LncRNA SH3BP5-AS1 Regulates the Proliferation and Cell Cycle of Non- Small Cell Lung Cancer Cells

IF 0.5 4区生物学 Q4 BIOCHEMICAL RESEARCH METHODS Current Proteomics Pub Date : 2023-10-25 DOI:10.2174/0115701646253656231013141100

Xiaowu Fan

{"title":"LncRNA SH3BP5-AS1 Regulates the Proliferation and Cell Cycle of Non- Small Cell Lung Cancer Cells","authors":"Xiaowu Fan","doi":"10.2174/0115701646253656231013141100","DOIUrl":null,"url":null,"abstract":" Background: Non-small cell lung cancer (NSCLC) consists of a class of heterogeneous diseases. Objective: LncRNAs are exceedingly implicated in the pathogenesis of NSCLC. Herein, the current study set out to illustrate the molecular mechanism of SH3BP5-AS1 in NSCLC cells. Methods: SH3BP5-AS1 expression in clinical NSCLC tissues and its impact on prognosis were analyzed by bioinformatics database. SH3BP5-AS1 expression patterns in NSCLC cell lines (A549/H1299/H1975/H460) and human normal lung epithelial cell lines (BEAS-2B) were examined by RT-qPCR. SH3BP5-AS1 was overexpressed in A549 or silenced in H1975 cells through transfection to assess its effect on proliferation, cell cycle distribution, and apoptosis, apoptosisrelated protein (Cleaved Caspase-3, Bax, Bcl-2) levels, invasive, migratory, and healing capacity through CCK-8, colony formation assay, flow cytometry, Western blot, Transwell, and cell scratch test. Results: SH3BP5-AS1 was under-expressed in NSCLC clinical tissues, and NSCLC patients with low SH3BP5-AS1 expression showed poor prognosis. A549/H1299/H1975/H460 cells had reduced levels of SH3BP5-AS1, with the relative level lowest/highest expression in A549/H1975 cells, respectively. SH3BP5-AS1 overexpression repressed A549 cell proliferation, slowed down cell cycle progression, enhanced apoptosis, elevated Cleared Caspase-3, Bax, suppressed Bcl-2 protein levels, and inhibited migratory, invasive, and scratch healing capacities, while SH3BP5-AS1 silencing brought about the opposite results in H1975 cells. Conclusion: SH3BP5-AS1 could suppress NSCLC cell proliferation, slow down cell cycle progression, stimulate apoptosis, and limit invasion and migration.","PeriodicalId":50601,"journal":{"name":"Current Proteomics","volume":null,"pages":null},"PeriodicalIF":0.5000,"publicationDate":"2023-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current Proteomics","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.2174/0115701646253656231013141100","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"BIOCHEMICAL RESEARCH METHODS","Score":null,"Total":0}

引用次数: 0

Abstract

Background: Non-small cell lung cancer (NSCLC) consists of a class of heterogeneous diseases. Objective: LncRNAs are exceedingly implicated in the pathogenesis of NSCLC. Herein, the current study set out to illustrate the molecular mechanism of SH3BP5-AS1 in NSCLC cells. Methods: SH3BP5-AS1 expression in clinical NSCLC tissues and its impact on prognosis were analyzed by bioinformatics database. SH3BP5-AS1 expression patterns in NSCLC cell lines (A549/H1299/H1975/H460) and human normal lung epithelial cell lines (BEAS-2B) were examined by RT-qPCR. SH3BP5-AS1 was overexpressed in A549 or silenced in H1975 cells through transfection to assess its effect on proliferation, cell cycle distribution, and apoptosis, apoptosisrelated protein (Cleaved Caspase-3, Bax, Bcl-2) levels, invasive, migratory, and healing capacity through CCK-8, colony formation assay, flow cytometry, Western blot, Transwell, and cell scratch test. Results: SH3BP5-AS1 was under-expressed in NSCLC clinical tissues, and NSCLC patients with low SH3BP5-AS1 expression showed poor prognosis. A549/H1299/H1975/H460 cells had reduced levels of SH3BP5-AS1, with the relative level lowest/highest expression in A549/H1975 cells, respectively. SH3BP5-AS1 overexpression repressed A549 cell proliferation, slowed down cell cycle progression, enhanced apoptosis, elevated Cleared Caspase-3, Bax, suppressed Bcl-2 protein levels, and inhibited migratory, invasive, and scratch healing capacities, while SH3BP5-AS1 silencing brought about the opposite results in H1975 cells. Conclusion: SH3BP5-AS1 could suppress NSCLC cell proliferation, slow down cell cycle progression, stimulate apoptosis, and limit invasion and migration.

