Home ABI3BP can inhibit the proliferation, invasion, and epithelial–mesenchymal transition of non-small-cell lung cancer cells
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ABI3BP can inhibit the proliferation, invasion, and epithelial–mesenchymal transition of non-small-cell lung cancer cells

  • Jian Wu , Xiaokun Yan EMAIL logo and Zewen Cheng
Published/Copyright: March 11, 2025

Abstract

Lung cancer, especially non-small-cell lung cancer (NSCLC), has a poor 5-year survival rate below 20%, with factors like smoking, air pollution, and genetic mutations contributing to its development. ABI3BP, an extracellular matrix protein, inhibits NSCLC progression by regulating key signaling pathways; however, its exact mechanisms remain elusive. This study aimed to explore ABI3BP’s role in NSCLC and its impact on these pathways. We found that ABI3BP expression was significantly reduced in NSCLC cells compared to normal controls. Overexpression of ABI3BP in NSCLC cells resulted in a substantial reduction in cell growth and motility and induced cell cycle arrest. Furthermore, its overexpression suppressed the epithelial–mesenchymal transition (EMT) process in NSCLC cells. In addition, ABI3BP overexpression inhibited the MAPK/ERK pathway in NSCLC cells. Collectively, ABI3BP functions as a tumor suppressor in NSCLC by targeting the MAPK/ERK axis, thereby regulating cell proliferation, motility, and EMT. These findings suggest that ABI3BP represents a potential therapeutic target for NSCLC treatment.

Graphical abstract

1 Introduction

Lung cancer remains one of the most prevalent malignancies worldwide, accounting for a significant proportion of cancer-related deaths in both men and women [1,2]. Non-small-cell lung cancer (NSCLC) represents approximately 85% of all lung cancer cases, with more than 60% of patients being diagnosed at advanced stages [3]. The 5-year survival rate for NSCLC remains dismal, at less than 20% [4]. Although smoking is a primary cause of lung cancer, a considerable number of cases occur in non-smokers due to factors such as air pollution, environmental exposure, genetic mutations, and single nucleotide polymorphisms [5]. These observations underscore the urgent need for novel diagnostic and therapeutic strategies that address both the etiology and progression of NSCLC.

The ABI family member 3 binding protein (ABI3BP) is a key extracellular matrix protein known to regulate cell proliferation, differentiation, and signal transduction in various tissues [6]. ABI3BP is integral to modulating key signaling pathways, particularly the MAPK/ERK pathway [7], which plays a vital role in cell proliferation, differentiation, and survival [8]. By inhibiting this pathway, ABI3BP can suppress uncontrolled cell growth, thereby impeding the progression of malignancies. Additionally, ABI3BP interacts with other critical pathways, including the PI3K/Akt and TGF-β cascades, both of which are involved in tumorigenesis and metastasis [6]. Through these interactions, ABI3BP exerts a wide range of biological effects, including cell cycle arrest, epithelial–mesenchymal transition (EMT) inhibition, and reduced invasive potential [6,9]. ABI3BP’s activity is not limited to lung cancer; it has also demonstrated tumor-suppressive functions in other malignancies, such as esophageal and breast cancers, where it downregulates oncogenic signals, making it a versatile tumor suppressor across different cancer types [10,11]. Notably, ABI3BP interacts with oncogenic pathways, potentially serving as a multifaceted regulator of tumor biology [12]. Reduced expression of ABI3BP has been associated with tumor progression and metastasis, highlighting its pivotal role in tumor suppression.

In NSCLC, however, the specific role of ABI3BP remains inadequately understood. This study investigates the therapeutic potential of ABI3BP in NSCLC, hypothesizing that it suppresses NSCLC progression through the regulation of key signaling pathways.

2 Materials and methods

2.1 Cell lines and cell culture

Human NSCLC cell lines HCC-827, A549, NCI-H460, and H1975, as well as normal bronchial epithelial cells (BEAS-2B), were purchased from ATCC. All cell lines were cultured in RPMI-1640 medium (Gibco, USA) supplemented with 10% fetal bovine serum (FBS, Gibco), 100 U/mL penicillin, and 100 μg/mL streptomycin (Gibco). Cells were maintained at 37°C in a humidified incubator with 5% CO2.

