miR-483-5p通过下调CDK15促进肾上腺皮质癌增殖和侵袭

目的探讨miR-483-5p在肾上腺皮质癌中的作用及其可能的作用机制。方法荧光定量PCR法检测miR-483-5p和CDK15在肾上腺皮质癌组织和细胞系中的表达,CCK-8增殖试验测定miR-483-5p对细胞增殖的影响,Transwell法检测ACC细胞侵袭性的变化。荧光素酶试验和挽救实验验证miR-483-5p与CDK15相关的分子机制。结果miR-483-5p在肾上腺皮质癌组织中高表达(2.36±1.02 vs 1.09±0.43),CDK15在肾上腺皮质癌组织中低表达(0.57±0.26 vs 1.06±0.32)。荧光素酶检测证实CDK15是miR-483-5p的直接靶点。过表达miR-483-5p可通过下调CDK15的表达促进ACC细胞的增殖(24 h:0.26±0.03 vs 0.23±0.04,48 h:0.56±0.05 vs 0.41±0.03,72 h:0.73±0.04 vs 0.59±0.03)和侵袭能力(95.78±4.66 vs 23.89±2.52)。结论miR-483-5p可通过下调CDK15的表达促进肾上腺皮质癌的发生发展,其可作为肾上腺皮质癌的潜在生物标志物及治疗肾上腺皮质癌的新的作用靶点。

miR-483-5p promote adrenocortical cancer proliferation and invasion via down-regulation of CDK15

Objective To investigate the role of miR-483-5p in adrenocortical cancer(ACC)and its possible mechanism.Methods Quantitative real-time polymerase chain reaction was conducted to estimate the expression of miR-483-5p and CDK15 in ACC tissues and cell lines.The effects of miR-483-5p on proliferation were determined in vitro using CCK-8 proliferation assays,the changes of invasion of ACC cells were examined by Transwell.The molecular mechanism underlying the relevance between miR-483-5p and CDK15 was confirmed by luciferase assay and rescue assays.Results We found a relatively higher miR-483-5p(2.36±1.02 vs 1.09±0.43)and lower CDK15(0.57±0.26 vs 1.06±0.32)expression in ACC specimens and cell lines.CDK15 was verified as a direct target of miR-483-5p by luciferase assay.over-expression of miR-483-5p promoted proliferation(24 h:0.26±0.03 vs 0.23±0.04,48 h:0.56±0.05 vs 0.41±0.03,72 h:0.73±0.04 vs 0.59±0.03)and invasion(95.78±4.66 vs 23.89±2.52)by down-regulating CDK15 expression.Conclusion miR-483-5p plays a tumorigenesis role in ACC progression by down-regulating CDK15 expression,which may lead to a novel insight to the potential biomarker and novel therapeutic strategies for ACC.