Cell Biochemistry and Biophysics最新文献_第8页

Macrophage Polarization-Based Analysis of the Role of the FOXM1/KIF20A Axis in Breast Cancer Metastasis. 基于巨噬细胞极化的FOXM1/KIF20A轴在乳腺癌转移中的作用分析

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-04-28 DOI: 10.1007/s12013-025-01755-w

Yuanbin Wang, Ruimin Ma, Qing Yang, Lijun Yang, Xiangli Li, Zhihao Wu

{"title":"Macrophage Polarization-Based Analysis of the Role of the FOXM1/KIF20A Axis in Breast Cancer Metastasis.","authors":"Yuanbin Wang, Ruimin Ma, Qing Yang, Lijun Yang, Xiangli Li, Zhihao Wu","doi":"10.1007/s12013-025-01755-w","DOIUrl":"https://doi.org/10.1007/s12013-025-01755-w","url":null,"abstract":"To investigate the potential molecular processes underlying the function of forkhead box M1 (FOXM1)-mediated macrophage polarization in breast cancer (BC). The expression levels of Kinesin family member 20 A (KIF20A) and FOXM1 in BC tissues and tumor-associated macrophages (TAMs) were determined using RT-qPCR. Following co-culture of macrophages with BC cells, the impact of FOXM1 on the proliferation, invasive migration ability, and epithelial-mesenchymal transition (EMT) of BC cells was assessed using cell counting kit-8, Transwell, and Western blot assays respectively. Both the chromatin immunoprecipitation (ChIP) test and the dual luciferase reporter gene assay were used to confirm the connection between FOXM1 and KIF20A. Furthermore, the effect of FOXM1 on BC cell growth in vivo was evaluated via subcutaneous tumor formation assay conducted in nude mice. BC cell growth and metastasis were aided by M2 macrophage polarization. KIF20A and FOXM1 expression levels were markedly elevated in both TAMs and BC tissues. FOXM1 drived M2 polarization of macrophages by transcriptionally activating KIF20A. In vitro studies have demonstrated that FOXM1, through its regulation of KIF20A, enhanced BC cell proliferation, migration, invasion, and EMT. The upregulation of KIF20A expression by FOXM1 promotes M2 polarization of macrophages, thereby facilitating BC cell proliferation and metastasis.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143952237","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Synergistic Enhancement of Apo2L/TRAIL and DR4-Induced Apoptosis by Arsenic Trioxide in Triple-Negative Breast Cancer Cells: A Comparison to Conventional Chemotherapy. 三氧化二砷协同增强Apo2L/TRAIL和dr4诱导的三阴性乳腺癌细胞凋亡：与常规化疗的比较

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-04-28 DOI: 10.1007/s12013-025-01764-9

Soraya Moomivand, Mohsen Nikbakht, Ahmad Majd, Maryam Bikhof Torbati, Seyed Asadoullah Mousavi