2.2 Reagents and antibodies

Adenoviral vectors expressing ABI3BP (ad-ABI3BP) and control adenovirus (ad-NC) were purchased from Vigene Biosciences (China). Western blot analyses were performed using primary antibodies from Abcam, including anti-ABI3BP (ab154189, 1:1,000), anti-E-cadherin (ab40772, 1:1,000), anti-N-cadherin (ab18203, 1:1,000), anti-α-SMA (ab5694, 1:1,000), anti-AKT (ab8805, 1:1,000), anti-phospho-AKT (ab38449, 1:1000), anti-ERK1/2 (ab184699, 1:1,000), and anti-phospho-ERK1/2 (ab201015, 1:1,000). Horseradish peroxide (HRP)-conjugated secondary antibodies were diluted at 1:5,000 (Abcam).

2.3 Adenovirus infection

Cells were infected with ad-ABI3BP or ad-NC adenoviruses at a multiplicity of infection of 100. The infection process was carried out for 24 h in serum-free medium, followed by incubation in complete medium for further experiments.

2.4 Immunoblot analysis

Samples were separated on sodium dodecyl sulfate-polyacrylamide gel electrophoresis gels and transferred to polyvinylidene difluoride membranes (Millipore, USA). After blocking with 5% non-fat milk, membranes were incubated overnight at 4°C with the primary antibodies, followed by incubation with HRP-conjugated secondary antibodies for 1 h at room temperature. Protein bands were visualized using an enhanced chemiluminescence detection kit (Beyotime), and band intensities were quantified using ImageJ software.

2.5 Cell viability assay

Cell viability was assessed using the Cell Counting Kit-8 (CCK-8, Beyotime) following the manufacturer’s instructions. Absorbance was measured at 450 nm using a microplate reader (Thermo Fisher, USA).

2.6 Migration and invasion assays

Cell migration and invasion were evaluated using Transwell assays (Corning, USA). For the migration assay, 1 × 10⁵ cells in serum-free medium were placed in the upper chamber of a Transwell insert. The lower chamber was filled with RPMI-1640 medium containing 10% FBS. For the invasion assay, the upper chamber was pre-coated with Matrigel (Corning), and 2 × 10⁵ cells were seeded. After 24 h, cells on the lower surface of the insert were fixed in 4% paraformaldehyde and stained with 0.1% crystal violet. The number of migrated or invaded cells was counted in five randomly selected fields using a light microscope (Zeiss, Germany).

2.7 FCM assay

The cells were washed with PBS and fixed using 70% ethanol at −20°C for 2 h. Subsequently, the cells were stained with propidium iodide at 4°C. The stained cells were then analyzed using a flow cytometer (BD, USA).

2.8 Statistical analysis

Data are expressed as mean ± standard deviation (SD). Statistical significance was determined using one-way ANOVA followed by Tukey’s post hoc test for multiple comparisons. A p-value of <0.05 was considered statistically significant.

3 Results

3.1 ABI3BP expression was significantly downregulated in NSCLC cells

To assess the expression of ABI3BP in NSCLC, we first measured its levels through the TCGA database. We observed that ABI3BP had a lower TPM value in NSCLC tissues compared to normal tissues (Figure 1a). Subsequently, we detected the expression of ABI3BP in both normal bronchial epithelial cells (BEAS-2B) and NSCLC cell lines (HCC-827, A549, NCI-H460, and H1975). Immunoblot analysis revealed that ABI3BP expression was significantly lower in all NSCLC cell lines compared to normal bronchial epithelial cells (Figure 1b). Quantification of ABI3BP protein levels confirmed the marked reduction in its expression in NSCLC cells (Figure 1b). Thus, ABI3BP expression was significantly downregulated in NSCLC cells.

Figure 1 
                  ABI3BP expression was significantly downregulated in NSCLC cells. (a) TCGA database showed the TPM (transcripts per million) value of ABI3BP in 338 normal tissues and 486 tumor tissues. (b) Immunoblot showing ABI3BP protein expression levels in normal bronchial epithelial cells (BEAS-2B) and NSCLC cell lines (HCC-827, A549, NCI-H460, H1975). Quantification of ABI3BP protein expression was shown. Data are represented as mean ± SD. *p < 0.05, **p < 0.01. NSCLC, non-small-cell lung cancer.
Figure 1

ABI3BP expression was significantly downregulated in NSCLC cells. (a) TCGA database showed the TPM (transcripts per million) value of ABI3BP in 338 normal tissues and 486 tumor tissues. (b) Immunoblot showing ABI3BP protein expression levels in normal bronchial epithelial cells (BEAS-2B) and NSCLC cell lines (HCC-827, A549, NCI-H460, H1975). Quantification of ABI3BP protein expression was shown. Data are represented as mean ± SD. *p < 0.05, **p < 0.01. NSCLC, non-small-cell lung cancer.

