Volume 50, Issue 5

As one of the volatile anaesthetic drugs commonly used in clinical anaesthesia, sevoflurane is extensively used in general anaesthesia surgery because of its rapid induction, hemodynamic stability, and rapid metabolism. However, postoperative cognitive dysfunction (POCD) is the most prevalent complications of its clinical application. Neuroinflammation and neuronal apoptosis are currently believed to be the primary mechanisms responsible for the development of cognitive dysfunction. MicroRNAs (miRNAs) can negatively regulate the expression of target genes, thereby influencing neurological and cognitive processes. Therefore, the effects and potential mechanisms of miRNAs on cognitive function may provide new ideas for the prevention and treatment of sevoflurane-induced POCD, a topic of intense research interest at the moment. The mechanisms involved in sevoflurane-induced POCD, the regulation of miRNAs expression by sevoflurane, and the effects of miRNAs on target genes and downstream signalling pathways were reviewed in order to obtain a comprehensive understanding of the effects of miRNAs on cognitive function.

Objectives This study compares the effectiveness and safety of bexagliflozin and tirzepatide in type 2 diabetes mellitus, focusing on HbA1c, body weight, fasting plasma glucose, blood pressure, hypoglycemia, and adverse events using data from randomized controlled trials. Methods A systematic review and meta-analysis of randomized controlled trials (RCTs) was conducted using MEDLINE, EMBASE, PubMed, Google Scholar, and Cochrane. Eligible studies included head-to-head and placebo-controlled RCTs on bexagliflozin and tirzepatide. Primary outcome: HbA1c reduction; secondary outcomes: body weight, fasting plasma glucose, blood pressure, hypoglycemia, and adverse events. In this meta-analysis, the efficacy of bexagliflozin and tirzepatide was compared across key outcomes. Results Tirzepatide showed significant reduction in HbA1c (Mean difference [MD]: −1.29 %, p<0.001), while bexagliflozin had minimal reduction (MD: −0.18 %, p=0.28). In weight loss, tirzepatide outperformed bexagliflozin (MD: −11.18 kg, p<0.001 vs. −1.68 kg, p=0.04). Tirzepatide significantly reduced fasting plasma glucose (MD: −1.48 mmol/L, p<0.001) and systolic blood pressure (MD: −8.01 mmHg, p<0.001), while bexagliflozin showed non-significant effects. Safety analysis revealed no significant differences in major adverse cardiovascular events or serious adverse events. Bexagliflozin was associated with higher odds of treatment-emergent adverse events (OR: 1.71, p=0.009) and a trend toward increased gastrointestinal events (OR: 3.66, p=0.07). Conclusions Tirzepatide had a favorable safety profile with no significant increase in adverse events. Tirzepatide demonstrated superior efficacy in glycemic control, weight reduction, and cardiovascular parameters compared to bexagliflozin, alongside a more favorable safety profile. These findings support tirzepatide as a promising therapeutic option in type 2 diabetes mellitus management.

Objectives Despite the wide acceptability of laboratory assessments during the fasting state in clinical practice, emerging evidence suggests that non-fasting testing offers a convenient alternative, especially for the estimation of lipid profile. The present study aimed to compare fasting and non-fasting lipid, liver, and renal profiles and define desirable cut-off values for the main determinants of dyslipidemia in non-fasting in apparently healthy adults. Methods A total of 485 apparently healthy adults aged between 30 and 60 years in Southern, Sri Lanka were recruited in the present cross-sectional study. Fasting lipid profile, liver, and renal parameters were estimated in the fasting and non-fasting states on the same day in the same individuals. Results Significant mean differences between non-fasting and fasting triglyceride, high density lipoprotein cholesterol (HDL cholesterol), low density lipoprotein cholesterol (LDL cholesterol), very low-density lipoprotein cholesterol, and creatinine were found as +0.048 mmol/L, −0.080 mmol/L, −0.213 mmol/L, +0.013 mmol/L, and −40.842 μmol/L respectively. There were no significant differences in total cholesterol (TC), non-HDL cholesterol, alanine transaminase, aspartate aminotransferase, and urea between fasting and non-fasting serum samples. Conclusions Small differences and strong correlations in lipid, liver, and renal parameters between fasting and non-fasting states revealed that the non-fasting sample could be used in the screening of healthy adults for dyslipidemia, abnormalities in the liver, and renal functions, except for the estimation of serum creatinine. The optimal cut-off values for non-fasting TC, triglyceride, and LDL cholesterol were 5.33 mmol/L, 1.70 mmol/L, and 3.62 mmol/L, respectively, to diagnose dyslipidemia in apparently healthy adults.

