High mobility group AT-hook 2 promotes tumorigenicity of pancreatic cancer cells via upregulating ANLN

Exp Cell Res. 2020 Aug 1;393(1):112088. doi: 10.1016/j.yexcr.2020.112088. Epub 2020 May 12.

Abstract

HMGA2 is associated with the regulation of cellular biological processes in various human disorders and cancer progression, yet little is known about how HMGA2 controls tumorigenesis. This study uncovered the mechanism of HMGA2-mediated regulation of tumorigenicity in pancreatic cancer. We showed that HMGA2 was highly expressed in pancreatic cancer cells and correlated with poor prognosis. HMGA2 expression knockdown inhibited the tumorigenicity of pancreatic cancer cells. Conversely, overexpression of HMGA2 promoted tumorigenicity. Combination of ChIP-Seq, RNA-Seq and dual-luciferase reporter assays revealed HMGA2 could directly regulate ANLN expression. Furthermore, we found ANLN could mediate the HMGA2-induced effects on pancreatic cancer cells. The identification of the regulatory mechanism of HMGA2 and ANLN will provide insights into the progression for human pancreatic cancer.

Keywords: ANLN; HMGA2; Pancreatic cancer; Tumorigenicity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Carcinogenesis / genetics
  • Cell Movement / physiology
  • Cell Proliferation / physiology
  • Cell Transformation, Neoplastic / genetics
  • Gene Expression Regulation, Neoplastic / genetics
  • HMGA2 Protein / metabolism*
  • Humans
  • Mice, Nude
  • Microfilament Proteins / metabolism*
  • Pancreatic Neoplasms / metabolism*
  • Pancreatic Neoplasms / mortality
  • Up-Regulation

Substances

  • ANLN protein, human
  • Anln protein, mouse
  • HMGA2 Protein
  • HMGA2 protein, human
  • Microfilament Proteins