3.2 Overexpression of ABI3BP in NSCLC cells led to a marked reduction in cell growth as well as motility

Next, we evaluated the effect of ABI3BP overexpression on cell viability using the CCK8 assay. HCC-827 and NCI-H460 cells were transfected with either control (ad-NC) or ABI3BP-expressing adenovirus (ad-ABI3BP), and the overexpression efficiency was confirmed by Immunoblot (Figure 2a). Further, CCK-8 assays showed that overexpression of ABI3BP led to a significant decrease in cell viability in both NSCLC cell lines compared to the control and ad-NC groups (Figure 2b). However, its overexpression has modest effects on the viability of BEAS-2B cells (Figure 2b). Colony formation assays further confirmed that the overexpression of ABI3BP suppressed the proliferation of HCC-827 and NCI-H460 cells (Figure 2c). Transwell migration and invasion assays were performed using HCC-827 and NCI-H460 cells. The results indicated that overexpression of ABI3BP significantly reduced the migratory capacity of both cell lines compared to the control groups (Figure 2d). In contrast, ABI3BP overexpression did not affect the migration of BEAS-2B cells, as confirmed by Transwell assays (Figure 2d). Additionally, the invasive ability of HCC-827 and NCI-H460 cells was also markedly suppressed following ABI3BP overexpression (Figure 2e). Further, the overexpression of ABI3BP led to the cell cycle arrest in HCC-827 and NCI-H460 cells (Figure 2f). Therefore, overexpression of ABI3BP in NSCLC cells resulted in a significant reduction in cell growth as well as motility.

Figure 2 
                  Overexpression of ABI3BP in NSCLC cells led to a marked reduction in cell growth as well as motility. (a) Immunoblot showing ABI3BP protein levels in HCC-827 and NCI-H460 cells upon the indicated infection. GAPDH was used as the loading control. Quantification of relative ABI3BP expression is shown on the right. (b) Cell viability assay (CCK8) results for BEAS-2B, HCC-827, and NCI-H460 cells following overexpression of ABI3BP. The survival rate (%) is shown for the control, ad-NC, and ad-ABI3BP groups. (c) Colony formation assays showed the effects of ABI3BP overexpression on the proliferation of HCC-827 and NCI-H460 cells. The colony numbers were counted. (d) Transwell migration assay of BEAS-2B, HCC-827, and NCI-H460 cells with images showing migrated cells in each group. Quantification of migrated cells is shown on the right. (e) Transwell invasion assay of HCC-827 and NCI-H460 cells with images showing invaded cells in each group. (f) FCM assays showed the effects on the cell cycle of HCC-827 and NCI-H460 cells. The cells at different phases were calculated. Quantification of invaded cells is shown on the right. Data are represented as mean ± SD. **p < 0.01, ad-ABI3BP vs ad-NC. NSCLC, non-small-cell lung cancer. NC, negative control.
Figure 2

Overexpression of ABI3BP in NSCLC cells led to a marked reduction in cell growth as well as motility. (a) Immunoblot showing ABI3BP protein levels in HCC-827 and NCI-H460 cells upon the indicated infection. GAPDH was used as the loading control. Quantification of relative ABI3BP expression is shown on the right. (b) Cell viability assay (CCK8) results for BEAS-2B, HCC-827, and NCI-H460 cells following overexpression of ABI3BP. The survival rate (%) is shown for the control, ad-NC, and ad-ABI3BP groups. (c) Colony formation assays showed the effects of ABI3BP overexpression on the proliferation of HCC-827 and NCI-H460 cells. The colony numbers were counted. (d) Transwell migration assay of BEAS-2B, HCC-827, and NCI-H460 cells with images showing migrated cells in each group. Quantification of migrated cells is shown on the right. (e) Transwell invasion assay of HCC-827 and NCI-H460 cells with images showing invaded cells in each group. (f) FCM assays showed the effects on the cell cycle of HCC-827 and NCI-H460 cells. The cells at different phases were calculated. Quantification of invaded cells is shown on the right. Data are represented as mean ± SD. **p < 0.01, ad-ABI3BP vs ad-NC. NSCLC, non-small-cell lung cancer. NC, negative control.

3.3 ABI3BP overexpression suppressed the EMT process of NSCLC cells

Since EMT plays a crucial role in cancer metastasis, we examined whether ABI3BP influences EMT markers in NSCLC cells. Western Immunoblot analysis revealed that ABI3BP overexpression increased the expression of the epithelial marker E-cadherin and decreased the expression of mesenchymal markers N-cadherin and α-SMA in both HCC-827 (Figure 3a) and NCI-H460 (Figure 3b) cells. These findings suggest that ABI3BP inhibits EMT, thereby reducing the invasive potential of NSCLC cells.

