Department of Radiology, The First Affiliated Hospital of Naval Medical University, Shanghai 200433, P.R. China.
Department of Urology, Chinese People's Liberation Army (PLA) General Hospital/PLA Medical School, Beijing 100853, P.R. China.
Int J Mol Med. 2021 Jun;47(6). doi: 10.3892/ijmm.2021.4926. Epub 2021 Apr 13.
Prostate cancer is a main health risk for males with a high incidence and mortality. The present study aimed to examine the effects of long non‑coding RNA (lncRNA) MIR4435‑2HG binding with ST8SIA1 on the proliferation, invasion and migration of prostate cancer cells via the activation of the FAK/AKT/β‑catenin signaling pathway. The expression of MIR4435‑2HG and ST8SIA1 in prostate cancer cell lines, and the transfection efficacy were analyzed by RT‑qPCR. The proliferation, clone formation ability, and the invasion and migration of transfected cells were detected by CCK‑8 assay, clone formation assay, Transwell assay and wound healing assay, respectively. Plasmids were injected subcutaneously into mice to construct a xenograft tumor model. The expression levels of proteins related to proliferation, apoptosis, invasion and migration, and the FAK/AKT/β‑catenin pathway were detected by western blot analysis. The results revealed that MIR4435‑2HG expression was increased in the prostate cancer cell lines and MIR4435‑2HG expression was the highest in the PC‑3 cells. Interference with MIR4435‑2HG inhibited the proliferation, clone formation ability, and the invasion and migration of PC‑3 cells, as well as tumor growth by suppressing the activation of the FAK/AKT/β‑catenin signaling pathway. MIR4435‑2HG was demonstrated to target ST8SIA1. ST8SIA1 expression was also increased in the prostate cancer cell lines and MIR4435‑2HG expression was the highest in the PC‑3 cells. Interference with ST8SIA1 inhibited the promoting effects of MIR4435‑2HG on the proliferation, invasion and migration of PC‑3 cells, as well as tumor growth by suppressing the activation of the FAK/AKT/β‑catenin signaling pathway. On the whole, the present study demonstrates that interference with MIR4435‑2HG, combined with ST8SIA1, inhibits the proliferation, invasion and migration of prostate cancer cells and by blocking the activation of the FAK/AKT/β‑catenin signaling pathway.
前列腺癌是男性面临的主要健康风险之一，具有较高的发病率和死亡率。本研究旨在探讨长链非编码 RNA（lncRNA）MIR4435-2HG 与 ST8SIA1 结合对前列腺癌细胞增殖、侵袭和迁移的影响，以及 FAK/AKT/β-catenin 信号通路的激活。通过 RT-qPCR 分析前列腺癌细胞系中 MIR4435-2HG 和 ST8SIA1 的表达及转染效率。通过 CCK-8 检测、克隆形成实验、Transwell 检测和划痕愈合实验分别检测转染细胞的增殖、克隆形成能力以及侵袭和迁移能力。通过质粒注射构建皮下移植瘤模型。通过 Western blot 分析检测与增殖、凋亡、侵袭和迁移相关的蛋白及 FAK/AKT/β-catenin 通路的表达水平。结果表明，MIR4435-2HG 在前列腺癌细胞系中表达增加，其中 PC-3 细胞中表达最高。干扰 MIR4435-2HG 抑制了 PC-3 细胞的增殖、克隆形成能力以及侵袭和迁移能力，并通过抑制 FAK/AKT/β-catenin 信号通路的激活抑制了肿瘤生长。MIR4435-2HG 被证实靶向 ST8SIA1。ST8SIA1 在前列腺癌细胞系中的表达也增加，其中 PC-3 细胞中表达最高。干扰 ST8SIA1 抑制了 MIR4435-2HG 对 PC-3 细胞增殖、侵袭和迁移以及肿瘤生长的促进作用，通过抑制 FAK/AKT/β-catenin 信号通路的激活。综上所述，本研究表明，干扰 MIR4435-2HG 联合 ST8SIA1 通过阻断 FAK/AKT/β-catenin 信号通路的激活，抑制前列腺癌细胞的增殖、侵袭和迁移。
