LncRNA SNHG6 enhances the radioresistance and promotes the growth of cervical cancer cells by sponging miR-485-3p
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PRIMARY RESEARCH
Cancer Cell International Open Access
LncRNA SNHG6 enhances the radioresistance and promotes the growth of cervical cancer cells by sponging miR‑485‑3p Jin Liu1, Xiaojiao Liu2 and Rong Li1*
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. Keywords: SNHG6, miR-485-3p, STYX, Cervical cancer Background Cervical cancer (CC) is a malignant cancer worldwide and endangers the health of females [1–3]. Studies have shown that no less than 530,000 people are diagnosed with CC each year and 280,000 people are passed away because of this cancer [1–3]. Even if the development in surgery and medicine therapy, the overall survival of CC patients remains pessimistic [4, 5]. Therefore, the *Correspondence: [email protected] 1 Department of Obstetrics and Gynecology, The First Affiliated Hospital of Xi’an Jiaotong University, No. 277 Yanta West Road, Xi’an 710061, Shaanxi, China Full list of author information is available at the end of the article
molecular mechanism underlying CC progression still need to be further identified. The aim of our present study was to explore the mechanism underneath the progression of CC. Long non-coding RNAs (lncRNAs) are transcripts almost without the ability to code proteins, which are characterized with the length more than 200 nt. Studies have revealed the important role of lncRNAs in regulating protein-coding genes and carcinogenesis [6]. LncRNAs can modulate their target genes at transcriptional or post-transcriptional level. Functionally, lncRNAs can affect various biological processes in cancers, such as cell proliferation, migration and invasion [7, 8]. For instance, lncRNA PVT1 can reduce the radioresistance of
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