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Updated: Feb 5, 2026

miRNA Expression Analyses in Prostate Cancer Clinical Tissues
11:29

miRNA Expression Analyses in Prostate Cancer Clinical Tissues

Published on: September 8, 2015

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KLF4, a miR-32-5p targeted gene, promotes cisplatin-induced apoptosis by upregulating BIK expression in prostate

Lu Zhang1,2, Xiaojie Li1,3, Yulin Chao1

  • 1Department of Urology of the First Affiliated Hospital & Institute of Cancer Stem Cell, Dalian Medical University, Dalian, Liaoning, 116044, People's Republic of China.

Cell Communication and Signaling : CCS
|September 5, 2018
PubMed
Abstract

Insights

Chemotherapy resistance in prostate cancer is a challenge. This study shows that increased KLF4, regulated by miR-32-5p, enhances cisplatin-induced apoptosis and prostate cancer chemosensitivity.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Chemotherapeutic insensitivity is a significant obstacle in prostate cancer treatment.
  • Krüppel-like factor 4 (KLF4) has emerged as a key player in prostate cancer, but its role in chemoresistance is unclear.

Purpose of the Study:

  • To investigate the biological role of KLF4 in the chemotherapeutic insensitivity of prostate cancer.
  • To elucidate the molecular mechanisms underlying KLF4's function in prostate cancer chemoresistance.

Main Methods:

  • Western blotting and CCK8 assays to assess KLF4's role in cisplatin-induced apoptosis.
  • RNA sequencing, q-RT-PCR, western blotting, and ChIP to explore the molecular mechanism.
  • Bioinformatic analysis and luciferase assays to confirm miR-32-5p-mediated KLF4 expression.

Main Results:

  • KLF4 was induced by cisplatin in prostate cancer cells, promoting apoptosis.
  • KLF4 directly upregulated the transcription of BIK by binding to its promoter.
  • Downregulation of miR-32-5p upon cisplatin treatment increased KLF4 expression, enhancing chemosensitivity.

Conclusions:

  • KLF4 is a critical regulator of cisplatin-induced apoptosis in prostate cancer.
  • The miR-32-5p-KLF4-BIK signaling axis is crucial for modulating prostate cancer chemosensitivity.

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