MicroRNA-141 inhibits tumor growth and minimizes therapy resistance in colorectal cancer

Mol Med Rep. 2017 Mar;15(3):1037-1042. doi: 10.3892/mmr.2017.6135. Epub 2017 Jan 23.

Abstract

Colorectal cancer (CRC) is one of most common cancers and causes of cancer-associated mortality worldwide, due to its recurrence, metastasis and therapy resistance. Cancer stem cells (CSC) have been demonstrated to be vital for tumor initiation and recurrence. microRNAs may act as an oncogenes or tumor suppressors in numerous cancers. The present study demonstrated that microRNA-141 (miR‑141) was downregulated in CSC compared with differentiated cancer cells, and in tumor compared with healthy tissue. miR‑141 may inhibit CRC cell proliferation and the maintenance of CSC stemness, thereby enhancing drug susceptibility. In addition, the present study identified cyclin D2 as a novel target gene of miR‑141. In conclusion, the antitumor role of miR‑141 and its target cyclin D2 may suggest the development of miR‑141 as a potential therapeutic agent.

MeSH terms

  • 3' Untranslated Regions
  • Antineoplastic Agents / pharmacology
  • Cell Cycle / drug effects
  • Cell Cycle / genetics
  • Cell Differentiation / drug effects
  • Cell Differentiation / genetics
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Colorectal Neoplasms / genetics*
  • Colorectal Neoplasms / pathology
  • Colorectal Neoplasms / therapy
  • Cyclin D2 / genetics
  • Drug Resistance, Neoplasm / genetics
  • Gene Expression Profiling
  • Gene Expression Regulation, Neoplastic
  • Humans
  • MicroRNAs / genetics*
  • Neoplastic Stem Cells / drug effects
  • Neoplastic Stem Cells / metabolism
  • Neoplastic Stem Cells / pathology
  • RNA Interference

Substances

  • 3' Untranslated Regions
  • Antineoplastic Agents
  • Cyclin D2
  • MIRN141 microRNA, human
  • MicroRNAs