Figure 3 
                  ABI3BP overexpression suppressed the EMT process of NSCLC cells. (a) and (b) Immunoblot showing E-cadherin, N-cadherin, and α-SMA protein levels in HCC-827 (a) and NCI-H460 (b) cells upon the indicated infection. GAPDH was used as the loading control. Quantification of relative E-cadherin, N-cadherin, and α-SMA expression is shown on the right. Data are represented as mean ± SD. **p < 0.01, ad-ABI3BP vs ad-NC. NSCLC, non-small-cell lung cancer. NC, negative control.
Figure 3

ABI3BP overexpression suppressed the EMT process of NSCLC cells. (a) and (b) Immunoblot showing E-cadherin, N-cadherin, and α-SMA protein levels in HCC-827 (a) and NCI-H460 (b) cells upon the indicated infection. GAPDH was used as the loading control. Quantification of relative E-cadherin, N-cadherin, and α-SMA expression is shown on the right. Data are represented as mean ± SD. **p < 0.01, ad-ABI3BP vs ad-NC. NSCLC, non-small-cell lung cancer. NC, negative control.

3.4 ABI3BP overexpression suppressed MAPK/ERK pathway in NSCLC cells

To explore the molecular mechanisms by which ABI3BP regulates NSCLC cell proliferation and migration, we investigated the MAPK/ERK pathway. Immunoblot analysis revealed that overexpression of ABI3BP reduced the phosphorylation of ERK and Akt in both HCC-827 (Figure 4a) and NCI-H460 (Figure 4b) cells, indicating that ABI3BP inhibits the MAPK/ERK pathway. These results suggest that ABI3BP suppresses NSCLC progression by modulating the MAPK/ERK pathway.

Figure 4 
                  ABI3BP overexpression suppressed the MAPK/ERK pathway in NSCLC cells. (a) and (b) Immunoblot showing ERK and AKT protein levels and phosphorylation levels in HCC-827 (a) and NCI-H460 (b) cells upon the indicated infection. GAPDH was used as the loading control. Quantification of relative phosphorylation levels of ERK and AKT is shown on the right. Data are represented as mean ± SD. **p < 0.01, ad-ABI3BP vs ad-NC. NSCLC, non-small-cell lung cancer. NC, negative control.
Figure 4

ABI3BP overexpression suppressed the MAPK/ERK pathway in NSCLC cells. (a) and (b) Immunoblot showing ERK and AKT protein levels and phosphorylation levels in HCC-827 (a) and NCI-H460 (b) cells upon the indicated infection. GAPDH was used as the loading control. Quantification of relative phosphorylation levels of ERK and AKT is shown on the right. Data are represented as mean ± SD. **p < 0.01, ad-ABI3BP vs ad-NC. NSCLC, non-small-cell lung cancer. NC, negative control.

4 Discussion

NSCLC is the most prevalent form of lung cancer, comprising around 85% of all lung cancer diagnoses. It is highly aggressive, characterized by rapid cell proliferation, migration, and EMT, which collectively drive tumor progression and metastasis [13,14,15,16]. These biological processes are regulated by several key signaling pathways and proteins that ensure proper cellular function. Disruption of these pathways often leads to poor clinical outcomes in NSCLC patients. In our study, we explored the role of ABI3BP in regulating cell proliferation, migration, and EMT, providing insights into its potential therapeutic relevance in NSCLC.

EMT plays a crucial role in advancing cancer by enhancing the metastatic ability of cancer cells [17]. Through this process, epithelial cells acquire mesenchymal traits, thereby increasing their capacity for migration and invasion. EMT is also implicated in resistance to cancer therapies, making it a critical target in NSCLC treatment strategies. Our findings revealed that ABI3BP overexpression led to a significant reduction in EMT in NSCLC cells, as evidenced by altered levels of EMT markers, such as E-cadherin and N-cadherin. These results underscore the importance of targeting EMT to limit the metastatic potential of NSCLC.

ABI3BP, a vital extracellular matrix protein, is involved in the regulation of various cellular functions such as cell growth, differentiation, and programmed cell death. Its role as a tumor suppressor has been established in multiple cancer types, including esophageal and gallbladder cancers, where it inhibits cellular proliferation and migration [10,11]. ABI3BP’s interactions with key signaling pathways, including MAPK/ERK and PI3K/Akt, are essential for its tumor-suppressive activities. In this study, we observed that overexpression of ABI3BP in NSCLC cells led to reduced proliferation and invasion, consistent with its known role as a tumor suppressor.

