during pregnancy: A retrospective analysis
  249. Erratum
  250. Erratum to “Inhibition of miR-21 improves pulmonary vascular responses in bronchopulmonary dysplasia by targeting the DDAH1/ADMA/NO pathway”
  251. Erratum to: “Fer exacerbates renal fibrosis and can be targeted by miR-29c-3p”
  252. Retraction
  253. Retraction of “Study to compare the effect of casirivimab and imdevimab, remdesivir, and favipiravir on progression and multi-organ function of hospitalized COVID-19 patients”
  254. Retraction of “circ_0062491 alleviates periodontitis via the miR-142-5p/IGF1 axis”
  255. Retraction of “miR-223-3p alleviates TGF-β-induced epithelial-mesenchymal transition and extracellular matrix deposition by targeting SP3 in endometrial epithelial cells”
  256. Retraction of “SLCO4A1-AS1 mediates pancreatic cancer development via miR-4673/KIF21B axis”
  257. Retraction of “circRNA_0001679/miR-338-3p/DUSP16 axis aggravates acute lung injury”
  258. Retraction of “lncRNA ACTA2-AS1 inhibits malignant phenotypes of gastric cancer cells”
  259. Special issue Linking Pathobiological Mechanisms to Clinical Application for cardiovascular diseases
  260. Effect of cardiac rehabilitation therapy on depressed patients with cardiac insufficiency after cardiac surgery
  261. Special issue The evolving saga of RNAs from bench to bedside - Part I
  262. FBLIM1 mRNA is a novel prognostic biomarker and is associated with immune infiltrates in glioma
  263. Special Issue Computational Intelligence Methodologies Meets Recurrent Cancers - Part III
  264. Development of a machine learning-based signature utilizing inflammatory response genes for predicting prognosis and immune microenvironment in ovarian cancer
https://doi.org/10.1515/med-2023-0799
Keywords for this article
non-small cell lung cancer; anesthetics; propofol; astragaloside IV; autophagy
Creative Commons
BY 4.0

Articles in the same Issue

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  4. circ-IARS depletion inhibits the progression of non-small-cell lung cancer by circ-IARS/miR-1252-5p/HDGF ceRNA pathway
  5. circRNA ITGA7 restrains growth and enhances radiosensitivity by up-regulating SMAD4 in colorectal carcinoma
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  209. Clinical features and management of lymphoepithelial cyst
  210. Serum VEGF, high-sensitivity CRP, and cystatin-C assist in the diagnosis of type 2 diabetic retinopathy complicated with hyperuricemia
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  213. The causal relationship between immune cells and different kidney diseases: A Mendelian randomization study
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  215. Identification of diagnostic immune-related gene biomarkers for predicting heart failure after acute myocardial infarction
  216. Long-term administration of probiotics prevents gastrointestinal mucosal barrier dysfunction in septic mice partly by upregulating the 5-HT degradation pathway
  217. miR-192 inhibits the activation of hepatic stellate cells by targeting Rictor
  218. Diagnostic and prognostic value of MR-pro ADM, procalcitonin, and copeptin in sepsis
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  221. Electromagnetic fields exposure on fetal and childhood abnormalities: Systematic review and meta-analysis
  222. Characteristics of antibiotic resistance mechanisms and genes of Klebsiella pneumoniae
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  232. VISTA as a prospective immune checkpoint in gynecological malignant tumors: A review of the literature
  233. Case Reports
  234. Mycobacterium xenopi infection of the kidney and lymph nodes: A case report
  235. Genetic mutation of SLC6A20 (c.1072T > C) in a family with nephrolithiasis: A case report
  236. Chronic hepatitis B complicated with secondary hemochromatosis was cured clinically: A case report
  237. Liver abscess complicated with multiple organ invasive infection caused by hematogenous disseminated hypervirulent Klebsiella pneumoniae: A case report
  238. Urokinase-based lock solutions for catheter salvage: A case of an upcoming kidney transplant recipient
  239. Two case reports of maturity-onset diabetes of the young type 3 caused by the hepatocyte nuclear factor 1α gene mutation
  240. Immune checkpoint inhibitor-related pancreatitis: What is known and what is not
  241. Does total hip arthroplasty result in intercostal nerve injury? A case report and literature review
  242. Clinicopathological characteristics and diagnosis of hepatic sinusoidal obstruction syndrome caused by Tusanqi – Case report and literature review
  243. Synchronous triple primary gastrointestinal malignant tumors treated with laparoscopic surgery: A case report
  244. CT-guided percutaneous microwave ablation combined with bone cement injection for the treatment of transverse metastases: A case report
  245. Malignant hyperthermia: Report on a successful rescue of a case with the highest temperature of 44.2°C
  246. Anesthetic management of fetal pulmonary valvuloplasty: A case report
  247. Rapid Communication
  248. Impact of COVID-19 lockdown on glycemic levels during pregnancy: A retrospective analysis
  249. Erratum
  250. Erratum to “Inhibition of miR-21 improves pulmonary vascular responses in bronchopulmonary dysplasia by targeting the DDAH1/ADMA/NO pathway”
  251. Erratum to: “Fer exacerbates renal fibrosis and can be targeted by miR-29c-3p”
  252. Retraction
  253. Retraction of “Study to compare the effect of casirivimab and imdevimab, remdesivir, and favipiravir on progression and multi-organ function of hospitalized COVID-19 patients”
  254. Retraction of “circ_0062491 alleviates periodontitis via the miR-142-5p/IGF1 axis”
  255. Retraction of “miR-223-3p alleviates TGF-β-induced epithelial-mesenchymal transition and extracellular matrix deposition by targeting SP3 in endometrial epithelial cells”
  256. Retraction of “SLCO4A1-AS1 mediates pancreatic cancer development via miR-4673/KIF21B axis”
  257. Retraction of “circRNA_0001679/miR-338-3p/DUSP16 axis aggravates acute lung injury”
  258. Retraction of “lncRNA ACTA2-AS1 inhibits malignant phenotypes of gastric cancer cells”
  259. Special issue Linking Pathobiological Mechanisms to Clinical Application for cardiovascular diseases
  260. Effect of cardiac rehabilitation therapy on depressed patients with cardiac insufficiency after cardiac surgery
  261. Special issue The evolving saga of RNAs from bench to bedside - Part I
  262. FBLIM1 mRNA is a novel prognostic biomarker and is associated with immune infiltrates in glioma
  263. Special Issue Computational Intelligence Methodologies Meets Recurrent Cancers - Part III
  264. Development of a machine learning-based signature utilizing inflammatory response genes for predicting prognosis and immune microenvironment in ovarian cancer
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