Objectives Peripheral vascular disease (PVD) is an atherosclerotic disease by the occlusion of arteries in the lower extremities. Buerger’s disease is autoimmune due to inflammation of small and medium-sized vessels. The aim was to investigate the relations among adiponectin, leptin, resistin, and variants of ADIPOQ −11,377   C/G, LEP2548G/A, RETN −420   G/C in PVD and Buerger’s disease. Methods The study group consisted of 151 patients (127 PVD, 24 Buerger’s disease). Adiponectin, leptin, and resistin were analyzed by ELISA. ADIPOQ −11377   C/G, LEP2548G/A, and RETN −420   G/C were genotyped with designed primers, and probes in LightCycler 480. Results Adiponectin was found to be insignificantly higher in the PVD than that Buerger’s disease (p=0.17). Leptin was found to be significantly lower in the Buerger’s disease than in the PVD (p=0.018). The relationships were among age and leptin (r= −0.264; p=0.047), ankle brachial index (ABI) (r= −0.206; p=0.045), adiponectin (r=0.210; p=0.026) in PVD. In Buerger’s disease, resistin and leptin had a significant relationship (r= −0.508; p=0.019). Conclusions It is thought that the high serum leptin levels observed in the Buerger group carrying the ADIPOQ GG genotype and the PVD group carrying the RETN GG genotype may be related to the etiopathogenesis of both diseases. Our study is the first to examine the proteins and genetic variations of adipokines in the PVD and Buerger’s disease in Turkish population, and will provide direction for future studies to be conducted with the variants of leptin, adiponectin, resistin, and related proteins.

Objectives Erythrocyte membrane disorders are caused by a deficiency of structural proteins in the erythrocyte membrane. Accurate differential diagnosis within this group of disorders (is essential for appropriate management. The eosin-5′-maleimide (EMA) binding assay is a novel test that is used for the differential diagnosis of erythrocyte membrane disorders. In this study, we have examined and reported blood counts, reticulocyte indices, and the EMA binding assay results with clinical findings of cases admitted to our laboratory for suspected red blood cell (RBC) membrane disorder. Methods We performed the EMA binding assay on the blood samples of 103 patients who were screened for hereditary erythrocyte membrane disorders at the Flow Cytometry Laboratory of Ankara Numune Training and Research Hospital. The total cohort was grouped as patients with hereditary spherocytosis (HS) (n=36) and control group (patients without erythrocyte membrane disorders (n=60), and non-HS patients with a preliminary diagnosis of hemolytic anemia (n=7). The control group included during data collection, the results of the EMA binding assay were recorded along with demographic features, clinical information, morphologic features, blood count parameters, RBC and reticulocyte indices, and a conventional osmotic fragility (OF) test. Receiver Operating Characteristics (ROC) analyses were performed to evaluate the diagnostic accuracy of the EMA binding assay and reticulocyte parameters. Results Both EMA testing and flow cytometric (FC) OF test were significantly lower in overall (n=36), ≤10-year-old (n=12), and >10-year-old (n=24) patients with HS than in healthy controls (p<0.001). The EMA binding assay had 100 % sensitivity and specificity in screening HS. Conclusions Combined with conventional blood tests, clinical findings, and medical history, the EMA binding assay is a reliable and convenient tool for screening for HS and differentiating hereditary erythrocyte membrane disorders.

