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长链非编码RNA SNHG6通过吸附miR-485-3p增强宫颈癌细胞的放射抗性并促进其生长。

LncRNA SNHG6 enhances the radioresistance and promotes the growth of cervical cancer cells by sponging miR-485-3p.

作者信息

Liu Jin, Liu Xiaojiao, Li Rong

机构信息

Department of Obstetrics and Gynecology, The First Affiliated Hospital of Xi'an Jiaotong University, No. 277 Yanta West Road, Xi'an, 710061 Shaanxi China.

Department of Mammary Gland & Thyroid Surgery, Sichuan Gem Flower Hospital, No. 26 Tongjixiang Road, Chengdu, 610213 Sichuan China.

出版信息

Cancer Cell Int. 2020 Aug 31;20:424. doi: 10.1186/s12935-020-01448-9. eCollection 2020.

Abstract

BACKGROUND

Cervical cancer (CC) is the one of most common malignant gynecological tumors, which is characterized with the high mortality and recurrence rate. Previous studies have elucidated the oncogenic role of small nucleolar RNA host gene 6 (SNHG6) in some types of human cancers, whereas it is unclear whether it functions as an oncogene in CC. This study was aimed at unveiling the role of SNHG6 in CC.

METHODS

qRT-PCR analysis was implemented to evaluate the expression levels of SNHG6, miR-485-3p and STYX in CC cells. RNA pull down assay and luciferase reporter assay were conducted to verify the interaction between miR-485-3p and SNHG6 or STYX. Functional assays, such as colony formation assay, JC-1 assay and TUNEL assay were applied to detect the biological behaviors of CC cells. The resistance of CC cells to radiation was evaluated by colony formation assay.

RESULTS

SNHG6 was expressed at a high level in CC cells. Silenced SNHG6 suppressed cell proliferation but promoted cell apoptosis. Additionally, silenced SNHG6 could sensitize CC cells to radiation treatment. miR-485-3p could bind to both SNHG6 and STYX. Knockdown of miR-485-3p or overexpression of STYX could abolish the effects of SNHG6 silencing on CC cell growth.

CONCLUSIONS

LncRNA SNHG6 enhances the radioresistance of CC cells and promotes CC cell growth by sponging miR-485-3p to release STYX.

摘要

背景

宫颈癌(CC)是最常见的妇科恶性肿瘤之一,其特点是死亡率和复发率高。先前的研究已经阐明了小核仁RNA宿主基因6(SNHG6)在某些类型的人类癌症中的致癌作用,然而其在宫颈癌中是否作为癌基因发挥作用尚不清楚。本研究旨在揭示SNHG6在宫颈癌中的作用。

方法

采用qRT-PCR分析评估SNHG6、miR-485-3p和STYX在宫颈癌细胞中的表达水平。进行RNA下拉试验和荧光素酶报告试验以验证miR-485-3p与SNHG6或STYX之间的相互作用。应用集落形成试验、JC-1试验和TUNEL试验等功能试验来检测宫颈癌细胞的生物学行为。通过集落形成试验评估宫颈癌细胞对辐射的抗性。

结果

SNHG6在宫颈癌细胞中高表达。沉默SNHG6可抑制细胞增殖但促进细胞凋亡。此外,沉默SNHG6可使宫颈癌细胞对放射治疗敏感。miR-485-3p可与SNHG6和STYX结合。敲低miR-485-3p或过表达STYX可消除SNHG6沉默对宫颈癌细胞生长的影响。

结论

长链非编码RNA SNHG6通过海绵吸附miR-485-3p释放STYX来增强宫颈癌细胞的放射抗性并促进宫颈癌细胞生长。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2814/7457785/67ccf1d65d62/12935_2020_1448_Fig1_HTML.jpg

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