Involvement of NEAT1/miR-133a axis in promoting cervical cancer progression via targeting SOX4

J Cell Physiol. 2019 Aug;234(10):18985-18993. doi: 10.1002/jcp.28538. Epub 2019 Apr 1.

Abstract

NEAT1 is an important tumor oncogenic gene in various tumors. Nevertheless, its involvement remains poorly studied in cervical cancer. Our study explored the functional mechanism of NEAT1 in cervical cancer. NEAT1 level in several cervical cancer cells was quantified and we found NEAT1 was greatly upregulated in vitro. NEAT1 knockdown inhibited cervical cancer development through repressing cell proliferation, colony formation, capacity of migration, and invasion and also inducing the apoptosis. For another, microRNA (miR)-133a was downregulated in cervical cancer cells and NEAT1 negatively modulated miR-133a expression. Subsequently, we validated that miR-133a functioned as a potential target of NEAT1. Meanwhile, SOX4 is abnormally expressed in various cancers. SOX4 was able to act as a downstream target of miR-133a and silencing of SOX4 can restrain cervical cancer progression. In addition, in vivo assays were conducted to prove the role of NEAT1/miR-133a/SOX4 axis in cervical cancer. These findings implied that NEAT1 served as a competing endogenous RNA to sponge miR-133a and regulate SOX4 in cervical cancer pathogenesis. To sum up, it was implied that NEAT1/miR-133a/SOX4 axis was involved in cervical cancer development.

Keywords: NEAT1; SOX4; cervical cancer; miR-133a.

MeSH terms

  • Carcinogenesis / genetics
  • Cell Line, Tumor
  • Cell Movement / genetics
  • Cell Proliferation / genetics
  • Disease Progression
  • Female
  • Gene Expression Regulation, Neoplastic / genetics
  • HeLa Cells
  • Humans
  • MicroRNAs / genetics*
  • RNA, Long Noncoding / genetics*
  • SOXC Transcription Factors / genetics*
  • Uterine Cervical Neoplasms / genetics*
  • Uterine Cervical Neoplasms / pathology

Substances

  • MIRN133 microRNA, human
  • MicroRNAs
  • NEAT1 long non-coding RNA, human
  • RNA, Long Noncoding
  • SOX4 protein, human
  • SOXC Transcription Factors