Long non‑coding RNA SNHG12 regulates cell proliferation, invasion and migration in endometrial cancer by targeting miR‑4429

Abstract

long non-coding rna small nucleolar rna host gene 12 (SnHG12) has been demonstrated to be oncogenic. The aim of the present study was to examine the effects of SnHG12 on the progression of endometrial cancer (ec). The expression levels of SnHG12 and microrna (mir)-4429 were assessed in ec cell lines by reverse transcription-quantitative Pcr. Plasmids, including SnHG12 short hairpin rnas (shrnas), shrna negative control (nc), SnHG12 overexpression (oV), oV-nc, mir-4429 mimic and mimic-nc, were transfected into rl95-2 cells. Post-transfection, cell counting Kit-8, Transwell Matrigel and wound-healing assays were performed to assess cell proliferation, invasion and migration, respectively. cell cycle phase distribution was assessed by flow cytometry. The protein expression levels of matrix metalloproteinase (MMP)2 and MMP9 were detected by western blotting. mir-4429 target genes were predicted by bioinformatics analysis using target prediction online tools; the findings of this analysis were verified using a dual-luciferase reporter system. Identified as a target of miR-4429, SNHG12 was overexpressed in ec cell lines with decreased expression of mir-4429. Further experiments demonstrated that SnHG12 silencing and overexpression of mir-4429 markedly suppressed proliferation, migration and invasion of rl95-2 cells, arrested cells in the G 1 phase, and markedly downregulated the expression of MMP2 and MMP9. The opposite effects were observed in mir-4429 mimic-transfected rl95-2 cells after SNHG12 was overexpressed. The findings of the present study established the role of SnHG12 and mir-4429 in ec. Therefore, targeting the SnHG12/mir-4429 axis could serve as a potential future therapeutic target for treatment of ec.

ZIC2 upregulates lncRNA SNHG12 expression to promote endometrial cancer cell proliferation and migration by activating the Notch signaling pathway

“…4A ). Consistent with the results of a recent study ( 6 ), SNHG12 expression levels were revealed to be upregulated in EC cell lines, most notably in RL95-2 cells ( Fig. 4B ).…”

“…ZIC2 was predicted to bind to the promoter of SNHG12, which was demonstrated to promote EC progression in our previous study ( 6 ). ZIC2 has been reported to be dominantly located in the nucleus ( 25 ).…”

“…Therefore, it is pivotal to determine the key molecular mechanisms involved in EC cell proliferation and metastasis. In our previous study, SNHG12 was identified as a biomarker that could be used for the early diagnosis and targeted therapy of EC ( 6 ). The results of the present study demonstrated that the expression levels of ZIC2 were upregulated in patients with EC and EC cell lines, and ZIC2 bound to SNHG12 to positively regulate its expression.…”

“…Our previous study demonstrated that long non-coding RNA (lncRNA) small nucleolar RNA host gene 12 (SNHG12) promoted cell proliferation, invasion and migration by targeting microRNA-4429 in EC ( 6 ). However, the upstream mediators and involved underlying mechanisms were not identified.…”

Knockdown of long non‐coding RNA small nucleolar RNA host gene 9 or hexokinase 2 both suppress endometrial cancer cell proliferation and glycolysis

“…Moreover, the mRNA expression level of SNHG9 was lifted in the glioblastoma tissues, and the upregulation of SNHG9 accelerated aerobic glycolysis and cell proliferation in glioblastoma cells 11 . However, to the best of our knowledge, among the SNHGs family, only SNHG12, 23 SNHG16, 24 and SNHG5 25 have been reported to be involved in EC, and no research to date has reported the role of SNHG9 in EC. The results of the present study discovered that SNHG9 expression levels were upregulated in EC tissues and cells.…”