Objectives Hashimoto’s thyroiditis (HT) is a complex metabolic autoimmune disease. FOXs participate in many cellular metabolic processes and control many related genes. This study aimed to investigate FOXO1, FOXP1 and FOXP2 protein levels in HT disease. Methods The study included 38 patients diagnosed with HT and 38 healthy individuals at the Department of Endocrinology and Metabolic Diseases at Sivas Cumhuriyet University Hospital. Venous blood samples were taken from the individuals in the study groups and serum was obtained. Serum FOXO1, FOXP1 and FOXP2 protein levels were analyzed using the enzyme-linked immunosorbent assay (ELISA) method. Results Serum FOXO1 and FOXP2 protein levels were found to be lower in the HT patient group compared to the control group (p< 0.001 ). FOXP1 concentration was found to be lower in the patient group, but this decrease was not significant (p> 0.05 ). Thyroid stimulating hormone (TSH), anti TPO, antithyroglobulin (anti Tg) and AST levels were found to be higher in HT patients compared to the control group, while T4 levels were found to be lower. According to protein-protein interaction (PPI) analysis, these proteins were found to interact highly with each other and are generally involved in T cell mechanisms. Conclusions HT is a common autoimmune disease and is metabolically associated with many pathways. This cross-sectional study is only a preliminary study on the possible association between HT and FOX family proteins.

Objectives Infantile colic is a common disorder characterized by excessive crying in infants, with its etiology remaining largely unclear. In this study, the potential role of core circadian rhythm (CR) proteins in infantile colic was investigated. Methods Our study comprised 61 infants aged 0–3 months. Blood samples were collected intravenously from each individual. They were then centrifuged using the appropriate technique and divided into small portions. Cry1, Cry2, Per1, Per2, Clock, and Bmal1 protein levels in plasma samples were measured using enzyme-linked immunosorbent assay (ELISA) kits. A detailed questionnaire was administered to address various factors related to both the mother and the infant. The possible relationships between the measured CR protein levels and the gathered natal and sociodemographic data were then assessed using multiple regression analysis. Results The findings indicate that CR protein levels in infants with colic are significantly different from the control group, suggesting that CR dysregulation may be associated with colic symptoms. Furthermore, correlations were identified between these protein levels and variables, including vitamin D supplementation, nocturnal sleep patterns, the number of siblings, and maternal gestational diabetes. Statistically significant regression models, specifically those incorporating the Per2 variable, elucidated its associations with nocturnal sleep patterns, sibling counts, and gestational diabetes. Conclusions We argue that restoring CR protein levels to the normal range may improve the prognosis of infantile colic. These findings provide a novel perspective on the potential role of CR proteins in the infantile colic etiology, potentially paving the way for new treatment approaches in this area.

Objectives This study was to investigate the altered expression of SNHG6 in individuals suffering from traumatic brain injury (TBI), as well as the correlation between varying degrees of injury severity and patient’s prognosis, and to explore the impact of SNHG6 on oxygen-glucose deprivation (OGD)-induced cell damage. Methods A cohort of 121 patients with TBI were included in this study, including 71 mild patients and 50 severe patients. Reverse Transcription-Polymerase Chain Reaction (RT-qPCR) was used to determine the levels of SNHG6 and miR-101–3p. Receiver Operating Characteristic (ROC) curves were used to analyze the role of SNHG6 in distinguishing TBI patients with different degrees and TBI patients with different prognosis. The cell model was constructed by OGD damage, the cell proliferation capacity was detected by Cell Counting Kit-8 (CCK-8) assay, and the concentrations of inflammatory factors in the cells were detected by ELISA kit. Results Patients with severe TBI had higher levels of SNHG6 expression than those with mild TBI. And the expression of SNHG6 in patients with poor prognosis was higher than that in patients with good prognosis. SNHG6 could distinguish severe TBI patients from those mild TBI patients and predict the prognosis of patients with TBI. SNHG6 regulated cell proliferation and inflammation after OGD injury by inhibiting the expression of miR-101–3p. Conclusions SNHG6 may be a biomarker for TBI, SNHG6 may affect TBI by regulating the expression of miR-101–3p.