查看原文

微信好友朋友圈 QQ好友复制链接

本刊更多论文

LncRNA SH3BP5-AS1 调控非小细胞肺癌细胞的增殖和细胞周期

背景：非小细胞肺癌（NSCLC非小细胞肺癌（NSCLC）是一类异质性疾病。研究目的LncRNA 与 NSCLC 的发病机制有极大的关联。本研究旨在阐明 SH3BP5-AS1 在 NSCLC 细胞中的分子机制。研究方法通过生物信息学数据库分析SH3BP5-AS1在临床NSCLC组织中的表达及其对预后的影响。通过 RT-qPCR 检测了 SH3BP5-AS1 在 NSCLC 细胞系（A549/H1299/H1975/H460）和人类正常肺上皮细胞系（BEAS-2B）中的表达模式。在 A549 细胞中过表达 SH3BP5-AS1，或通过转染在 H1975 细胞中沉默 SH3BP5-AS1，并通过 CCK-8、集落形成试验、流式细胞术、Western 印迹、Transwell 和细胞划痕试验评估 SH3BP5-AS1 对细胞增殖、细胞周期分布、凋亡、凋亡相关蛋白（Caspase-3、Bax、Bcl-2）水平、侵袭、迁移和愈合能力的影响。结果显示SH3BP5-AS1在NSCLC临床组织中低表达，SH3BP5-AS1低表达的NSCLC患者预后较差。A549/H1299/H1975/H460细胞的SH3BP5-AS1水平降低，相对水平最低/最高的分别是A549/H1975细胞。SH3BP5-AS1的过表达抑制了A549细胞的增殖，减缓了细胞周期的进展，增强了细胞凋亡，提高了Caspase-3、Bax的清除率，抑制了Bcl-2蛋白水平，抑制了细胞的迁移、侵袭和划痕愈合能力，而SH3BP5-AS1的沉默则在H1975细胞中带来了相反的结果。结论SH3BP5-AS1能抑制NSCLC细胞增殖、减缓细胞周期进程、刺激细胞凋亡、限制侵袭和迁移。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文去求助

来源期刊

Current Proteomics BIOCHEMICAL RESEARCH METHODS-BIOCHEMISTRY & MOLECULAR BIOLOGY

CiteScore

1.60

自引率

0.00%

发文量

审稿时长

>0 weeks

期刊介绍： Research in the emerging field of proteomics is growing at an extremely rapid rate. The principal aim of Current Proteomics is to publish well-timed in-depth/mini review articles in this fast-expanding area on topics relevant and significant to the development of proteomics. Current Proteomics is an essential journal for everyone involved in proteomics and related fields in both academia and industry. Current Proteomics publishes in-depth/mini review articles in all aspects of the fast-expanding field of proteomics. All areas of proteomics are covered together with the methodology, software, databases, technological advances and applications of proteomics, including functional proteomics. Diverse technologies covered include but are not limited to: Protein separation and characterization techniques 2-D gel electrophoresis and image analysis Techniques for protein expression profiling including mass spectrometry-based methods and algorithms for correlative database searching Determination of co-translational and post- translational modification of proteins Protein/peptide microarrays Biomolecular interaction analysis Analysis of protein complexes Yeast two-hybrid projects Protein-protein interaction (protein interactome) pathways and cell signaling networks Systems biology Proteome informatics (bioinformatics) Knowledge integration and management tools High-throughput protein structural studies (using mass spectrometry, nuclear magnetic resonance and X-ray crystallography) High-throughput computational methods for protein 3-D structure as well as function determination Robotics, nanotechnology, and microfluidics.