MiR-31 regulates the cisplatin resistance by targeting Src in gallbladder cancer

Oncotarget. 2016 Dec 13;7(50):83060-83070. doi: 10.18632/oncotarget.13067.

Abstract

Background: Gallbladder cancer (GBC) is a malignant tumor highly resistant to chemotherapy. MicroRNAs (miRNAs) are found extensively involved in modulation of carcinogenesis and chemoresistance. This study aimed to investigate cisplatin (DDP)-susceptibility regulated by expression of the miRNAs and underlying pathways in GBC.

Results: The microRNA-31 (miR-31) was selected by microarray due to the biggest fold change between DDP-resistant and parental cells. Ectopic overexpression of miR-31 decreased cell proliferation, viability and invasion capacity, but promoted apoptosis in DDP-resistant cells and in xenograft tumor models. Cell apoptosis and DDP-chemosensitivity was remarkably increased by knockdown of Src proto-oncogene (Src) expression, which was subsequently reversed by rescue of Src expression in miR-31-expressing cells.

Methods: The microarray was used to select the candidate miRNA in two DDP-resistant GBC cell lines. The effect of regulated expression of the miRNA on cell migration, invasion, proliferation and apoptosis was examined by wound healing, transwell assays, CCK-8 assays, colony formation and flow cytometry assays, respectively. Xenograft tumor models were used to validate the function of the downstream target.

Conclusion: Our results demonstrated that miR-31reduced significantly in GBC cells rendering resistance to cisplatin, and upregulated expression of miR-31 augmented chemosensitivity, presenting a therapeutic potential to overcome drug resistance in GBC.

Keywords: DDP; drug resistance; gallbladder cancer; miR-31; src.

MeSH terms

  • Animals
  • Antineoplastic Agents / pharmacology*
  • Apoptosis / drug effects
  • Cell Line, Tumor
  • Cell Movement / drug effects
  • Cell Proliferation / drug effects
  • Cell Survival / drug effects
  • Cisplatin / pharmacology*
  • Dose-Response Relationship, Drug
  • Drug Resistance, Neoplasm* / genetics
  • Gallbladder Neoplasms / drug therapy*
  • Gallbladder Neoplasms / enzymology
  • Gallbladder Neoplasms / genetics
  • Gallbladder Neoplasms / pathology
  • Gene Expression Profiling / methods
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Male
  • Mice, Nude
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • Neoplasm Invasiveness
  • Oligonucleotide Array Sequence Analysis
  • Proto-Oncogene Mas
  • Proto-Oncogene Proteins c-akt / metabolism
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • RNA Interference
  • Signal Transduction / drug effects
  • Time Factors
  • Transfection
  • Tumor Burden / drug effects
  • Xenograft Model Antitumor Assays
  • bcl-2-Associated X Protein / metabolism
  • src-Family Kinases / genetics
  • src-Family Kinases / metabolism*

Substances

  • Antineoplastic Agents
  • BAX protein, human
  • BCL2 protein, human
  • MAS1 protein, human
  • MIRN31 microRNA, human
  • MicroRNAs
  • Proto-Oncogene Mas
  • Proto-Oncogene Proteins c-bcl-2
  • bcl-2-Associated X Protein
  • src-Family Kinases
  • Proto-Oncogene Proteins c-akt
  • Cisplatin