Experimental and Molecular Medicine (Mar 2020)

PROM2 promotes gemcitabine chemoresistance via activating the Akt signaling pathway in pancreatic cancer

  • Wenbin Li,
  • Yue Zhu,
  • Kelin Zhang,
  • Xianhuan Yu,
  • Haoming Lin,
  • Wenrui Wu,
  • Yaorong Peng,
  • Jian Sun

DOI
https://doi.org/10.1038/s12276-020-0390-4
Journal volume & issue
Vol. 52, no. 3
pp. 409 – 422

Abstract

Read online

Pancreatic cancer: Exploring a pathway to drug resistance A cell membrane protein called PROM2 promotes the resistance of pancreatic cancer to the anti-cancer drug gemcitabine, suggesting PROM2 and the molecular signaling pathway it stimulates could be targeted by new treatments. Researchers in China led by Jian Sun at Sun Yat-Sen University, Guangzhou, investigated the role of PROM2 in cultured human pancreatic cancer cells and in a mouse model of pancreatic cancer. Production and activity of PROM2 were increased in cancer cells, leading to increased resistance to gemcitabine. The researchers found that PROM2’s promotion of gemcitabine resistance was linked to its ability to bind to another protein called Akt. This interaction stimulates the Akt signaling pathway, sustaining cancer cells. Combining gemcitabine therapy with an Akt pathway inhibitor restored cancer cell sensitivity to gemcitabine, revealing a potential approach to developing drugs to overcome gemcitabine resistance.