The mechanism of Annexin A1 regulating the proliferation, apoptosis and migration of bladder cancer cells

Q4 Medicine

中华泌尿外科杂志 Pub Date : 2019-12-15 DOI:10.3760/CMA.J.ISSN.1000-6702.2019.12.012

Tao Wang, Peide Bai, Shunqiang Xie, Anran Sun, J. Xing

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引用次数: 0

Abstract

Objective Explore the function and regulatory mechanism of Annexin A1 (ANXA1) in bladder cancer cell proliferation, apoptosis and migration. Methods From February 2018 to June 2019, we use T24 cells as the model and divide it into over-expression control group (ctrl), ANXA1 over-expression group (ANXA1), knockdown control group (shctrl), ANXA1 knockdown group 1 (shANXA1-1), ANXA1 knockdown group 2 (shANXA1-2) and ANXA1 knockdown group 3 (shANXA1-3). 24 hours after the culture, the cells were collected and the mRNA expression level of ANXA1 was detected by Real-Time quantitative PCR. The cell activity was detected by CCK-8; the cell apoptosis and cycle were detected by flow cytometry. The cell migration was detected by Transwell assay. Results The Real-Time quantitative PCR showed that the expression of ANXA1 in the over expression group was significantly higher than that in the over expression control group (15 369.00±874.20 and 1.00±0.07, P 0.05), while the number of apoptosis in the knockdown group 2 and 3 were significantly higher than that in the knockdown control group (13.04%, 14.58% and 7.76%, P<0.001). Cell function analysis showed that the number of cells passing through the membrane of the over expression group was significantly higher than that of the over expression group (525.00±9.30 and 385.70±13.40, P<0.01), while that of the knockdown group 2 and 3 were significantly lower than that of the knockdown control group (214.70±6.40, 226.00±5.30 and 398.70±10.00, P<0.001). Conclusions Over-expression of ANXA1 significantly promoted the proliferation, cycle and migration of T24 cells and inhibited apoptosis. On the contrary, ANXA1 knockdown inhibited the proliferation, cycle and migration of T24 cells and promoted apoptosis. Key words: Urinary bladder neoplasms; Annexin A1; Cell proliferation; Cell apoptosis; Tumor invasion and metastasis

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膜联蛋白A1调节膀胱癌症细胞增殖、凋亡和迁移的机制

目的探讨膜联蛋白A1 (Annexin A1, ANXA1)在膀胱癌细胞增殖、凋亡和迁移中的作用及调控机制。方法2018年2月~ 2019年6月，以T24细胞为模型，将其分为过表达对照组(ctrl)、过表达组(ANXA1)、敲低对照组(shctrl)、敲低组1 (shANXA1-1)、敲低组2 (shANXA1-1)和敲低组3 (shANXA1-3)。培养24 h后收集细胞，采用Real-Time定量PCR检测ANXA1 mRNA表达水平。CCK-8检测细胞活性;流式细胞术检测细胞凋亡及周期。Transwell法检测细胞迁移。结果Real-Time定量PCR结果显示，过表达组的ANXA1表达量显著高于过表达对照组(15 369.00±874.20和1.00±0.07,P< 0.05)，而敲低组2和3的细胞凋亡数量显著高于敲低对照组(13.04%，14.58%和7.76%，P<0.001)。细胞功能分析显示，过表达组细胞膜穿过细胞数显著高于过表达组(525.00±9.30和385.70±13.40,P<0.01)，而敲除组2和3的细胞膜穿过细胞数显著低于敲除对照组(214.70±6.40,226.00±5.30和398.70±10.00,P<0.001)。结论过表达ANXA1可显著促进T24细胞的增殖、周期和迁移，抑制细胞凋亡。反之，ANXA1敲低抑制T24细胞的增殖、周期和迁移，促进细胞凋亡。关键词:膀胱肿瘤;膜联蛋白A1;细胞增殖;细胞凋亡;肿瘤的侵袭和转移

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来源期刊

中华泌尿外科杂志 Medicine-Nephrology

CiteScore

0.10

自引率

0.00%

发文量

14180

期刊介绍： Chinese Journal of Urology (monthly) was founded in 1980. It is a publicly issued academic journal supervised by the China Association for Science and Technology and sponsored by the Chinese Medical Association. It mainly publishes original research papers, reviews and comments in this field. This journal mainly reports on the latest scientific research results and clinical diagnosis and treatment experience in the professional field of urology at home and abroad, as well as basic theoretical research results closely related to clinical practice. The journal has columns such as treatises, abstracts of treatises, experimental studies, case reports, experience exchanges, reviews, reviews, lectures, etc. Chinese Journal of Urology has been included in well-known databases such as Peking University Journal (Chinese Journal of Humanities and Social Sciences), CSCD Chinese Science Citation Database Source Journal (including extended version), and also included in American Chemical Abstracts (CA). The journal has been rated as a quality journal by the Association for Science and Technology and as an excellent journal by the Chinese Medical Association.