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通过RNA干扰敲低SMYD3可抑制宫颈癌细胞在体外的生长和侵袭。

Knockdown of SMYD3 by RNA interference inhibits cervical carcinoma cell growth and invasion in vitro.

作者信息

Wang Shu-zhen, Luo Xue-gang, Shen Jing, Zou Jia-ning, Lu Yun-hua, Xi Tao

机构信息

School of Life Science and Technology, China Pharmaceutical University, Nanjing 210009, P R China.

出版信息

BMB Rep. 2008 Apr 30;41(4):294-9. doi: 10.5483/bmbrep.2008.41.4.294.

Abstract

Elevated expression of SMYD3 is a frequent genetic abnormality in several malignancies. Few studies knocking down SMYD3 expression in cervical carcinoma cells have been performed to date. In this paper, we established an inducible short hairpin RNA expression system to examine its role in maintaining the malignant phenotype of HeLa cells. After being induced by doxycycline, SMYD3 mRNA and protein expression were both reduced, and significant reductions in cell proliferation, colony formation and migration/invasion activity were observed in the SMYD3-silenced HeLa cells. The percentage of cells in sub-G1 was elevated and DNA ladder formation could be detected, indicating potent induction of apoptosis by SMYD3 knockdown. These findings imply that SMYD3 plays crucial roles in HeLa cell proliferation and migration/invasion, and that it may be a useful therapeutic target in human cervical carcinomas.

摘要

SMYD3的高表达是几种恶性肿瘤中常见的基因异常。迄今为止,很少有研究在宫颈癌细胞中敲低SMYD3的表达。在本文中,我们建立了一个可诱导的短发夹RNA表达系统,以研究其在维持HeLa细胞恶性表型中的作用。强力霉素诱导后,SMYD3的mRNA和蛋白表达均降低,并且在SMYD3沉默的HeLa细胞中观察到细胞增殖、集落形成及迁移/侵袭活性显著降低。亚G1期细胞的百分比升高,并且可以检测到DNA梯状条带的形成,这表明敲低SMYD3可有效诱导细胞凋亡。这些发现意味着SMYD3在HeLa细胞增殖及迁移/侵袭中起关键作用,并且它可能是人类宫颈癌中一个有用的治疗靶点。

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