Long non‐coding RNA SNHG6 promotes cell proliferation and migration through sponging miR‐4465 in ovarian clear cell carcinoma

Abstract

Dysregulation of small nucleolar RNA host gene 6 (SNHG6) exerts critical oncogenic effects and facilitates tumourigenesis in human cancers. However, little information about the expression pattern of SNHG6 in ovarian clear cell carcinoma (OCCC) is available, and the contributions of this long non‐coding RNA to the tumourigenesis and progression of OCCC are unclear. In the present study, we showed via quantitative real‐time PCR that SNHG6 expression was abnormally up‐regulated in OCCC tissues relative to that in unpaired normal ovarian tissues. High SNHG6 expression was correlated with vascular invasion, distant metastasis and poor survival. Further functional experiments demonstrated that knockdown of SNHG6 in OCCC cells inhibited cell proliferation, migration and invasion in vitro as well as tumour growth in vivo. Moreover, SNHG6 functioned as a competing endogenous RNA (ceRNA), effectively acting as a sponge for miR‐4465 and thereby modulating the expression of enhancer of zeste homolog 2 (EZH2). Taken together, our data suggest that SNHG6 is a novel molecule involved in OCCC progression and that targeting the ceRNA network involving SNHG6 may be a treatment strategy in OCCC.

Long noncoding RNA SNHG6 promotes proliferation and angiogenesis of cholangiocarcinoma cells through sponging miR-101-3p and activation of E2F8

“…overexpressed SNHG6 reduces cell apoptosis but promotes cell cycle, cell migration, invasion, EMT, and chemoresistance. SNHG6 exerts its function mainly by serving as miRNA sponge to antagonize the connections between multiple tumor suppressor miRNAs and their target mRNAs [19][20][21][22][23] . In this study, we analyzed public database and found that SNHG6 was also upregulated in CCA cell lines and tissues, and functional investigations showed that SNHG6 silencing inhibited cell proliferation, migration, and HUVECs tube formation, which indicated that SNHG6 functioned as an oncogene in CCA.…”

Long non‐coding RNA SNHG6 promotes the growth and invasion of non‐small cell lung cancer by downregulating miR‐101‐3p

“…It is known that the regulatory mechanisms of SNHG6 are mediated by sponging a variety of miRNAs . SNHG6 also acts as a competing endogenous RNA to upregulate E2F7 by sponging miR‐26a‐5p in LUAD .…”

“…Moreover, SNHG6 acts as the sponges of microRNAs (miRNAs) to participate in the pathogenesis of multiple malignancies. Accumulating evidence shows that SNHG6 acts as an oncogenic factor by sponging miR‐4465 in ovarian clear cell carcinoma and miR‐181a‐5p/−miR‐26a/b/−214 in CRC . These studies indicate that SNHG6 can mediate miRNA networks to participate in cancer progression.…”

Prognostic and clinicopathological significance of SNHG6 in human cancers: a meta-analysis

“…All of the included studies were performed in China and were published from 2016 to 2019 with a mean sample size of 71. In terms of the type of cancer, 5 studies referred to colorectal cancer [10][11][12][13][14], 2 studies related to glioma [15,26], 2 studies involved osteosarcoma [16,27], and the remaining cohorts were on ovarian cancer [18], lung cancer [19], oesophageal cancer [20], gastric cancer [21], and liver cancer [22]. Of the 14 studies included, 6 had survival dates in the original literature, and the survival dates for the others were determined with graphical survival plots following the published method proposed by Tierney et al [28].…”

“…With the development of high-throughput RNA sequencing techniques and bioinformatic algorithms, a spectrum of lncRNAs have been identified. The small nucleolar RNA host gene 6 (SNHG6; also termed U87HG), a subclass of lncRNA molecules, pervasively participates in gene modulation through functioning as an oncogene in different human cancers, including colorectal cancer [10][11][12][13][14], glioma [15], osteosarcoma [16], breast cancer [17], ovarian cancer [18], lung adenocarcinoma [19], oesophageal cancer [20], gastric cancer [21] and liver cancer [22]. Studies have proven that the upregulation of SNHG6 plays multiple critical roles in cell differentiation, proliferation, apoptosis, and multidrug resistance [23,24].…”