EMT in cervical cancer: its role in tumour progression and response to therapy

Cancer Lett. 2015 Jan 28;356(2 Pt B):321-31. doi: 10.1016/j.canlet.2014.09.021. Epub 2014 Sep 30.

Abstract

The prognosis of cervical patients significantly decreases as the cancer metastasizes to other parts of the body. The epithelial to mesenchymal transition (EMT) plays an important role in cervical cancer progression and metastasis. Recurrence is the primary cause of the increased number of deaths due to cervical cancer. Oncogenes, such as AEG1, Sam-68, FTS and miR-361-5p, induce EMT in cervical cancer. Tumour suppressors, such as LMX-1, SFRP1, klotho, and miR-155, suppress EMT in cervical cancer. Factors such as hypoxia, the radiation dose, cytokines, proteins, transcription factors, and signalling pathways also play an important role in the induction, progression and maintenance of EMT in cervical cancer. Overall, this review describes a wide range of factors with potential roles in EMT that have been identified to date, and this information could be important for the development of new and more effective therapeutics that ameliorate the negative impact of cervical pathogenesis via EMT.

Keywords: Cervical cancer; Epithelial Mesenchymal Transition; Mesenchymal transition (EMT); Oncogene; Therapeutics; Tumour-suppressor.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Antineoplastic Agents / therapeutic use*
  • Cell Transformation, Neoplastic / drug effects*
  • Cell Transformation, Neoplastic / pathology*
  • Disease Progression
  • Epithelial-Mesenchymal Transition*
  • Female
  • Gene Expression Regulation, Neoplastic / drug effects*
  • Humans
  • Signal Transduction / drug effects*
  • Uterine Cervical Neoplasms / drug therapy*
  • Uterine Cervical Neoplasms / pathology*

Substances

  • Antineoplastic Agents