子宫颈鳞状细胞癌中tRF-Glu38的表达及细胞增殖机制的研究OA

Objective This study aimed to investigate the expression of tRF-Glu38 in cervical squamous cell car-cinoma(CSCC)and its effect on CSCC cell proliferation.Methods The expression of tRF-Glu38 in CSCC tissues was detected by qRT-PCR.Cell proliferation was assessed using CCK-8 assay and colony formation assay.Down-stream target genes of tRF-Glu38 were predicted by bioinformatics and validated by dual-luciferase assay.Rescue ex-periments were conducted to verify the regulation of downstream target genes by tRF-Glu38 and their effects on cell pro-liferation.The impact of tRF-Glu38 on the growth and proliferation of transplanted tumors in nude mice was evalu-ated.Results The expression of tRF-Glu38 in 82 CSCC tissues(8.12±2.16)was significantly higher than that in adjacent normal tissues(3.32±1.06).tRF-Glu38 expression was closely associated with tumor size and differentia-tion.CCK-8 assays showed that overexpression of tRF-Glu38 promoted the proliferation of C33A and SiHa cells(both P<0.05),whereas knockdown of tRF-Glu38 inhibited their proliferation(both P<0.05).Colony formation assays re-vealed that the numbers of colonies in SiHa and C33A cells overexpressing tRF-Glu38 were 33.37±2.72 and 32.60±1.80,respectively,significantly higher than those in the control group(17.13±1.82 and 17.20±1.20)(both P<0.05).In the tRF-Glu38 knockdown group,colony numbers decreased to 11.53±1.04 and 10.20±1.30,respec-tively,significantly lower than the control(18.57±1.33 and 17.17±2.12)(both P<0.05).In vivo,tRF-Glu38 pro-moted the growth of CSCC xenografts in nude mice.Dual-luciferase assays confirmed that tRF-Glu38 bound to the 3′untranslated region of TP53I11,suppressing its expression and thereby promoting CSCC cell proliferation.Rescue ex-periments showed that overexpression of tRF-Glu38 decreased TP53I11 protein levels and increased NF-κB levels,whereas knockdown had the opposite effects.Further colony formation assays indicated that the tRF-Glu38/TP53I11/NF-κB signaling pathway promoted cervical cancer cell colony formation.Conclusion tRF-Glu38 is a novel oncogene in CSCC that promotes NF-κB expression by inhibiting TP53I11.The tRF-Glu38/TP53I11/NF-κB signaling pathway contributes to CSCC cell proliferation and growth.