Objectives The target of this study was to explore the value of miR-142-5p for diagnosis and prognosis in patients with acute coronary syndrome (ACS). Methods RT-qPCR was utilized to investigate serum miR-142-5p in 77 ACS patients, 65 stable angina pectoris (SAP) patients, and 70 healthy volunteers. Receiver Operating Characteristic (ROC) curves were developed to estimate the clinical diagnostic importance of miR-142-5p for ACS. Kaplan-Meier and Cox regression were utilized to estimate the prognostic value of miR-142-5p for the incidence of major adverse cardiovascular events (MACE) during the 6-month post-treatment surveillance period after percutaneous coronary intervention (PCI) in patients with ACS. Results Serum miR-142-5p was significantly higher in ACS patients than in healthy controls (HC) and SAP groups. ROC curve indicated that serum miR-142-5p was effective in distinguishing ACS patients from HC and also distinguishing ACS patients from SAP patients. Pearson correlation coefficients confirmed that miR-142-5p was positively correlated with cardiac troponin I (cTnI, r=0.690) and Gensini score (GS, r=0.734). Furthermore, patients with high miR-142-5p expression had a greater probability of developing MACE after PCI treatment (Log Rank=0.016), which is an independent prognostic biomarker for ACS. Conclusions miR-142-5p expression was significantly elevated in the serum of ACS patients. It not only demonstrates a strong correlation with an elevated risk of MACE following PCI, but also exhibits diagnostic utility and serves as an independent prognostic biomarker. It is a promising biomarker for the diagnosis and prognosis of ACS.

Objectives Timely prediction of esophageal varices (EV) in cirrhotic patients is an effective step in the clinical management of cirrhotic patients. The aim of this study was to investigate the potential of microRNA-186-5p (miR-186-5p) a risk factor for EV in cirrhotic patients. Methods Serum miR-186-5p was detected by RT-qPCR assay. ROC curve was employed to assess the possibility of miR-186-5p in the diagnosis of cirrhosis and EV. Moreover, the pathological mechanism of miR-186-5p target genes in EV was elucidated by GO and KEGG analysis. Results miR-186-5p was downregulated in cirrhotic patients and had high diagnostic value in identifying cirrhosis. Meanwhile, miR-186-5p expression was decreased in EV patients with cirrhosis. Downregulation of miR-186-5p may sensitively predict the occurrence of EV in cirrhotic patients. Moreover, pathomechanism analysis elaborated that miR-186-5p downstream target genes were highly accumulated in regulation of mRNA processing, endoplasmic reticulum-Golgi intermediate compartment, protein serine/threonine kinase activity,and autophagy-animal. Conclusions miR-186-5p has high accuracy in predicting cirrhosis occurrence and identifying EV.

Objectives The skin altered by burn injury has the capacity to revert to its normal function and structure. Nonetheless, the exact mechanism behind this restoration remains unclear. This study was to examine the function of miR-199a-5p in the migration and proliferation of fibroblasts affected by burn injury. Methods The miR-199a-5p expression was assessed using quantitative real-time polymerase chain reaction (qRT-PCR). The proliferation and migration capacity of human skin fibroblast (HSF) cells were measured by CCK-8 and Transwell assay. The protein levels of vascular endothelial growth factor A (VEGFA), phosphorylated phosphoinositide 3-kinases (p-PI3K), phosphorylated protein kinase B (p-AKT), and phosphorylated endothelial nitric oxide synthase (p-eNOS) were assessed via western blot assay. Results The miR-199a-5p levels were decreased in individuals with burn injuries as well as in burn-denatured HSF cells, at the same time, there was an increase in the VEGFA mRNA levels. miR-199a-5p negatively regulated VEGFA, which in turn suppressed the migration and proliferation of HSF cells. Additionally, miR-199a-5p inhibited the PI3K/AKT/eNOS signaling pathway through the regulation of VEGFA. Conclusions miR-199a-5p regulates proliferation and migration of burn degenerated fibroblasts by targeting VEGFA.

