miR-450b-5p induced by oncogenic KRAS is required for colorectal cancer progression

Oncotarget. 2016 Sep 20;7(38):61312-61324. doi: 10.18632/oncotarget.11016.

Abstract

The development and progression of CRC are regarded as a complicated network and progressive event including genetic and/or epigenetic alterations. Recent researches revealed that MicroRNAs are biomarkers and regulators of CRC progression. Analyses of published microarray datasets revealed that miR-450b-5p was highly up-regulated in CRC tissues. In addition, high expression of miR-450b-5p was significantly associated with KRAS mutation. However, the role of miR-450b-5p in the progression of CRC remains unknown. Here, we sought to validate the expression of miR-450b-5p in CRC tissues and investigate the role and underlying mechanism of miR-450b-5p in the progression of CRC. The results revealed that miR-450b-5p was up-regulated in CRC tissues, high expression level of miR-450b-5p was positively associated with poor differentiation, advanced TNM classification and poor prognosis. Moreover, miR-450b-5p was especially high in KRAS-mutated cell lines and could be up-regulated by KRAS/AP-1 signaling. Functional validation revealed that overexpression of miR-450b-5p promoted cell proliferation and tumor growth while inhibited apoptosis of CRC cells. Furthermore, we demonstrated that miR-450b-5p directly bound the 3'-UTRs of SFRP2 and SIAH1, and activated Wnt/β-Catenin signaling. In conclusion, miR-450b-5p induced by oncogenic KRAS is required for colorectal cancer progression. Collectively, our work helped to understand the precise role of miR-450b-5p in the progression of CRC, and might promote the development of new therapeutic strategies against CRC.

Keywords: KRAS; Wnt/β-Catenin pathway; colorectal cancer; miR-450b-5p; progression.

MeSH terms

  • 3' Untranslated Regions
  • Animals
  • Apoptosis
  • Biomarkers, Tumor / genetics
  • Cell Differentiation
  • Cell Line, Tumor
  • Cell Proliferation
  • Colorectal Neoplasms / genetics*
  • Colorectal Neoplasms / metabolism*
  • Disease Progression
  • Epigenesis, Genetic
  • Female
  • Gene Expression Regulation, Neoplastic
  • Genes, ras
  • HCT116 Cells
  • Humans
  • Membrane Proteins / metabolism
  • Mice
  • Mice, Inbred BALB C
  • MicroRNAs / metabolism*
  • Neoplasm Transplantation
  • Nuclear Proteins / metabolism
  • Oligonucleotide Array Sequence Analysis
  • Prognosis
  • Signal Transduction
  • Treatment Outcome
  • Ubiquitin-Protein Ligases / metabolism
  • ras Proteins / genetics*

Substances

  • 3' Untranslated Regions
  • Biomarkers, Tumor
  • MIRN450 microRNA, human
  • Membrane Proteins
  • MicroRNAs
  • Nuclear Proteins
  • SFRP2 protein, human
  • Ubiquitin-Protein Ligases
  • seven in absentia proteins
  • ras Proteins