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Oncol Rep. 2019 Mar;41(3):1789-1796. doi: 10.3892/or.2019.6975. Epub 2019 Jan 22.

Downregulated Krüppel‑like factor 4 expression is associated with the aggressiveness of prostate cancer.

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Department of Urology, The Affiliated Hospital of Zunyi Medical College, Zunyi, Guizhou 563003, P.R. China.


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.

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