PAX5 诱导的 LINC01194 上调通过 miR-486-5p 调控 GOLPH3 表达在前列腺癌中发挥致癌作用。
PAX5-induced upregulation of LINC01194 exerts oncogenic properties by regulating GOLPH3 expression via miR-486-5p in prostate cancer.
机构信息
Department of Laboratory Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
出版信息
Eur Rev Med Pharmacol Sci. 2021 Mar;25(6):2528-2541. doi: 10.26355/eurrev_202103_25416.
OBJECTIVE
Several studies have demonstrated that long non-coding RNA can act as crucial roles during the progression of various tumors, including prostate cancer (PCa). We aimed to determine lncRNA LINC01194(LINC01194) expression in prostate cancer (PCa) and examine its influence on tumor behaviors of PCa cells.
PATIENTS AND METHODS
RT-PCR was performed to examine LINC01194 and PAX5's expression levels in PCa tissues and cell lines. Luciferase reporter and chromatin immunoprecipitation (ChIP) assays were performed to explore whether PAX5 could activate the transcription of LINC01194. Cell viability, migration and invasion were assessed by CCK-8, colony formation, transwell assay and Wound-healing assays. Bioinformatics and Dual-Luciferase assays were used to investigate the interaction between LINC01194 and miR-486-5p, as well as between miR-486-5p and GOLPH3. Western blot was applied for detecting the expressions of the related proteins.
RESULTS
LINC01194 was highly expressed in PCa specimens and cell lines. PAX5 could bind directly to LINC01194 promoter region and activate its transcription. Functionally, the proliferation and metastasis of PCa cells were substantially impeded by LINC01194 silencing in vitro and in vivo. Mechanistically, LINC01194 promoted PCa progression by serving as a sponge of miR-486-5p to increase GOLPH3 expression.
CONCLUSIONS
Our study identifies LINC01194 as a tumor promotor in PCa and implicates the LINC01194/miR-486-5p/GOLPH3 axis in the PCa progression.
目的
多项研究表明，长非编码 RNA 在包括前列腺癌（PCa）在内的多种肿瘤的进展中可以发挥关键作用。本研究旨在确定前列腺癌（PCa）中 lncRNA LINC01194 的表达，并研究其对 PCa 细胞肿瘤行为的影响。
患者和方法
采用 RT-PCR 检测 PCa 组织和细胞系中 LINC01194 和 PAX5 的表达水平。通过荧光素酶报告和染色质免疫沉淀（ChIP）实验检测 PAX5 是否能激活 LINC01194 的转录。通过 CCK-8、集落形成、Transwell 实验和划痕愈合实验评估细胞活力、迁移和侵袭。生物信息学和双荧光素酶实验用于研究 LINC01194 与 miR-486-5p 以及 miR-486-5p 与 GOLPH3 之间的相互作用。Western blot 用于检测相关蛋白的表达。
结果
LINC01194 在 PCa 标本和细胞系中高表达。PAX5 可直接与 LINC01194 启动子区域结合并激活其转录。功能上，LINC01194 沉默可显著抑制体外和体内 PCa 细胞的增殖和转移。机制上，LINC01194 通过作为 miR-486-5p 的海绵来增加 GOLPH3 表达，从而促进 PCa 的进展。
结论
本研究鉴定了 LINC01194 作为 PCa 的肿瘤促进因子，并提示了 LINC01194/miR-486-5p/GOLPH3 轴在 PCa 进展中的作用。
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