Beyond these general cellular effects, ABI3BP exerts specific control over EMT, as well as cell proliferation and migration in NSCLC [18]. Our research demonstrated that ABI3BP overexpression decreased EMT-related markers, notably reducing N-cadherin levels while increasing E-cadherin expression. In addition, ABI3BP was shown to suppress NSCLC cell migration and invasion, suggesting that its inhibition of these processes may be a crucial factor in reducing tumor progression and metastasis. This highlights ABI3BP as a significant modulator of EMT and an inhibitor of NSCLC progression.

ABI3BP overexpression inhibited the MAPK/ERK pathway in NSCLC cells. Previous studies have reported that the MAPK/ERK pathway plays critical in mediating cancer cell proliferation, and its alteration could affect the proliferation of cancer cells, including NSCLC cells [19,20]. The MAPK/ERK and PI3K/Akt pathways are pivotal in regulating cellular processes like proliferation, migration, and survival. Dysregulation of these pathways is common in cancer and is linked to enhanced tumor growth and metastasis [19,20]. The MAPK/ERK pathway is primarily activated in response to growth stimuli, facilitating cell proliferation and survival, while the PI3K/Akt pathway similarly drives cell growth and migration. Both pathways are intimately involved in regulating EMT, and their dysregulation accelerates NSCLC progression. In this study, we found that ABI3BP suppresses the activation of both ERK and Akt, thereby inhibiting NSCLC cell proliferation and EMT. These findings suggest that modulating these pathways through ABI3BP could be a promising approach to NSCLC therapy.

We propose that future research could include in vivo tumor formation experiments in nude mice to further validate the conclusions and clarify the downstream molecular mechanism through multi-omics analysis. Moreover, while we focused on specific pathways, other signaling networks may also contribute to the tumor-suppressive effects of ABI3BP that have not yet been explored. Future research should aim to expand on these findings and investigate the clinical applications of ABI3BP as a therapeutic target.

In summary, our study highlights the tumor-suppressive role of ABI3BP in NSCLC, revealing its ability to regulate key signaling pathways involved in cell proliferation, migration, and EMT. ABI3BP presents a promising target for therapeutic strategies aimed at controlling NSCLC progression. Further research into its mechanistic interactions could lead to the development of novel treatments for NSCLC patients, potentially improving their prognosis.


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  1. Funding information: Authors state no funding involved.

  2. Author contributions: Jian Wu, Xiaokun Yan, Zewen Cheng – designed the study and carried them out; Jian Wu, Xiaokun Yan, Zewen Cheng – supervised the data collection; Jian Wu, Xiaokun Yan, Zewen Cheng – analyzed the data; Jian Wu, Xiaokun Yan, Zewen Cheng – interpreted the data; Jian Wu, Xiaokun Yan – prepared the manuscript for publication and reviewed the draft of the manuscript. All authors have read and approved the manuscript.

  3. Conflict of interest: Authors state no conflict of interest.

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

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Received: 2024-10-10
Revised: 2024-12-03
Accepted: 2024-12-09
Published Online: 2025-03-11

