LncRNA SNHG16调节miR-212-3p/FAM3C轴对食管癌细胞增殖迁移和侵袭的影响OACSTPCD

Objective:To investigate the effect of long non-coding small nucleolar RNA host gene 16(LncRNA SNHG16)targeting microRNA-212-3p(miR-212-3p)/Family with sequence similarity 3 mem-ber C(FAM3C)axis on the proliferation,migration,and invasion of esophageal cancer cells.Methods:Hu-man esophageal cancer cells KYSE-510 were cultured in vitro and divided into five groups:control group,si-NC group,si-SNHG16 group,si-SNHG16+inhibitor NC group,and si-SNHG16+miR-212-3p inhibitor group.The expression levels of LncRNA SNHG16,miR-212-3p,and FAM3C mRNA were detected using RT-qPCR.The proliferation of KYSE-510 cells was assessed using the CCK-8 assay,apoptosis was analyzed by flow cytometry,migration was evaluated by wound healing assay,and invasion was measured by Transwell assay.The dual-luciferase reporter assay was used to verify the targeting relationship between LncRNA SNHG16 and miR-212-3p,as well as between miR-212-3p and FAM3C.Results:Compared with the con-trol and si-NC groups,the si-SNHG16 group showed decreased levels of LncRNA SNHG16 and FAM3C mR-NA,reduced OD values,lower wound healing rates,decreased invasion numbers,and increased miR-212-3p levels and apoptosis rates(P＜0.05).Compared with the si-SNHG16+inhibitor NC group,the si-SNHG16+miR-212-3p inhibitor group showed decreased miR-212-3p levels and apoptosis rates,and in-creased FAM3C mRNA levels,OD values,wound healing rates,and invasion numbers(P＜0.05),with no difference in LncRNA SNHG16 levels(P＞0.05).Bioinformatics prediction revealed the presence of target binding sites between miR-212-3p and both LncRNA SNHG16 and FAM3C,which was further validated by the dual-luciferase reporter assay(P＜0.05).Conclusion:LncRNA SNHG16 is upregulated in esophageal cancer.Knockdown of LncRNA SNHG16 can target and upregulate miR-212-3p,inhibiting the expression of FAM3C,thereby suppressing the proliferation,migration,and invasion of esophageal cancer cells and promo-ting apoptosis.