Department of Urology, The Affiliated Hospital of Zunyi Medical College, Zunyi, Guizhou 563003, P.R. China.
Oncol Rep. 2019 Mar;41(3):1789-1796. doi: 10.3892/or.2019.6975. Epub 2019 Jan 22.
Krüppel‑like factor 4 (KLF4) is a transcription factor and putative tumor suppressor. However, little is known about its role in the progression of prostate cancer. The aim of the present study was to examine the expression and potential role of KLF4 in prostate cancer. KLF4 and E‑cadherin expression in 60 prostate cancer tissues and 60 benign prostatic hyperplasia tissues was characterized by immunohistochemistry. The levels of KLF4 expression in prostate cancer cells were determined by reverse transcription‑quantitative polymerase chain reaction and western blot analysis. LNCaP cells were transduced with lentivirus to induce KLF4 overexpression. The effects of KLF4 overexpression on proliferation, cell cycle and migration were determined by MTT, flow cytometry, wound healing and Transwell migration assays. KLF4 was identified to be primarily expressed in the cytoplasm of non‑tumor prostate tissues. The percentage of KLF4+ tissues among prostate cancer tissues (16.67%) was significantly lower compared with that of non‑tumor tissues (84.67%; P<0.05). Downregulated KLF4 expression was associated with higher stage, positive lymph node metastasis and higher Gleason scores of prostate cancer (all P<0.05). Induction of KLF4 overexpression significantly inhibited the proliferation, wound healing and migration of LNCaP cells and induced their cell cycle arrest at S phase. Furthermore, E‑cadherin expression was downregulated in prostate cancer tissues and KLF4 overexpression enhanced the levels of E‑cadherin expression in LNCaP cells. In conclusion, downregulated KLF4 expression was associated with aggressiveness of prostate cancer, and KLF4 overexpression inhibited the proliferation, wound healing and migration of prostate cancer cells by inducing cell cycle arrest and E‑cadherin expression.
Krüppel 样因子 4(KLF4)是一种转录因子和潜在的肿瘤抑制因子。然而,其在前列腺癌进展中的作用知之甚少。本研究旨在研究 KLF4 在前列腺癌中的表达和潜在作用。通过免疫组织化学法检测 60 例前列腺癌组织和 60 例良性前列腺增生组织中 KLF4 和 E-钙黏蛋白的表达。通过逆转录-定量聚合酶链反应和 Western blot 分析检测前列腺癌细胞中 KLF4 的表达水平。用慢病毒转导 LNCaP 细胞诱导 KLF4 过表达。通过 MTT、流式细胞术、划痕愈合和 Transwell 迁移实验测定 KLF4 过表达对增殖、细胞周期和迁移的影响。鉴定出 KLF4 主要在非肿瘤前列腺组织的细胞质中表达。前列腺癌组织中 KLF4+组织的百分比(16.67%)明显低于非肿瘤组织(84.67%;P<0.05)。下调的 KLF4 表达与前列腺癌的更高分期、阳性淋巴结转移和更高的 Gleason 评分相关(均 P<0.05)。诱导 KLF4 过表达显著抑制 LNCaP 细胞的增殖、划痕愈合和迁移,并诱导其细胞周期停滞在 S 期。此外,E-钙黏蛋白在前列腺癌组织中表达下调,KLF4 过表达增强了 LNCaP 细胞中 E-钙黏蛋白的表达水平。总之,下调的 KLF4 表达与前列腺癌的侵袭性相关,KLF4 过表达通过诱导细胞周期停滞和 E-钙黏蛋白表达抑制前列腺癌细胞的增殖、划痕愈合和迁移。