Anticancer effect of miR-96 inhibitor in bladder cancer cell lines

Ting Xu1,2, Xiao-Wen Du1, Jun-Biao Hu1

  • 1Department of Urology, Jinhua People's Hospital, Jinhua, Zhejiang 321000, P.R. China.

Oncology Letters
|February 23, 2018
PubMed

Insights

MicroRNA-96 (miR-96) inhibition suppressed bladder cancer cell proliferation and invasion while promoting apoptosis. HERG1 was identified as a direct target of miR-96, suggesting miR-96 as a potential therapeutic target for bladder cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Bladder cancer is a significant health concern with a need for novel therapeutic targets.
  • MicroRNAs (miRNAs) play crucial roles in cancer development and progression.
  • The specific role of microRNA-96 (miR-96) in bladder cancer remains to be fully elucidated.

Purpose of the Study:

  • To investigate the role of miR-96 in bladder cancer cell proliferation, invasion, and apoptosis.
  • To identify the molecular mechanisms underlying miR-96's function in bladder cancer.
  • To explore the potential of targeting miR-96 as a therapeutic strategy for bladder cancer.

Main Methods:

  • Reverse transcription-polymerase chain reaction (RT-PCR) and western blotting were used to assess miR-96 and HERG1 expression.
  • Transfection with miR-96 inhibitors was employed to modulate miR-96 levels in bladder cancer cell lines.
  • MTT, flow cytometry, and Transwell assays were utilized to evaluate cell viability, apoptosis, and invasion.
  • Dual-luciferase reporter assays were performed to confirm the direct targeting of HERG1 by miR-96.

Main Results:

  • miR-96 was significantly upregulated in bladder cancer cell lines (T24 and 5637) compared to normal uroepithelial cells (SV-HUC-1).
  • Inhibition of miR-96 suppressed bladder cancer cell proliferation and invasion, induced apoptosis, and caused G1 cell cycle arrest.
  • The human ether-à-go-go-related (HERG1) potassium channel was also overexpressed in bladder cancer cells and its expression was inversely correlated with miR-96 inhibition.
  • Dual-luciferase assays confirmed that miR-96 directly targets HERG1.

Conclusions:

  • miR-96 inhibition demonstrates anticancer effects on bladder cancer cells by reducing proliferation and invasion and promoting apoptosis.
  • HERG1 is identified as a direct and functional target of miR-96 in bladder cancer.
  • These findings support miR-96 as a promising therapeutic target for bladder cancer treatment.

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