MicroRNA-31 is overexpressed in cutaneous squamous cell carcinoma and regulates cell motility and colony formation ability of tumor cells

PLoS One. 2014 Jul 28;9(7):e103206. doi: 10.1371/journal.pone.0103206. eCollection 2014.


Cutaneous squamous cell carcinoma (cSCC) is a malignancy of epidermal keratinocytes that is responsible for approximately 20% of skin cancer-related death yearly. We have previously compared the microRNA (miRNA) expression profile of cSCC to healthy skin and found the dysregulation of miRNAs in human cSCC. In this study we show that miR-31 is overexpressed in cSCC (n = 68) compared to healthy skin (n = 34) and precancerous skin lesions (actinic keratosis, n = 12). LNA in situ hybridization revealed that miR-31 was specifically up-regulated in tumor cells. Mechanistic studies of inhibition of endogenous miR-31 in human metastatic cSCC cells revealed suppressed migration, invasion and colony forming ability, whereas overexpression of miR-31 induced these phenotypes. These results indicate that miR-31 regulates cancer-associated phenotypes of cSCC and identify miR-31 as a potential target for cSCC treatment.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Carcinoma, Squamous Cell / genetics*
  • Carcinoma, Squamous Cell / pathology
  • Cell Cycle / genetics
  • Cell Line, Tumor
  • Cell Movement / genetics*
  • Cell Proliferation
  • Gene Expression Regulation, Neoplastic
  • Gene Expression*
  • Humans
  • MicroRNAs / genetics*
  • Neoplastic Stem Cells / metabolism
  • Skin Neoplasms / genetics*
  • Skin Neoplasms / pathology
  • Transfection
  • Tumor Stem Cell Assay
  • Up-Regulation


  • MIRN31 microRNA, human
  • MicroRNAs

Grant support

This work was supported by the Swedish Research Council (Vetenskapsrådet), Cancerfonden (CAN 2012/730), the Swedish Society of Medicine (Svenska Läkaresällskapet), the Swedish Psoriasis Association (Psoriasisförbundet), the European Skin Research Foundation, the Welander and Finsens Foundation, the Tore Nilssons Foundation, the Lars Hierta Memorial Foundation, the Sigurt and Elsa Golje Memorial Foundation, the Centre of Excellence for Research on Inflammation and Cardiovascular Disease, the Karolinska Institute, and the Stockholm County Council. N.X.L. was supported by the Swedish Society for Medical Research. A.P. was supported by the LEO Pharma Research Foundation. E.S. was supported by the Stockholm County Council. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.