Yao Lin-Ya, Ma Jun, Zeng Xue-Ming, Ou-Yang Jun
Department of Urology, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, P.R. China.
Department of Urology, Kunshan Chinese Medicine Hospital Affiliated to Nanjing University of Chinese Medicine, Kunshan, Jiangsu 215300, P.R. China.
Oncol Lett. 2020 Dec;20(6):353. doi: 10.3892/ol.2020.12215. Epub 2020 Oct 11.
The aim of the present study was to determine the effect of microRNA (miR)-155-5p on the expression of testican-1 (SPOCK1) and the invasion and migration of prostate cancer cells . Bioinformatics analysis and molecular biology assays revealed that SPOCK1 may be a direct target gene of miR-155-5p. In addition, a negative correlation was identified between SPCOK1 and miR-155-5p expression in prostate tumor tissues and cell lines. miR-155-5p mimic transfection inhibited SPOCK1 expression in PC3 cells and decreased cell migration and invasion abilities, while the expression of vimentin, N-cadherin, E-cadherin, β-catenin, matrix metalloproteinase (MMP)3 and MMP9 was upregulated. In summary, SPOCK1 was found to be a target gene of miR155-5p in prostate cancer, and miR-155-5p acts as a tumor-suppressor gene and may inhibit SPOCK1-mediated prostate cancer progression.
本研究的目的是确定微小RNA（miR）-155-5p对睾丸蛋白聚糖-1（SPOCK1）表达以及前列腺癌细胞侵袭和迁移的影响。生物信息学分析和分子生物学检测显示，SPOCK1可能是miR-155-5p的直接靶基因。此外，在前列腺肿瘤组织和细胞系中，SPCOK1与miR-155-5p表达之间存在负相关。miR-155-5p模拟物转染抑制了PC3细胞中SPOCK1的表达，降低了细胞迁移和侵袭能力，同时波形蛋白、N-钙黏蛋白、E-钙黏蛋白、β-连环蛋白、基质金属蛋白酶（MMP）3和MMP9的表达上调。总之，发现SPOCK1是前列腺癌中miR155-5p的靶基因，miR-155-5p作为肿瘤抑制基因，可能抑制SPOCK1介导的前列腺癌进展。
