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linc00675在肺癌组织和细胞中的表达及其抑制肺癌细胞迁移和侵袭的机制
引用本文:赵凌燕,梁宗安,曾茄,熊小敏.linc00675在肺癌组织和细胞中的表达及其抑制肺癌细胞迁移和侵袭的机制[J].现代肿瘤医学,2021,0(1):16-21.
作者姓名:赵凌燕  梁宗安  曾茄  熊小敏
作者单位:1.四川大学华西临床医学院呼吸与危重症医学科,四川 成都 610041; 2.广元市中心医院呼吸与危重症医学科,四川 广元 628000
基金项目:四川省卫生和计划委员会科技发展项目(编号:180563218);广元市科技计划项目(编号:2017ZCZDYF021)。
摘    要:目的:探讨linc00675在肺癌组织和细胞中的表达以及其对肺癌细胞迁移、侵袭的影响。方法:采用qRT-PCR检测linc00675在35例肺癌组织和癌旁组织及肺癌细胞株SPCA1、A549、NCI-H446和人肺正常上皮细胞BEAS-2B中的表达。利用细胞转染实验对肺癌细胞SPCA1进行LV-linc00675和siRNA-linc00675及相关阴性对照的转染,采用qRT-PCR检测linc00675的表达水平。采用Transwell实验检测过表达及干扰linc00675表达对SPCA1细胞迁移和侵袭能力的影响。通过Western blot实验检测细胞上皮标志蛋白 E-钙黏蛋白(E-cadherin)、间质标志蛋白 N-钙黏蛋白(N-cadherin)、波形蛋白(Vimentin)的表达水平。结果:linc00675在肺癌组织中的表达显著低于癌旁组织,在肺癌细胞株中的表达显著低于人肺正常上皮细胞。转染LV-linc00675可显著增加linc00675在肺癌细胞中的表达,转染siRNA-linc00675可显著降低linc00675在肺癌细胞中的表达。Transwell实验结果显示,过表达linc00675可显著抑制肺癌细胞的迁移和侵袭能力,干扰linc00675表达可显著增强肺癌细胞的迁移和侵袭能力。Western blot实验结果显示,过表达linc00675可显著抑制SPCA1细胞上皮间质转化(EMT)的发生,干扰linc00675表达后SPCA1细胞发生了明显的EMT。结论:linc00675在肺癌细胞中发挥抑癌作用,linc00675可能通过抑制肺癌细胞EMT的发生从而减弱其迁移和侵袭能力,提示linc00675可能成为肺癌治疗的新靶点。

关 键 词:linc00675  肺癌  迁移  侵袭

Expression of linc00675 in lung cancer tissues and cells and its mechanism of inhibiting migration and invasion of lung cancer cells
ZHAO Lingyan,LIANG Zongan,ZENG Jia,XIONG Xiaomin.Expression of linc00675 in lung cancer tissues and cells and its mechanism of inhibiting migration and invasion of lung cancer cells[J].Journal of Modern Oncology,2021,0(1):16-21.
Authors:ZHAO Lingyan  LIANG Zongan  ZENG Jia  XIONG Xiaomin
Institution:1.Department of Respiratory and Critical Medicine,Huaxi Clinical Medical College of Sichuan University,Sichuan Chengdu 610041, China;2.Department of Respiratory and Critical Medicine,Guangyuan City Central Hospital,Sichuan Guangyuan 628000,China.
Abstract:Objective:To investigate the expression of linc00675 in lung cancer tissues and cells and its effect on migration and invasion of lung cancer cells.Methods:The expression of linc00675 was detected by qRT-PCR in 35 lung cancer tissues and adjacent tissues,lung cancer cell lines SPCA1,A549,NCI-H446 and human lung normal epithelial cells BEAS-2B.The cell transfection experiment was used to transfer LV-linc00675 and siRNA-linc00675 and related negative controls into lung cancer cell SPCA1,the expression level of linc00675 was detected by qRT-PCR.Transwell assay was used to detect the effect of overexpression and interference with the expression of linc00675 on the migration and invasion of SPCA1 cells.The expression levels of epithelial marker protein E-cadherin,interstitial marker protein N-cadherin and Vimentin were detected by Western blot.Results:The expression of linc00675 in lung cancer tissues was significantly lower than that in adjacent tissues,and the expression in lung cancer cell lines was significantly lower than that in normal lung epithelial cells.Transfection of LV-linc00675 significantly increased the expression of linc00675,and transfection of siRNA-linc00675 significantly decreased the expression of linc00675 in lung cancer cells.Transwell results showed that overexpression of linc00675 significantly inhibited the migration and invasion of lung cancer cells,and interference with the expression of linc00675 significantly enhanced the migration and invasion of lung cancer cells.Western blot showed that overexpression of linc00675 significantly inhibited the occurrence of EMT in SPCA1 cells,and EMT was observed in SPCA1 cells after interfering with the expression of linc00675.Conclusion:Linc00675 plays an anti-cancer role in lung cancer cells.Linc00675 may decrease its migration and invasion ability by inhibiting the occurrence of EMT in lung cancer cells,suggesting that linc00675 may become a new target for lung cancer treatment.
Keywords:linc00675  lung cancer  migration  invasion
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