{"title":"Synergistic Enhancement of Apo2L/TRAIL and DR4-Induced Apoptosis by Arsenic Trioxide in Triple-Negative Breast Cancer Cells: A Comparison to Conventional Chemotherapy.","authors":"Soraya Moomivand, Mohsen Nikbakht, Ahmad Majd, Maryam Bikhof Torbati, Seyed Asadoullah Mousavi","doi":"10.1007/s12013-025-01764-9","DOIUrl":"https://doi.org/10.1007/s12013-025-01764-9","url":null,"abstract":"Triple-negative breast cancer (TNBC) is an aggressive subtype lacking hormonal and HER2 receptors, making it highly resistant to treatment. Apo2L/TRAIL, a tumor necrosis factor-related ligand, induces apoptosis in cancer cells via the death receptor DR4. However, TNBC often develops resistance to TRAIL-mediated apoptosis, limiting its therapeutic potential. This study investigates whether arsenic trioxide (ATO) can overcome TRAIL resistance by modulating the Apo2L/TRAIL pathway and enhancing the effects of carboplatin (CP) and cyclophosphamide (CY). TNBC cell lines BT-20 and MDA-MB-231 were treated with ATO, CP, CY, and their combinations. Cell viability was measured using the MTT assay, while real-time PCR and Western blot analysis assessed Apo2L/TRAIL and DR4 expression. Statistical analysis was performed using ANOVA with Dunnett's post hoc test. ATO induced dose-dependent cytotoxicity in TNBC cells, which was significantly enhanced in combination treatments. The highest reductions in cell viability were observed with 3 µM ATO plus 5000 µM CP or 500 µM CY (p < 0.0001). ATO markedly upregulated Apo2L/TRAIL and DR4 at both mRNA and protein levels, with the most pronounced effects seen in ATO-CY combinations. These findings indicate that ATO sensitizes TNBC cells to TRAIL-mediated apoptosis by upregulating DR4 and Apo2L/TRAIL, while also exhibiting strong synergistic cytotoxicity with CP and CY. This highlights ATO's potential as an adjuvant therapy to improve TNBC treatment efficacy and overcome chemoresistance, warranting further clinical exploration.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143956535","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A Computational Approach for Designing a Peptide-Based Acetyl-CoA Synthetase 2 Inhibitor: A New Horizon for Anticancer Development. 设计肽类乙酰辅酶A合成酶2抑制剂的计算方法：抗癌发展的新视野。

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-04-27 DOI: 10.1007/s12013-025-01729-y

Musab Ali, Ernest Oduro-Kwateng, Ibrahim Oluwatobi Kehinde, Narasimham L Parinandi, Mahmoud E S Soliman

{"title":"A Computational Approach for Designing a Peptide-Based Acetyl-CoA Synthetase 2 Inhibitor: A New Horizon for Anticancer Development.","authors":"Musab Ali, Ernest Oduro-Kwateng, Ibrahim Oluwatobi Kehinde, Narasimham L Parinandi, Mahmoud E S Soliman","doi":"10.1007/s12013-025-01729-y","DOIUrl":"https://doi.org/10.1007/s12013-025-01729-y","url":null,"abstract":"Acetyl-CoA Synthetase 2 (ACSS2) has emerged as a new target for anticancer development owing to its high expression in various tumours and its enhancement of malignancy. Stressing the growing interest in peptide-derived drugs featuring better selectivity and efficacy, a computational protocol was applied to design a peptide inhibitor for ACSS2. Herein, 3600 peptide sequences derived from ACSS2 nucleotide motif were generated by classifying the 20 amino acids into six physiochemical groups. De novo modeling maintained essential binding interactions, and a refined library of 16 peptides was derived using Support Vector Machine filters to ensure proper bioavailability, toxicity, and therapeutic relevance. Structural and folding predictions, along with molecular docking, identified the top candidate, Pep16, which demonstrated significantly higher binding affinity (91.1 ± 1.6 kcal/mol) compared to a known inhibitor (53.7 ± 0.7 kcal/mol). Further molecular dynamics simulations and binding free energy calculations revealed that Pep16 enhances ACSS2 conformational variability, occupies a larger binding interface, and achieved firm binding. MM/GBSA analysis highlighted key electrostatic interactions with specific ACSS2 residues, including ARG 373, ARG 526, ARG 628, ARG 631, and LYS 632. Overall, Pep16 appears to lock the ACSS2 nucleotide pocket into a compact, rigid conformation, potentially blocking ATP binding and catalytic activity, and may serve as a novel specific ACSS2 inhibitor. Though, we urge further research to confirm and compare its therapeutic potential to existing inhibitors. We also believe that this systematic methodology would represent an indispensable tool for prospective peptide-based drug discovery.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143952126","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Molecular Mechanism of Notch Signaling and Macrophages in Deep Vein Thrombosis: A Comprehensive Review. Notch信号和巨噬细胞在深静脉血栓形成中的分子机制综述

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-04-25 DOI: 10.1007/s12013-025-01761-y