Objectives This study investigates diagnosis of upper respiratory diseases with similar clinical symptoms, specifically COVID-19, originated from the SARS-CoV-2 virus, and Influenza infections associated with Influenza viruses. Effective treatment relies on rapid and accurate diagnosis, especially due to pandemic potential. This research aims to develop a multiplex lateral flow assay (LFA) based diagnosis method for detecting SARS-CoV-2 and Influenza A H1N1 viruses simultaneously. Methods Lateral flow assay utilizing gold nanoparticles were developed with specific monoclonal antibodies targeting the nucleocapsid (NP) protein of SARS-CoV-2 and the hemagglutinin (HA) protein of Influenza A H1N1. Multiplexing was achieved by immobilizing two different capture antibodies for both targets on the same test. Recombinant antigens were employed to perform analytical assessments of specificity and cross-reactivity. Results The limit of detection (LOD) of the developed system in both single and multiplex formats was found to be: 1 ng/mL for SARS-CoV-2 NP, 1 × 10 3  PFU/mL for active viruses and 5 ng/mL for Influenza A H1N1 HA. Negative control experiments confirmed no cross-reactivity among target antigens, demonstrating high assay specificity. The low LOD values and absence of cross-reactivity indicate excellent analytical sensitivity and specificity. Simultaneous detection of both pathogens offers significant advantages for rapid clinical decision-making and infection control. Conclusions Our research presents a potential diagnostic approach utilizing a singular LFA platform for the early and accurate detection of COVID-19 and Influenza infections. The proposed multiplex strategy could improve public health outcomes by facilitating rapid therapeutic intervention and successful disease management during respiratory infection epidemics.

Objectives In this study, the aim is to investigate the clinical findings as well as laboratory and echocardiographic differences in infants with respiratory syncytial virus (RSV) bronchiolitis hospitalized in the pediatric intensive care unit (PICU) compared to those hospitalized in the general pediatric ward and thus contribute to the establishment of a novel evidence-based medical scoring. Methods The study was conducted by retrospectively reviewing the files of 58 infants aged 1–12 months who were hospitalized in the PICU and general pediatric ward of Health Sciences University of Bursa City Hospital with a definite diagnosis of RSV bronchiolitis between September 2022 and April 2023. Results There were significant differences in clinical findings (Bronchiolitis Score of Sant Joan de Déu↑), laboratory tests [blood gas (pH↓-PaCO 2 ↑-lactate↑) and N-terminal pro-B-type natriuretic peptide (NT-proBNP↑)] and echocardiographic parameters [systolic pulmonary artery pressure (sPAP↑), right ventricular Tei index (RVTX↑), left ventricular systolic eccentricity index (LVEls↑) and tricuspid annular planar systolic excursion (TAPSE↓)] in infants hospitalized in PICU compared to those hospitalized in general pediatric ward. Multivariate regression analysis revealed that the best indicator to add to the clinical score in terms of PICU hospitalization was NT-ProBNP (OR: 1.007, 95 % CI 1.002–1.011, p=0.003). Conclusions The severity of RSV bronchiolitis can be evaluated more objectively with new scoring methods to be developed by adding laboratory and echocardiographic parameters, especially NT-proBNP, to clinical scoring systems.

