Department of Biochemistry & Molecular Biology, Harbin Medical University, Harbin, 150086, Heilongjiang, China.
Teaching Experiment Center of Biotechnology, Harbin Medical University, Harbin, 150086, Heilongjiang, China.
Med Oncol. 2022 May 16;39(5):94. doi: 10.1007/s12032-022-01689-w.
Prostate cancer (PCa) is the second most common cause of cancer-related mortality in men. Prostate cancer metastasis usually observed at the last stage is the major cause of prostate cancer-related death. Long non-coding RNAs were reported to be involved in tumorigenesis and progression of prostate cancer. This study aimed to investigate the effects and related mechanisms of AC245100.4 in prostate cancer. Knockdown and overexpression of AC245100.4 was used to detect the effect of AC245100.4 on cell migration. qRT-PCR was used to confirm the downstream target of AC245100.4. RAP-MS was used to find pathways related to AC245100.4. Western blot was performed to detect the expression of p-p38 and p38. We found that AC245100.4 promoted the migration of prostate cancer cells via regulating PAR2. The AC245100.4 or PAR2 knockdown resulted in a decrease in Vimentin but an increase in E-cadherin protein levels, while the AC245100.4 or PAR2 overexpression got the opposite results. Moreover, we discovered that AC245100.4 activated the p38-MAPK via regulating PAR2. In brief, these results have suggested that AC245100.4 and PAR2 served as oncogenic factors in cellular migration in PCa cells.
前列腺癌（PCa）是男性癌症相关死亡的第二大主要原因。前列腺癌转移通常发生在晚期，是导致前列腺癌相关死亡的主要原因。长链非编码 RNA 被报道参与前列腺癌的发生和发展。本研究旨在探讨 AC245100.4 在前列腺癌中的作用及相关机制。通过敲低和过表达 AC245100.4 来检测 AC245100.4 对细胞迁移的影响。qRT-PCR 用于确认 AC245100.4 的下游靶标。RAP-MS 用于寻找与 AC245100.4 相关的途径。Western blot 用于检测 p-p38 和 p38 的表达。我们发现 AC245100.4 通过调节 PAR2 促进前列腺癌细胞的迁移。AC245100.4 或 PAR2 的敲低导致波形蛋白减少，E-钙黏蛋白增加，而 AC245100.4 或 PAR2 的过表达则得到相反的结果。此外，我们发现 AC245100.4 通过调节 PAR2 激活 p38-MAPK。总之，这些结果表明 AC245100.4 和 PAR2 作为致癌因子在前列腺癌细胞的细胞迁移中发挥作用。