© 2025 the author(s), published by De Gruyter

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

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  60. FTO alleviated the diabetic nephropathy progression by regulating the N6-methyladenosine levels of DACT1
  61. Clinical relevance of inflammatory markers in the evaluation of severity of ulcerative colitis: A retrospective study
  62. Zinc valproic acid complex promotes osteoblast differentiation and exhibits anti-osteoporotic potential
  63. Primary pulmonary synovial sarcoma in the bronchial cavity: A case report
  64. Metagenomic next-generation sequencing of alveolar lavage fluid improves the detection of pulmonary infection
  65. Uterine tumor resembling ovarian sex cord tumor with extensive rhabdoid differentiation: A case report
  66. Genomic analysis of a novel ST11(PR34365) Clostridioides difficile strain isolated from the human fecal of a CDI patient in Guizhou, China
  67. Effects of tiered cardiac rehabilitation on CRP, TNF-α, and physical endurance in older adults with coronary heart disease
  68. Changes in T-lymphocyte subpopulations in patients with colorectal cancer before and after acupoint catgut embedding acupuncture observation
  69. Modulating the tumor microenvironment: The role of traditional Chinese medicine in improving lung cancer treatment
  70. Alterations of metabolites related to microbiota–gut–brain axis in plasma of colon cancer, esophageal cancer, stomach cancer, and lung cancer patients
  71. Research on individualized drug sensitivity detection technology based on bio-3D printing technology for precision treatment of gastrointestinal stromal tumors
  72. CEBPB promotes ulcerative colitis-associated colorectal cancer by stimulating tumor growth and activating the NF-κB/STAT3 signaling pathway
  73. Oncolytic bacteria: A revolutionary approach to cancer therapy
  74. A de novo meningioma with rapid growth: A possible malignancy imposter?
  75. Diagnosis of secondary tuberculosis infection in an asymptomatic elderly with cancer using next-generation sequencing: Case report
  76. Hesperidin and its zinc(ii) complex enhance osteoblast differentiation and bone formation: In vitro and in vivo evaluations
  77. Research progress on the regulation of autophagy in cardiovascular diseases by chemokines
  78. Anti-arthritic, immunomodulatory, and inflammatory regulation by the benzimidazole derivative BMZ-AD: Insights from an FCA-induced rat model
  79. Immunoassay for pyruvate kinase M1/2 as an Alzheimer’s biomarker in CSF
  80. The role of HDAC11 in age-related hearing loss: Mechanisms and therapeutic implications
  81. Evaluation and application analysis of animal models of PIPNP based on data mining
  82. Therapeutic approaches for liver fibrosis/cirrhosis by targeting pyroptosis
  83. Fabrication of zinc oxide nanoparticles using Ruellia tuberosa leaf extract induces apoptosis through P53 and STAT3 signalling pathways in prostate cancer cells
  84. Haplo-hematopoietic stem cell transplantation and immunoradiotherapy for severe aplastic anemia complicated with nasopharyngeal carcinoma: A case report
  85. Modulation of the KEAP1-NRF2 pathway by Erianin: A novel approach to reduce psoriasiform inflammation and inflammatory signaling
  86. The expression of epidermal growth factor receptor 2 and its relationship with tumor-infiltrating lymphocytes and clinical pathological features in breast cancer patients
  87. Innovations in MALDI-TOF Mass Spectrometry: Bridging modern diagnostics and historical insights
  88. BAP1 complexes with YY1 and RBBP7 and its downstream targets in ccRCC cells
  89. Hypereosinophilic syndrome with elevated IgG4 and T-cell clonality: A report of two cases
  90. Electroacupuncture alleviates sciatic nerve injury in sciatica rats by regulating BDNF and NGF levels, myelin sheath degradation, and autophagy
  91. Polydatin prevents cholesterol gallstone formation by regulating cholesterol metabolism via PPAR-γ signaling
  92. RNF144A and RNF144B: Important molecules for health
  93. Analysis of the detection rate and related factors of thyroid nodules in the healthy population
  94. Artesunate inhibits hepatocellular carcinoma cell migration and invasion through OGA-mediated O-GlcNAcylation of ZEB1
  95. Endovascular management of post-pancreatectomy hemorrhage caused by a hepatic artery pseudoaneurysm: Case report and review of the literature
  96. Efficacy and safety of anti-PD-1/PD-L1 antibodies in patients with relapsed refractory diffuse large B-cell lymphoma: A meta-analysis
  97. SATB2 promotes humeral fracture healing in rats by activating the PI3K/AKT pathway
  98. Overexpression of the ferroptosis-related gene, NFS1, corresponds to gastric cancer growth and tumor immune infiltration
  99. Understanding risk factors and prognosis in diabetic foot ulcers
  100. Atractylenolide I alleviates the experimental allergic response in mice by suppressing TLR4/NF-kB/NLRP3 signalling
  101. FBXO31 inhibits the stemness characteristics of CD147 (+) melanoma stem cells
  102. Immune molecule diagnostics in colorectal cancer: CCL2 and CXCL11