Sisira Joy, Anusha Prasannan, Kaliyamurthi Venkatachalam, Ambika Binesh

{"title":"Molecular Mechanism of Notch Signaling and Macrophages in Deep Vein Thrombosis: A Comprehensive Review.","authors":"Sisira Joy, Anusha Prasannan, Kaliyamurthi Venkatachalam, Ambika Binesh","doi":"10.1007/s12013-025-01761-y","DOIUrl":"https://doi.org/10.1007/s12013-025-01761-y","url":null,"abstract":"Deep vein thrombosis is an acute medical condition, and the molecular basis of this etiology will be crucial in the discovery of more advanced therapies. This review has focused at the Notch signaling pathway, which plays a significant role in different physiological activities such as homeostasis, development, and disease. Also, reveal macrophage function in inflammation and thrombosis in depth, with a focus on their polarization and interaction with the endothelium during thrombosis. In this context, some essential cellular and molecular mechanisms relevant to thrombus pathogenesis, DVT aetiology and risk factors, as well as elements and composition of the Notch pathway, are covered in the end, with a focus on elements that distinguish canonical from non-canonical signaling pathways and their biological relevance to macrophages. Notch signaling has been shown to influence macrophage activation and polarization, influencing their function in thrombosis breakdown and resolution. This interplay between Notch signaling and macrophages may reveal possible treatment targets for DVT. Discuss the physiological role of Notch signaling in vascular biology, as well as how it contributes to thrombosis. The difficulties in implementing these discoveries in clinical practice are discussed, along with the status of ongoing clinical trials and experimental investigations focussing on macrophage-directed treatments and Notch inhibitors. These molecular insights synthesis provides a basis for the creation of novel strategies for the efficient management of DVT.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143957049","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Correction: Chaperone-Mediated Autophagy Reactivation Protects Against Severe Acute Pancreatitis-Associated Liver Injury Through Upregulating Keap1/Nrf2 Signaling Pathway and Inhibiting NLRP3 Inflammasome Activation. 更正：伴侣介导的自噬再激活通过上调Keap1/Nrf2信号通路和抑制NLRP3炎性体激活来保护严重急性胰腺炎相关肝损伤。

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-04-22 DOI: 10.1007/s12013-025-01760-z

Zhongbiao Li, Yue Yu, Xihao Zhao, Yue Qu, Jiang Wang, Dianliang Zhang

引用次数: 0

Structural and Energetic Insights into the Binding of _L- and _D-Arginine Analogs with Neuropilin-1 (NRP1): Molecular Docking, Molecular Dynamics and DFT Calculations. L-和d -精氨酸类似物与Neuropilin-1 （NRP1）结合的结构和能量见解：分子对接，分子动力学和DFT计算。

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-04-20 DOI: 10.1007/s12013-025-01754-x

Mahmoud A A Ibrahim, Dina E M Mohamed, Khlood A A Abdeljawaad, Alaa H M Abdelrahman, Shaban R M Sayed, Mohamed A El-Tayeb, Peter A Sidhom, Paul W Paré