Objectives The study aimed to explore the potential mechanism of Kushen Herpes Tincture in treating herpes zoster in aging people based on network pharmacology. Methods Four herbs in Kushen Herpes Tincture were screened for transdermal active ingredients by TCMSP and HERB databases. Topological Polar Surface Area (TPSA) smaller than 60 Å square (Å 2 ) was used to screen the good at cell membrane-penetrating compounds. Potential targets of compounds were gathered from TCMSP, HERB, and SwissTargetPrediction. GeneCards and DisGeNET databases were used to screen herpes zoster-related targets. The targets were analyzed for protein interactions and KEGG enrichment. Among the top 20 targets, STAT3 and EGFR were subjected to cell experiment validation. Results Kushen Herpes Tincture was predicted to act on 51 herpes zoster-related targets. These targets were retraced to 103 cell membrane-penetrating compounds. Protein interactions proposed STAT3 and EGFR as two among the top 10 targets. The key KEGG pathway contained C-type lectin receptor signaling pathway, PI3K-Akt signaling pathway, etc. STAT3 and EGFR were upregulated in human keratinocyte and human epithelial cells after varicella-zoster virus infection, while decreased by Kushen Herpes Tincture treatment. Kushen Herpes Tincture restricted varicella-zoster virus replication in vitro . Conclusions Kushen Herpes Tincture may exert its therapeutic effect on aging herpes zoster through multi-component action on multi-targets and multi-pathways, including STAT3 and EGFR.

Objectives Calcium/calmodulin-dependent protein kinase-2 (CaMKII) is a serine/threonine kinase prevalent in neuronal cells, playing a key role in memory, learning, and synaptic plasticity. Nonspecific CaMKII inhibition can prevent apoptosis in neuronal cells and reduce glutamate-induced cell death. Additionally, variations in CaMKK enzyme levels affect hemopoietic stem cell proliferation, although the effects of CaMKII on stem cell responses during stress remain unclear. This study aims to explore CaMKII’s impact on the survival and proliferation of mesenchymal stem cells under stress and analyze the expression of its isoforms (alpha, beta, gamma, and delta) in these conditions. Methods The study included the characterization of MSCs, followed by an evaluation of the effects of KN-93, a CaMKII inhibitor, on the viability and proliferation of stem cells both in the presence and absence of H 2 O 2 treatment. The toxicity caused by the application of 1 mM H 2 O 2 further increased by inhibitor treatment. Additionally changes in the gene expression levels of CaMKII isoforms were analyzed. Results The application of H 2 O 2 significantly decreased the total expression levels of CaMKII, with a significant reduction in the delta isoform. Furthermore, CaMKII inhibition by KN-93 increased the toxicity induced by H 2 O 2 . Viability and proliferation of stem cells were negatively impacted by the combined treatment of KN-93 and H 2 O 2 compared to H 2 O 2  alone. Conclusions Our findings provide a strong foundation to understand the response mechanisms of MSCs under stress conditions and could inform strategies for targeted stem cell therapies in oxidative stress conditions.

Objectives This study aims to elucidate the interactions between laryngeal cancer cells (HEp-2) and endothelial cells (HUVEC) within the head and neck squamous cell cancer (HNSCC) microenvironment using direct and indirect in vitro co-cultivation systems. Methods Conditioned mediums (CM) of HEp-2 and HUVEC were generated, followed by the construction of co-culture systems. Confocal microscopy, XTT assay, trypan blue viability assay, real-time cell analysis system (RTCA), and quantitative real-time polymerase chain reaction (qRT-PCR) were used to assess cell morphology, proliferation, migration, invasion, and the expression of cancer-associated genes ( CDH2 , CCL21 , CXCL8 , ITGB , MMP2 , MMP9 , and  VIM ). Results We observed that the HEp2 co-culture effect altered HUVEC morphology, also reduced cell proliferation significantly, increased migration (p<0.05), and invasion of the cells. The mRNA levels of CXCL8 and ITGB were downregulated significantly, while the expression level of CCL21 mRNA was markedly upregulated (88.4-fold) compared to mono-culture HUVECs (p<0.05). Meanwhile, the HEp-2s showed a spindle-shaped and scattered morphology after co-culture with HUVEC. In addition, a higher relative migration rate (p<0.05) but significantly reduced proliferation and invasion rates of HEp2s were detected. Conclusions Reciprocal interactions between HEp2 and HUVEC significantly modulate cellular behaviors and gene expression, suggesting that these interactions play a crucial role in laryngeal cancer progression and offering potential insights for HNSCC treatment strategies.

