The mechanism of lncRNA SNHG16 in mediating the proliferation and metastasis of clear cell renal cell carcinoma cells via regulating miR-506-3p

CHENG Tao; GU Mingli; XU Weiqiang

doi:10.3969/j.issn.1002-7386.2026.02.001

Abstract：Objective To investigate the effects of long non-coding RNA(lncRNA)SNHG16 by targeting miR-506-3p on cell proliferation and metastasis of clear cell renal cell carcinoma(ccRCC)and its mechanism.Methods The ENCORI/starBase database was used to predict the binding sites of lncRNA SNHG16 and PTBP1 to miR-506-3p.The interaction of lncRNA SNHG16 and PTBP1 with miR-506-3p was determined by dual-luciferase reporter assay and RNA immunoprecipitation assay.The expression levels of lncRNA SNHG16 in ccRCC cell lines(Caki-1,A498,ACHN,786-O and OSRC-2)versus human normal renal cortical proximal tubular epithelial cells(HK-2)were measured by quantitative reverse-transcription polymerase chain reaction(qRT-PCR).Meanwhile,miR-506-3p level and PTBP1 mRNA expression in A498 cells were measured by qRT-PCR as well.A498 cells were transfected with short hairpin RNA targeting lncRNA SNHG16(sh-lncRNA SNHG16)and its negative control(shNC),miR-506-3p inhibitor and its negative control(NC inhibitor),miR-506-3p mimic(miR-506-3p)and its negative control(miR-NC),PTBP1-overexpressing plasmid(pcDNA3.1-PTBP1),and the empty vector pcDNA3.1.Subcellular localization of lncRNA SNHG16 was determined by cytoplasmic RNA isolation.The proliferative,migratory and invasive abilities of A498 cells were assessed by cell counting kit-8(CCK-8)assay,EdU and Transwell assays,respectively.Western blot was conducted to measure the protein expression of PTBP1.Results qRT-PCR results showed that compared with normal cells,lncRNA SNHG16 was significantly upregulated in ccRCC cells(P<0.05),which was localized in the cytoplasm(P<0.05).Compared with shNC group,the viability,proliferation,migration and invasion were significantly reduced in A498 cells transfected with sh-lncRNA SNHG16(P<0.05).Overexpression of miR-506-3p significantly decreased the luciferase activity of SNHG16-WT in A498 cells(P<0.05),and Ago2 antibody was significantly enriched in both lncRNA SNHG16 and miR-506-3p(P<0.05).Overexpression of miR-506-3p downregulated lncRNA SNHG16(P<0.05).Knockdown of miR-506-3p significantly weakened the inhibitory effects of silenced lncRNA SNHG16 on the proliferation,migration and invasion of ccRCC cells(P<0.05).Restoration of miR-506-3p inhibited luciferase activity of PTBP1-WT and mRNA and protein levels of PTBP1 in A498 cells(P<0.05).PTBP1 overexpression attenuated the suppressive effects of miR-506-3p on the proliferation,migration and invasion of ccRCC cells(P<0.05).Conclusion LncRNA SNHG16 is upregulated in ccRCC,and knockdown of lncRNA SNHG16 inhibits the proliferation and metastasis of ccRCC cells by targeting the miR-506-3p/PTBP1 axis.