{"title":"TRIM67 与ENAH相互作用,调节肺癌细胞的凋亡和自噬。","authors":"Rui Liu, Kun Miao, Ling Gao, Ling He","doi":"10.4149/gpb_2023037","DOIUrl":null,"url":null,"abstract":"<p><p>The aim of this study was to further clarify the functional mechanism of the triangular 67 (TRIM67) gene in lung cancer cells. We detected the expression of TRIM67 in lung cancer cells by RT-qPCR and Western blot, transfected si-NC, si-TRIM67, and pcDNA-ENAH into the cells. The expression of TRIM67 and ENAH was detected by Western blot and immunofluorescence localization, and CO-IP and GST pull-down experiments verified the interaction. Flow cytometry, Western blot, and transmission electron microscopy (TEM) evaluated the apoptosis and autophagy levels. TRIM67 was highly expressed in lung cancer cell lines. Knockdown of TRIM67 promoted apoptosis and autophagy of A549 and NCI-H1299 cells. TRIM67 interacted with the ENAH protein. ENAH restored the effect of knocking down TRIM67 and further inhibited apoptosis and autophagy of A549 and NCI-H1299 cells. TRIM67 inhibits apoptosis and autophagy of lung cancer cells by interacting with ENAH.</p>","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"43 2","pages":"163-173"},"PeriodicalIF":1.3000,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"TRIM67 interacts with ENAH to regulate the apoptosis and autophagy of lung cancer cells.\",\"authors\":\"Rui Liu, Kun Miao, Ling Gao, Ling He\",\"doi\":\"10.4149/gpb_2023037\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The aim of this study was to further clarify the functional mechanism of the triangular 67 (TRIM67) gene in lung cancer cells. We detected the expression of TRIM67 in lung cancer cells by RT-qPCR and Western blot, transfected si-NC, si-TRIM67, and pcDNA-ENAH into the cells. The expression of TRIM67 and ENAH was detected by Western blot and immunofluorescence localization, and CO-IP and GST pull-down experiments verified the interaction. Flow cytometry, Western blot, and transmission electron microscopy (TEM) evaluated the apoptosis and autophagy levels. TRIM67 was highly expressed in lung cancer cell lines. Knockdown of TRIM67 promoted apoptosis and autophagy of A549 and NCI-H1299 cells. TRIM67 interacted with the ENAH protein. ENAH restored the effect of knocking down TRIM67 and further inhibited apoptosis and autophagy of A549 and NCI-H1299 cells. TRIM67 inhibits apoptosis and autophagy of lung cancer cells by interacting with ENAH.</p>\",\"PeriodicalId\":12514,\"journal\":{\"name\":\"General physiology and biophysics\",\"volume\":\"43 2\",\"pages\":\"163-173\"},\"PeriodicalIF\":1.3000,\"publicationDate\":\"2024-03-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"General physiology and biophysics\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.4149/gpb_2023037\",\"RegionNum\":4,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"General physiology and biophysics","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.4149/gpb_2023037","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0
摘要
本研究旨在进一步阐明三角形 67(TRIM67)基因在肺癌细胞中的功能机制。我们通过 RT-qPCR 和 Western 印迹检测了 TRIM67 在肺癌细胞中的表达,并将 si-NC、si-TRIM67 和 pcDNA-ENAH 转染到细胞中。通过 Western blot 和免疫荧光定位检测了 TRIM67 和 ENAH 的表达,CO-IP 和 GST pull-down 实验验证了其相互作用。流式细胞术、Western印迹和透射电子显微镜(TEM)评估了细胞凋亡和自噬水平。TRIM67在肺癌细胞系中高表达。敲除TRIM67可促进A549和NCI-H1299细胞的凋亡和自噬。TRIM67与ENAH蛋白相互作用。ENAH恢复了敲除TRIM67的效果,并进一步抑制了A549和NCI-H1299细胞的凋亡和自噬。TRIM67通过与ENAH相互作用抑制肺癌细胞的凋亡和自噬。
TRIM67 interacts with ENAH to regulate the apoptosis and autophagy of lung cancer cells.
The aim of this study was to further clarify the functional mechanism of the triangular 67 (TRIM67) gene in lung cancer cells. We detected the expression of TRIM67 in lung cancer cells by RT-qPCR and Western blot, transfected si-NC, si-TRIM67, and pcDNA-ENAH into the cells. The expression of TRIM67 and ENAH was detected by Western blot and immunofluorescence localization, and CO-IP and GST pull-down experiments verified the interaction. Flow cytometry, Western blot, and transmission electron microscopy (TEM) evaluated the apoptosis and autophagy levels. TRIM67 was highly expressed in lung cancer cell lines. Knockdown of TRIM67 promoted apoptosis and autophagy of A549 and NCI-H1299 cells. TRIM67 interacted with the ENAH protein. ENAH restored the effect of knocking down TRIM67 and further inhibited apoptosis and autophagy of A549 and NCI-H1299 cells. TRIM67 inhibits apoptosis and autophagy of lung cancer cells by interacting with ENAH.
期刊介绍:
General Physiology and Biophysics is devoted to the publication of original research papers concerned with general physiology, biophysics and biochemistry at the cellular and molecular level and is published quarterly by the Institute of Molecular Physiology and Genetics, Slovak Academy of Sciences.