Objectives Letrozole (LTZ), an aromatase inhibitor, is associated with significant side effects such as uterine toxicity. This study investigated the potential of hesperidin (HSP) and taurine (TAU), both natural antioxidant molecules, to mitigate LTZ-induced uterine toxicity. Methods A total of 48 female rats were divided into six groups and treated orally for 30 days as follows: Control (sham), LTZ (1 mg/kg), HSP (100 mg/kg), TAU (100 mg/kg), LTZ+HSP, and LTZ+TAU. Histopathological, gene expression, and biochemical analyses were conducted on uterine tissues and serum samples. Results LTZ caused a significant decrease in serum IL-1β, IL-6, estradiol, and FSH levels (p<0.05). It reduced SOD, CAT activities, and GSH levels while increasing tissue MDA levels. Additionally, it led to a significant increase in Bax, caspase-3, COX-2, iNOS, and TNF-α gene expression. HSP and TAU did not significantly alter hormone levels (p>0.05). However, HSP significantly reduced oxidative stress (p<0.05), decreased the expression of genes related to apoptosis and inflammation (p<0.05), and significantly lowered serum cytokine levels while increasing the expression of anti-apoptotic genes. Both HSP and TAU mitigated LTZ-induced cystic dilatation and hyperemia in the uterine glands. TAU did not significantly affect IL-1β and IL-6 levels or the expression of apoptosis-related genes (p>0.05). Although TAU exhibited effects similar to HSP in certain parameters, its protective efficacy was comparatively less pronounced. Conclusions The results suggest that HSP is a promising agent for mitigating LTZ-induced uterine toxicity. However, further studies with different doses and application protocols are required to more definitively elucidate the potential effects of TAU.

Objectives Although many synthetic anticancer drugs are available, a significant proportion of human therapeutics in the anticancer armamentarium are derived from natural products. The aim of this study to examine the anticancer effects of natural compounds against non-small cell lung cancer (NSCLC) and breast cancer, which remain among the world’s greatest obstacles. Methods Coronilla orientalis MILLER (CO) was collected in Erzincan, Türkiye, prepared, and extracted with 70 % ethanol. CO was then tested against A549 NSCLC and MCF-7 breast cancer cells using the MTT assay. To explore its potential anticancer mechanism, the apoptotic effects of CO in A549 and MCF-7 cells and the kinase inhibitory effects of CO were investigated using the Annexin V/ethidium homodimer III staining assay and the ADP-Glo kinase assay, respectively. Molecular docking studies were also performed for several major components of CO in the ATP binding site of EGFR. Results The results showed that CO, with IC 50 values of 2.37 ± 0.59 μg/mL and 7.60 ± 1.18 μg/mL, exhibited anticancer activity against A549 cells and MCF-7 cells, respectively. CO was also selectively cytotoxic between Jurkat cells and PBMCs (healthy). CO-treated A549 and MCF-7 cells were found to undergo significant apoptosis and CO was found to inhibit EGFR. Molecular docking studies revealed the interaction of some defined components of CO with key residues in the ATP binding site of EGFR. Conclusions Taken together, this research has shown that CO has a great deal of potential as an inhibitor of the anticancer function against NSCLC and breast cancer, and warrants further investigation.