  103. Inhibiting CXCR6 promotes senescence of activated hepatic stellate cells with limited proinflammatory SASP to attenuate hepatic fibrosis
  104. Cadmium toxicity, health risk and its remediation using low-cost biochar adsorbents
  105. Pulmonary cryptococcosis with headache as the first presentation: A case report
  106. Solitary pulmonary metastasis with cystic airspaces in colon cancer: A rare case report
  107. RUNX1 promotes denervation-induced muscle atrophy by activating the JUNB/NF-κB pathway and driving M1 macrophage polarization
  108. Morphometric analysis and immunobiological investigation of Indigofera oblongifolia on the infected lung with Plasmodium chabaudi
  109. The NuA4/TIP60 histone-modifying complex and Hr78 modulate the Lobe2 mutant eye phenotype
  110. Experimental study on salmon demineralized bone matrix loaded with recombinant human bone morphogenetic protein-2: In vitro and in vivo study
  111. A case of IgA nephropathy treated with a combination of telitacicept and half-dose glucocorticoids
  112. Analgesic and toxicological evaluation of cannabidiol-rich Moroccan Cannabis sativa L. (Khardala variety) extract: Evidence from an in vivo and in silico study
  113. Wound healing and signaling pathways
  114. Combination of immunotherapy and whole-brain radiotherapy on prognosis of patients with multiple brain metastases: A retrospective cohort study
  115. To explore the relationship between endometrial hyperemia and polycystic ovary syndrome
  116. Research progress on the impact of curcumin on immune responses in breast cancer
  117. Biogenic Cu/Ni nanotherapeutics from Descurainia sophia (L.) Webb ex Prantl seeds for the treatment of lung cancer
  118. Dapagliflozin attenuates atrial fibrosis via the HMGB1/RAGE pathway in atrial fibrillation rats
  119. Glycitein alleviates inflammation and apoptosis in keratinocytes via ROS-associated PI3K–Akt signalling pathway
  120. ADH5 inhibits proliferation but promotes EMT in non-small cell lung cancer cell through activating Smad2/Smad3
  121. Apoptotic efficacies of AgNPs formulated by Syzygium aromaticum leaf extract on 32D-FLT3-ITD human leukemia cell line with PI3K/AKT/mTOR signaling pathway
  122. Novel cuproptosis-related genes C1QBP and PFKP identified as prognostic and therapeutic targets in lung adenocarcinoma
  123. Bee venom promotes exosome secretion and alters miRNA cargo in T cells
  124. Treatment of pure red cell aplasia in a chronic kidney disease patient with roxadustat: A case report
  125. Comparative bioinformatics analysis of the Wnt pathway in breast cancer: Selection of novel biomarker panels associated with ER status
  126. Kynurenine facilitates renal cell carcinoma progression by suppressing M2 macrophage pyroptosis through inhibition of CASP1 cleavage
  127. RFX5 promotes the growth, motility, and inhibits apoptosis of gastric adenocarcinoma cells through the SIRT1/AMPK axis
  128. ALKBH5 exacerbates early cardiac damage after radiotherapy for breast cancer via m6A demethylation of TLR4
  129. Phytochemicals of Roman chamomile: Antioxidant, anti-aging, and whitening activities of distillation residues
  130. Circadian gene Cry1 inhibits the tumorigenicity of hepatocellular carcinoma by the BAX/BCL2-mediated apoptosis pathway
  131. The TNFR-RIPK1/RIPK3 signalling pathway mediates the effect of lanthanum on necroptosis of nerve cells
  132. Longitudinal monitoring of autoantibody dynamics in patients with early-stage non-small-cell lung cancer undergoing surgery
  133. The potential role of rutin, a flavonoid, in the management of cancer through modulation of cell signaling pathways
  134. Construction of pectinase gene engineering microbe and its application in tobacco sheets
  135. Construction of a microbial abundance prognostic scoring model based on intratumoral microbial data for predicting the prognosis of lung squamous cell carcinoma
  136. Sepsis complicated by haemophagocytic lymphohistiocytosis triggered by methicillin-resistant Staphylococcus aureus and human herpesvirus 8 in an immunocompromised elderly patient: A case report
  137. Sarcopenia in liver transplantation: A comprehensive bibliometric study of current research trends and future directions
  138. Advances in cancer immunotherapy and future directions in personalized medicine
  139. Ecology and Environmental Science
  140. Optimization and comparative study of Bacillus consortia for cellulolytic potential and cellulase enzyme activity
  141. The complete mitochondrial genome analysis of Haemaphysalis hystricis Supino, 1897 (Ixodida: Ixodidae) and its phylogenetic implications
  142. Epidemiological characteristics and risk factors analysis of multidrug-resistant tuberculosis among tuberculosis population in Huzhou City, Eastern China
  143. Indices of human impacts on landscapes: How do they reflect the proportions of natural habitats?
  144. Genetic analysis of the Siberian flying squirrel population in the northern Changbai Mountains, Northeast China: Insights into population status and conservation
