Long noncoding RNA BLACAT1 promotes cell proliferation and invasion in human cervical cancer

长链非编码RNA BLACAT1促进人宫颈癌细胞增殖和侵袭

阅读:6
作者:Dan Shan, Yumin Shang, Tongxiu Hu

Abstract

Cervical cancer is one of the leading causes of mortality in females worldwide. Predisposition to distant metastasis has reduced the prognosis of this malignancy, thus the identification of a novel agent for metastatic cervical cancer is required. Long noncoding RNAs (LncRNAs) have been reported to serve significant roles in human tumorigenesis. The present study aimed to investigate the effects of a newly discovered LncRNA bladder cancer associated transcript 1 (non-protein coding) (BLACAT1) on cell proliferation and metastasis in cervical cancer. A total of 100 patients with cervical cancer were included, and tumor tissues as well as the adjacent non-cancerous counterparts were collected for reverse transcription-quantitative polymerase chain reaction analysis. It was demonstrated that BLACAT1 was highly expressed in human cervical cancer tissues and cell lines. The knockdown of BLACAT1 with specific short hairpin RNA reduced colony formation rates in ME180 and C33A cells. Cell cycle and cell proliferation assays revealed that depletion of BLACAT1 in ME180, and C33A cells arrested the cell cycle at the G0/G1 phase and inhibited cell proliferation. Transwell assays demonstrated that the knockdown of BLACAT1 inhibited cell migration and invasion in ME180, and C33A cells. Moreover, wound-healing assays supported the aformentioned observations. Western blot analysis showed that the knockdown of BLACAT1 in ME180 and C33A cells decreased the protein levels of cyclin B1, cell division cycle 25C, and N-cadherin, while increasing the protein level of E-cadherin. These findings indicated the oncogenic potential of BLACAT1 in cervical cancer, which may provide novel insights for the clinical diagnosis and treatment of cervical cancer.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。