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.

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It was previously reported that long non-coding RNA (lncRNA) small nucleolar RNA host gene 12 (SNHG12) promoted the proliferation, invasion and migration of endometrial cancer (EC) cells; however, the upstream underlying mechanism remains unclear. The present study aimed to determine the possible underlying mechanism of SNHG12 regulating EC. The Encyclopedia of RNA Interactomes database was used to analyze whether SNHG12 could bind to Zic family member 2 (ZIC2) and the expression levels of ZIC2 in patients with EC. ZIC2 expression levels in EC cell lines were analyzed using western blotting and reverse transcription-quantitative PCR. RL95-2 cells were subsequently transfected with short hairpin RNA targeting ZIC2, or ZIC2 or SNHG12 overexpression plasmids. Cell proliferation, migration and invasion were analyzed using Cell Counting Kit-8, colony formation, wound healing and Transwell assays, respectively. The binding between ZIC2 and SHNG12 was verified using dual luciferase reporter and chromatin immunoprecipitation assays. The results of the present study revealed that the expression levels of ZIC2 were upregulated in the tissues of patients with EC and EC cell lines. ZIC2 knockdown inhibited RL95-2 cell proliferation, migration and invasion. The protein expression levels of Ki67, proliferating cell nuclear antigen, MMP2 and MMP9 were also downregulated following the knockdown of ZIC2. ZIC2 was predicted to bind to SNHG12 and positively regulate SNHG12 expression. Further experiments demonstrated that the effects of the knockdown of ZIC2 on RL95-2 cells were partially reversed by SNHG12 overexpression. In addition, ZIC2 knockdown inhibited Notch signaling activation, while SNHG12 overexpression reversed this effect. In conclusion, the findings of the present study indicated that ZIC2 may upregulate SNHG12 expression to promote EC cell proliferation and migration by activating the Notch signaling pathway.

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