MiR-212-5p inhibits the malignant behavior of clear cell renal cell carcinoma cells by targeting TBX15.

肾透明细胞癌 小RNA 转染 细胞生长 细胞培养 癌症研究 分子生物学 荧光素酶 细胞 免疫印迹 报告基因 HEK 293细胞 生物 化学 基因表达 基因 肾细胞癌 医学 病理 生物化学 遗传学
作者
Deng Jh,Zheng Gy,Li Hz,Ji Zg
出处
期刊:European Review for Medical and Pharmacological Sciences 卷期号:23 (24): 10699-10707 被引量:19
标识
DOI:10.26355/eurrev_201912_19770
摘要

Objective To investigate the role of microRNA-212-5p (miR-212-5p) in clear cell renal cell carcinoma (ccRCC) and to explore the potential underlying mechanisms. Materials and methods 32 pairs of ccRCC clinical samples were collected. Renal ccRCC cells (786-O) and embryonic kidney cells (293T) were cultured in vitro. The ability of cell proliferation was detected by 3-(4,5)-dimethylthiazol(-z-y1)-3,5-diphenyl tetrazolium bromide (MTT) assay. Transwell migration assay was used to detect the abilities of cell invasion and migration. The relative protein and mRNA expressions of miR-212-5p were detected by Western blot and quantitative Real-time polymerase chain reaction (qRT-PCR) analysis, respectively. Furthermore, bioinformatics online sites and luciferase reporter gene assay were performed to predict and verify the potential targets of miR-212-5p, respectively. Results The expression level of miR-212-5p in ccRCC tissues and cell lines was significantly inhibited. Bioinformatics online sites and luciferase reporter gene assay confirmed that T-box transcription factor TBX15 (TBX15) was the potential target gene of miR-212-5p. In vitro experiments demonstrated that the proliferation, cell cycle, cell invasion and migration of ccRCC cells were obviously restricted after up-regulation of miR-212-5p. However, the above functional effects were significantly abolished in ccRCC cells after co-transfection with miR-212-5p mimics and LV-TBX15. Conclusions MiR-212-5p acted as a tumor suppressor gene in ccRCC. Through targeting TBX15, miR-212-5p significantly inhibited the malignant behavior of ccRCC cells. Our findings revealed that miR-212-5p/TBX15 axis might be a potential therapeutic target for the treatment of ccRCC.

科研通智能强力驱动
Strongly Powered by AbleSci AI
更新
大幅提高文件上传限制,最高150M (2024-4-1)

科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
炙热衣完成签到,获得积分10
1秒前
与我常在发布了新的文献求助10
2秒前
4秒前
4秒前
Apr9810h发布了新的文献求助10
4秒前
5秒前
明理宛秋完成签到 ,获得积分10
6秒前
搞怪山晴发布了新的文献求助10
8秒前
maggiexjl完成签到,获得积分10
10秒前
10秒前
胖子东发布了新的文献求助10
10秒前
11秒前
11秒前
科研通AI2S应助甩看文献采纳,获得10
12秒前
Lucas应助you采纳,获得10
13秒前
燕晓啸完成签到 ,获得积分0
13秒前
郑大王完成签到,获得积分20
13秒前
坚定幻嫣发布了新的文献求助10
14秒前
14秒前
Bismarck发布了新的文献求助10
15秒前
NN123完成签到,获得积分10
15秒前
酷波er应助给一采纳,获得10
15秒前
今后应助等待泥猴桃采纳,获得10
15秒前
酷波er应助高兴南琴采纳,获得10
16秒前
17秒前
YY完成签到,获得积分10
17秒前
diorzhang发布了新的文献求助10
18秒前
落后的楼房完成签到,获得积分10
18秒前
丁一发布了新的文献求助20
18秒前
理科学不会完成签到,获得积分10
19秒前
19秒前
Zz发布了新的文献求助10
22秒前
dou完成签到 ,获得积分10
22秒前
研友_LBrm9L完成签到,获得积分10
24秒前
25秒前
荔枝发布了新的文献求助10
25秒前
26秒前
26秒前
26秒前
27秒前
高分求助中
Evolution 10000
Sustainability in Tides Chemistry 2800
юрские динозавры восточного забайкалья 800
Diagnostic immunohistochemistry : theranostic and genomic applications 6th Edition 500
Chen Hansheng: China’s Last Romantic Revolutionary 500
China's Relations With Japan 1945-83: The Role of Liao Chengzhi 400
Classics in Total Synthesis IV 400
热门求助领域 (近24小时)
化学 医学 生物 材料科学 工程类 有机化学 生物化学 物理 内科学 纳米技术 计算机科学 化学工程 复合材料 基因 遗传学 催化作用 物理化学 免疫学 量子力学 细胞生物学
热门帖子
关注 科研通微信公众号,转发送积分 3150293
求助须知:如何正确求助?哪些是违规求助? 2801435
关于积分的说明 7844751
捐赠科研通 2458905
什么是DOI,文献DOI怎么找? 1308810
科研通“疑难数据库(出版商)”最低求助积分说明 628582
版权声明 601727