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MicroRNA-31 functions as a tumor suppressor and increases sensitivity to mitomycin-C in urothelial bladder cancer by

Tianyuan Xu1, Liang Qin1, Zhaowei Zhu2

  • 1Department of Urology, Ruijin Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.

Oncotarget
|April 7, 2016
PubMed

Insights

MicroRNA-31 (miR-31) is significantly reduced in urothelial bladder cancer (UBC), correlating with higher recurrence risks. Restoring miR-31 inhibits UBC progression and enhances chemotherapy effectiveness, suggesting its therapeutic potential.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Urothelial bladder cancer (UBC) is a prevalent genitourinary malignancy with diverse clinical behaviors.
  • MicroRNAs (miRNAs) play crucial roles in cancer, but the specific function of miR-31 in UBC remains unclear.
  • Understanding miR-31's role is vital for developing novel diagnostic and therapeutic strategies for UBC.

Purpose of the Study:

  • To investigate the role and mechanism of miR-31 in urothelial bladder cancer.
  • To determine if miR-31 levels correlate with UBC prognosis and clinical outcomes.
  • To explore the therapeutic potential of miR-31 in UBC treatment.

Main Methods:

  • Quantitative analysis of miR-31 expression in UBC tumor samples and normal urothelium.
  • Prognostic analysis using the EORTC model to assess the correlation between miR-31 levels and UBC recurrence/progression.
  • In vitro studies involving miR-31 mimic transfection in UBC cell lines to evaluate effects on proliferation, migration, and invasion.
  • Identification of miR-31 direct targets using bioinformatics and experimental validation.
  • In vivo studies using UBC xenografts to assess the impact of miR-31 on tumor growth and chemotherapy response.

Main Results:

  • Down-regulation of miR-31 was observed in UBC tissues, particularly in invasive cases, compared to normal urothelium.
  • Reduced miR-31 levels significantly correlated with increased risks of recurrence and progression in noninvasive UBC.
  • Overexpression of miR-31 suppressed UBC cell proliferation, migration, and invasion by targeting Integrin α5 (ITGA5).
  • miR-31 overexpression enhanced sensitivity to mitomycin-C (MMC) by promoting apoptosis and deactivating Akt/ERK signaling, effects reversed by ITGA5 restoration.
  • In vivo, miR-31 inhibited tumor growth and potentiated MMC efficacy in UBC xenografts.

Conclusions:

  • miR-31 acts as a tumor suppressor in urothelial bladder cancer.
  • Down-regulation of miR-31 is a significant prognostic predictor for UBC recurrence and progression.
  • miR-31 represents a promising therapeutic target for enhancing conventional chemotherapy in UBC.
Keywords:
bladder cancerchemotherapyintegrin α5microRNA-31mitomycin-C

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