{"title":"Structural and Energetic Insights into the Binding of L- and D-Arginine Analogs with Neuropilin-1 (NRP1): Molecular Docking, Molecular Dynamics and DFT Calculations.","authors":"Mahmoud A A Ibrahim, Dina E M Mohamed, Khlood A A Abdeljawaad, Alaa H M Abdelrahman, Shaban R M Sayed, Mohamed A El-Tayeb, Peter A Sidhom, Paul W Paré","doi":"10.1007/s12013-025-01754-x","DOIUrl":"https://doi.org/10.1007/s12013-025-01754-x","url":null,"abstract":"Neuropilin-1 (NRP1) is a transmembrane glycoprotein that binds numerous ligands, including vascular endothelial growth factor A (VEGFA) that stimulates blood vessel formation. Preclinical trials propose that NRP1 inhibition blocks neoplasm cell proliferation and slows tumor growth by suppressing angiogenesis. As such, VEGFA/NRP1 signaling is a potential target for carcinoma inhibition. Since arginine (Arg) regulates nutrient-responsive rapamycin signaling, which in turn regulates cell growth and metabolism, Arg, as well as simple structural variations of L- and D-Arg, were selected to study in-silico structural and energetic influences of such ligands on NRP1 signaling. Initially, AutoDock Vina1.1.2 software performance was assessed to predict binding modes of Arg analogs with NRP1 based on the available experimental data. Molecular docking and molecular dynamics (MD) simulations over 100 ns were run to inspect the potency of Arg analogs to bind with NRP1. Analog-NRP1 complex binding affinities (ΔGbinding) were evaluated using the MM/GBSA approach. Results indicated that L-/D-Agd- and L-/D-Agn-NRP1 complexes exhibited binding affinities greater than the co-crystallized L-homoarginine ligand (calc.-31.2 kcal.mol-1) with ΔGbinding values of -40.5/-40.6 and -40.0/-36.2 kcal.mol-1, respectively. Structural and energetic analyses were performed to examine further L-/D-Agd and L-/D-Agn. Quantum mechanical calculations were performed to confirm the outcomes obtained from docking computations and MD simulations.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143960409","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Structural Mechanisms Driving the Selective Efficacy of Oxamniquine against Schistosoma mansoni and Schistosoma japonicum. 奥氨喹对曼氏血吸虫和日本血吸虫选择性作用的结构机制研究。

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-04-19 DOI: 10.1007/s12013-025-01756-9

Kehinde F Paul-Odeniran, Emmanuel A Iwuchukwu, Paul O Odeniran

{"title":"Structural Mechanisms Driving the Selective Efficacy of Oxamniquine against Schistosoma mansoni and Schistosoma japonicum.","authors":"Kehinde F Paul-Odeniran, Emmanuel A Iwuchukwu, Paul O Odeniran","doi":"10.1007/s12013-025-01756-9","DOIUrl":"https://doi.org/10.1007/s12013-025-01756-9","url":null,"abstract":"Oxamniquine (OXA) exhibits selective efficacy against different Schistosoma species, with the highest activity observed in Schistosoma mansoni sulfotransferase (SmSULT) and the lowest in Schistosoma japonicum sulfotransferase (SjSULT). This study utilises advanced atomistic and molecular simulations to elucidate the structural dynamics induced by OXA binding to SmSULT and SjSULT, aiming to unravel the underpinnings of this selective efficacy. Binding free energy (BFE) analyses revealed a markedly higher affinity of OXA for SmSULT (-48.04 kcal/mol) compared to wtSjSULT (-22.84 kcal/mol), with a significant restoration of binding affinity (-39.23 kcal/mol) observed in SjSULT following the mutation of Val139 to Gly139. Comprehensive conformational assessments highlighted that SmSULT-OXA achieves its superior efficacy by stabilising the protein structure, in stark contrast to the erratic conformational behaviour of wild-type SjSULT. Notably, this erratic behaviour is ameliorated upon mutation, leading to a restoration of OXA's efficacy in SjSULT. These insights elucidate the structural mechanisms underpinning OXA's selective efficacy and provide valuable perspectives on its targeted action against Schistosoma spp.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143956159","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

PM_2.5 Induced Vascular and Myocardial Calcification Impairs Ischemia-reperfusion Tolerance via Mitochondrial Dysregulation. PM2.5诱导的血管和心肌钙化通过线粒体失调损害缺血再灌注耐受性。

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-04-18 DOI: 10.1007/s12013-025-01758-7

