TNNT1 accelerates migration, invasion and EMT progression in lung cancer cells.

IF 2.3 3区医学 Q3 ONCOLOGY

Thoracic Cancer Pub Date : 2024-08-01 Epub Date: 2024-07-07 DOI:10.1111/1759-7714.15400

Xiaobin Ge, Guangzhong Du, Qingchen Zhou, Bing Yan, Gonglei Yue

{"title":"TNNT1 accelerates migration, invasion and EMT progression in lung cancer cells.","authors":"Xiaobin Ge, Guangzhong Du, Qingchen Zhou, Bing Yan, Gonglei Yue","doi":"10.1111/1759-7714.15400","DOIUrl":null,"url":null,"abstract":"Background: Clinically, most patients with lung cancer (LC) die from tumor spread and metastasis. Specific metastasis-related molecules can provide reference for clinical prediction of efficacy, evaluation of prognosis, and search for the best treatment plan. Troponin T1 (TNNT1) is highly expressed in various cancer tissues, which affects malignant behavior of tumor cells and is related to patients' survival and prognosis. However, the role and molecular mechanism of TNNT1 in LC invasion and metastasis have not yet been investigated.Methods: Gene expression profiling interactive analysis (GEPIA) online analysis was used to analyze TNNT1 expression in LC tissues. Quantitative real-time-polymerase chain reaction (qRT-PCR) or western blot were performed to measure TNNT1 or epithelial-to-mesenchymal transition (EMT)-related and Wnt/β-catenin pathway-related protein expression in LC cells. After TNNT1 knockdown, cell scratch healing and transwell assays were introduced to assess cell migration and invasion, respectively.Results: TNNT1 expression in LC tissues and cells was increased. TNNT1 knockdown notably impaired LC cell migration, invasion and EMT. TNNT1 knockdown inhibited Wnt/β-catenin pathway of LC cells. Lithium chloride (LiCl) addition partially restored the inhibition of TNNT1 knockdown on migration, invasion, EMT and Wnt/β-catenin of LC cells.Conclusion: TNNT1 knockdown attenuated LC migration, invasion and EMT, possibly through Wnt/β-catenin signaling.","PeriodicalId":23338,"journal":{"name":"Thoracic Cancer","volume":" ","pages":"1749-1756"},"PeriodicalIF":2.3000,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11320084/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Thoracic Cancer","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1111/1759-7714.15400","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/7/7 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"ONCOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

Background: Clinically, most patients with lung cancer (LC) die from tumor spread and metastasis. Specific metastasis-related molecules can provide reference for clinical prediction of efficacy, evaluation of prognosis, and search for the best treatment plan. Troponin T1 (TNNT1) is highly expressed in various cancer tissues, which affects malignant behavior of tumor cells and is related to patients' survival and prognosis. However, the role and molecular mechanism of TNNT1 in LC invasion and metastasis have not yet been investigated.

Methods: Gene expression profiling interactive analysis (GEPIA) online analysis was used to analyze TNNT1 expression in LC tissues. Quantitative real-time-polymerase chain reaction (qRT-PCR) or western blot were performed to measure TNNT1 or epithelial-to-mesenchymal transition (EMT)-related and Wnt/β-catenin pathway-related protein expression in LC cells. After TNNT1 knockdown, cell scratch healing and transwell assays were introduced to assess cell migration and invasion, respectively.

Results: TNNT1 expression in LC tissues and cells was increased. TNNT1 knockdown notably impaired LC cell migration, invasion and EMT. TNNT1 knockdown inhibited Wnt/β-catenin pathway of LC cells. Lithium chloride (LiCl) addition partially restored the inhibition of TNNT1 knockdown on migration, invasion, EMT and Wnt/β-catenin of LC cells.

Conclusion: TNNT1 knockdown attenuated LC migration, invasion and EMT, possibly through Wnt/β-catenin signaling.

查看原文本刊更多论文

TNNT1 可加速肺癌细胞的迁移、侵袭和 EMT 进展。

背景：临床上，大多数肺癌患者死于肿瘤扩散和转移。特异性转移相关分子可为临床预测疗效、评估预后、寻找最佳治疗方案提供参考。肌钙蛋白 T1（TNNT1）在各种肿瘤组织中高表达，影响肿瘤细胞的恶性行为，与患者的生存和预后有关。然而，TNNT1在LC侵袭和转移中的作用和分子机制尚未得到研究：方法：采用基因表达谱交互分析（GEPIA）在线分析 LC 组织中 TNNT1 的表达。定量实时聚合酶链反应（qRT-PCR）或Western印迹检测TNNT1或上皮细胞向间质转化（EMT）相关蛋白和Wnt/β-catenin通路相关蛋白在LC细胞中的表达。敲除TNNT1后，引入细胞划痕愈合和Transwell试验分别评估细胞迁移和侵袭：结果：TNNT1在LC组织和细胞中的表达增加。结果：TNNT1 在 LC 组织和细胞中的表达增加。TNNT1 敲除抑制了 LC 细胞的 Wnt/β-catenin 通路。氯化锂（LiCl）的加入部分恢复了 TNNT1 敲除对 LC 细胞迁移、侵袭、EMT 和 Wnt/β-catenin 的抑制作用：结论：TNNT1敲除抑制了LC细胞的迁移、侵袭和EMT，可能是通过Wnt/β-catenin信号传导。

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分钟内获得全文求助全文

来源期刊

Thoracic Cancer ONCOLOGY-RESPIRATORY SYSTEM

CiteScore

5.20

自引率

3.40%

发文量

439

审稿时长

2 months

期刊介绍： Thoracic Cancer aims to facilitate international collaboration and exchange of comprehensive and cutting-edge information on basic, translational, and applied clinical research in lung cancer, esophageal cancer, mediastinal cancer, breast cancer and other thoracic malignancies. Prevention, treatment and research relevant to Asia-Pacific is a focus area, but submissions from all regions are welcomed. The editors encourage contributions relevant to prevention, general thoracic surgery, medical oncology, radiology, radiation medicine, pathology, basic cancer research, as well as epidemiological and translational studies in thoracic cancer. Thoracic Cancer is the official publication of the Chinese Society of Lung Cancer, International Chinese Society of Thoracic Surgery and is endorsed by the Korean Association for the Study of Lung Cancer and the Hong Kong Cancer Therapy Society. The Journal publishes a range of article types including: Editorials, Invited Reviews, Mini Reviews, Original Articles, Clinical Guidelines, Technological Notes, Imaging in thoracic cancer, Meeting Reports, Case Reports, Letters to the Editor, Commentaries, and Brief Reports.