  145. Diversity and environmental drivers of Suillus communities in Pinus sylvestris var. mongolica forests of Inner Mongolia
  146. Global assessment of the fate of nitrogen deposition in forest ecosystems: Insights from 15N tracer studies
  147. Fungal and bacterial pathogenic co-infections mainly lead to the assembly of microbial community in tobacco stems
  148. Influencing of coal industry related airborne particulate matter on ocular surface tear film injury and inflammatory factor expression in Sprague-Dawley rats
  149. Temperature-dependent development, predation, and life table of Sphaerophoria macrogaster (Thomson) (Diptera: Syrphidae) feeding on Myzus persicae (Sulzer) (Homoptera: Aphididae)
  150. Agriculture
  151. Integrated analysis of transcriptome, sRNAome, and degradome involved in the drought-response of maize Zhengdan958
  152. Variation in flower frost tolerance among seven apple cultivars and transcriptome response patterns in two contrastingly frost-tolerant selected cultivars
  153. Heritability of durable resistance to stripe rust in bread wheat (Triticum aestivum L.)
  154. Molecular mechanism of follicular development in laying hens based on the regulation of water metabolism
  155. Animal Science
  156. Effect of sex ratio on the life history traits of an important invasive species, Spodoptera frugiperda
  157. Plant Sciences
  158. Hairpin in a haystack: In silico identification and characterization of plant-conserved microRNA in Rafflesiaceae
  159. Widely targeted metabolomics of different tissues in Rubus corchorifolius
  160. The complete chloroplast genome of Gerbera piloselloides (L.) Cass., 1820 (Carduoideae, Asteraceae) and its phylogenetic analysis
  161. Field trial to correlate mineral solubilization activity of Pseudomonas aeruginosa and biochemical content of groundnut plants
  162. Correlation analysis between semen routine parameters and sperm DNA fragmentation index in patients with semen non-liquefaction: A retrospective study
  163. Plasticity of the anatomical traits of Rhododendron L. (Ericaceae) leaves and its implications in adaptation to the plateau environment
  164. Effects of Piriformospora indica and arbuscular mycorrhizal fungus on growth and physiology of Moringa oleifera under low-temperature stress
  165. Effects of different sources of potassium fertiliser on yield, fruit quality and nutrient absorption in “Harward” kiwifruit (Actinidia deliciosa)
  166. Comparative efficiency and residue levels of spraying programs against powdery mildew in grape varieties
  167. The DREB7 transcription factor enhances salt tolerance in soybean plants under salt stress
  168. Using plant electrical signals of water hyacinth (Eichhornia crassipes) for water pollution monitoring
  169. Food Science
  170. Phytochemical analysis of Stachys iva: Discovering the optimal extract conditions and its bioactive compounds
  171. Review on role of honey in disease prevention and treatment through modulation of biological activities
  172. Computational analysis of polymorphic residues in maltose and maltotriose transporters of a wild Saccharomyces cerevisiae strain
  173. Optimization of phenolic compound extraction from Tunisian squash by-products: A sustainable approach for antioxidant and antibacterial applications
  174. Liupao tea aqueous extract alleviates dextran sulfate sodium-induced ulcerative colitis in rats by modulating the gut microbiota
  175. Toxicological qualities and detoxification trends of fruit by-products for valorization: A review
  176. Polyphenolic spectrum of cornelian cherry fruits and their health-promoting effect
  177. Optimizing the encapsulation of the refined extract of squash peels for functional food applications: A sustainable approach to reduce food waste
  178. Advancements in curcuminoid formulations: An update on bioavailability enhancement strategies curcuminoid bioavailability and formulations
  179. Impact of saline sprouting on antioxidant properties and bioactive compounds in chia seeds
  180. The dilemma of food genetics and improvement
  181. Bioengineering and Biotechnology
  182. Impact of hyaluronic acid-modified hafnium metalorganic frameworks containing rhynchophylline on Alzheimer’s disease
  183. Emerging patterns in nanoparticle-based therapeutic approaches for rheumatoid arthritis: A comprehensive bibliometric and visual analysis spanning two decades
  184. Application of CRISPR/Cas gene editing for infectious disease control in poultry
  185. Preparation of hafnium nitride-coated titanium implants by magnetron sputtering technology and evaluation of their antibacterial properties and biocompatibility
  186. Preparation and characterization of lemongrass oil nanoemulsion: Antimicrobial, antibiofilm, antioxidant, and anticancer activities
  187. Corrigendum
  188. Corrigendum to “Utilization of convolutional neural networks to analyze microscopic images for high-throughput screening of mesenchymal stem cells”
  189. Corrigendum to “Effects of Ire1 gene on virulence and pathogenicity of Candida albicans
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