Bhavana Sivakumar, Gino A Kurian

{"title":"PM2.5 Induced Vascular and Myocardial Calcification Impairs Ischemia-reperfusion Tolerance via Mitochondrial Dysregulation.","authors":"Bhavana Sivakumar, Gino A Kurian","doi":"10.1007/s12013-025-01758-7","DOIUrl":"https://doi.org/10.1007/s12013-025-01758-7","url":null,"abstract":"Cardiovascular diseases (CVD) are intricately linked to vascular dysfunction, with growing evidence implicating particulate matter (PM2.5) as a major factor. This study addresses the urgent need to understand how PM2.5 exposure influences cardiac vulnerability to ischemia-reperfusion (IR) injury by investigating the underlying mechanisms of vascular and myocardial alterations. The aim was to assess the progressive impact of PM2.5 exposure on vascular and myocardial function, mainly focusing on mitochondrial integrity and calcification processes. Adult Wistar female rats were subjected to PM2.5 at a concentration of 250 µg/m3 for 3 h daily over 1, 7, 14, and 21 days. Cardiac endurance to IR injury was assessed using the Langendorff perfusion method. Findings revealed that exposure for 7 days or more induced vascular calcification, upregulating calcification-related genes and causing calcium accumulation, while endothelial dysfunction and impaired vascular contractility manifested earlier. Myocardial calcification and hemodynamic impairments became evident after 14 days, correlating with progressive mitochondrial dysfunction in both vascular and cardiac tissues. By day 21, severe mitochondrial damage and elevated cardiac sensitivity to IR injury were observed, accompanied by increased metal deposition in the vasculature and myocardium. The study concludes that PM2.5 exposure drives a cascade of vascular and myocardial alterations, with vascular dysfunction preceding myocardial calcification. These findings emphasize the need for strategies to mitigate PM2.5 induced cardiovascular risks, particularly by targeting mitochondrial health and vascular integrity.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143955100","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The Regulatory Role of NcRNAs in Pyroptosis and Disease Pathogenesis. ncrna在焦亡和疾病发病机制中的调节作用。

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-04-18 DOI: 10.1007/s12013-025-01720-7

Shaocong Wang, Xinzhe Chen, Kun Wang, Sumin Yang

引用次数: 0

Identification of circRNA-Based Biomarkers and ceRNA Mechanism in Non-Small Cell Lung Cancer. 环状rna生物标志物的鉴定及其在非小细胞肺癌中的作用机制

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-04-18 DOI: 10.1007/s12013-025-01753-y

Zhengjia Liu, Xiyu Liu, Cong Yin, Zihao Liu, Haixiang Yu

{"title":"Identification of circRNA-Based Biomarkers and ceRNA Mechanism in Non-Small Cell Lung Cancer.","authors":"Zhengjia Liu, Xiyu Liu, Cong Yin, Zihao Liu, Haixiang Yu","doi":"10.1007/s12013-025-01753-y","DOIUrl":"https://doi.org/10.1007/s12013-025-01753-y","url":null,"abstract":"We aimed to identify circRNA as a biomarker in non-small cell lung cancer (NSCLC) and explore the underlying mechanism. circRNA and mRNA data were retrieved from GEO database. A series of bioinformatics analyses including differentially expressed analysis, weighted gene co-expression network analysis (WGCNA), Random Forest, and support vector machine algorithm were applied to identify the key circRNAs in NSCLC. ROC curves were used to evaluate and distinguish the roles of key circRNAs in cancer. The expression levels of circRNAs were validated via qPCR analysis. Finally, a ceRNA network was constructed. Herein, si-hsa_circ_0084443 was transfected into NSCLC cells to investigate its function in NSCLC. Five circRNAs (hsa_circ_0049271, hsa_circ_0029426, hsa_circ_0084443, hsa_circ_0015278, and hsa_circ_0024731) were identified as biomarkers in NSCLC. They exhibited potent diagnostic ability in identifying NSCLC, with AUC > 0.85. qPCR results suggested that hsa_circ_0049271, hsa_circ_0029426, and hsa_circ_0015278 were significantly downregulated and hsa_circ_0084443 and hsa_circ_0024731 were significantly upregulated in tumor tissue compared with the levels in normal tissues (P < 0.05). A ceRNA network was finally constructed. Knockdown of hsa_circ_0084443 inhibited cell growth, migration, invasion, and colony formation, and promoted apoptosis in NSCLC cell line. Five circRNAs were identified as biomarkers and demonstrated abnormal expression in NSCLC. Furthermore, ceRNA network was constructed, which can aid the mechanism exploration in the future.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143958344","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0