HIF-1α-regulated stanniocalcin-1 mediates gemcitabine resistance in pancreatic ductal adenocarcinoma via PI3K/AKT signaling pathway

Mol Carcinog. 2022 Sep;61(9):839-850. doi: 10.1002/mc.23420. Epub 2022 Jul 4.

Abstract

Pancreatic ductal adenocarcinoma (PDAC) has a poor response to the first-line chemotherapy drug gemcitabine. We previously identified stanniocalcin-1 as a gemcitabine-resistant-related gene, but its specific role and function in pancreatic cancer remain unclear. RT-qPCR and Western blot were used to evaluate differential protein and mRNA expressions. The biological functions of genes were determined using proliferation and drug-resistance experiments. Subcutaneous tumorigenesis experiment was performed on nude mice. Prognostic analysis was performed using public databases and our clinical data. We found HIF-1α-regulated STC1 expression mediated chemoresistance in pancreatic cancer. Deeper, we explored the action mechanism of STC1 and identified PI3K/AKT as the downstream signaling pathway of STC1. Furthermore, we analyzed clinical data and found that STC1 expression was related to the prognosis of gemcitabine-treated patients after surgery. In general, we proved the HIF-1α/STC1/PI3K-AKT axis participated in PDAC progression and chemoresistance, and STC1 may serve as a potential prognostic factor and therapeutic target for PDAC treatment.

Keywords: HIF-1α; PI3K/AKT pathway; STC1; gemcitabine resistance; pancreatic cancer.

MeSH terms

  • Animals
  • Carcinoma, Pancreatic Ductal* / drug therapy
  • Carcinoma, Pancreatic Ductal* / genetics
  • Carcinoma, Pancreatic Ductal* / metabolism
  • Cell Line, Tumor
  • Deoxycytidine / analogs & derivatives
  • Drug Resistance, Neoplasm / genetics
  • Gemcitabine
  • Glycoproteins
  • Hypoxia-Inducible Factor 1, alpha Subunit
  • Mice
  • Mice, Nude
  • Pancreatic Neoplasms* / drug therapy
  • Pancreatic Neoplasms* / genetics
  • Pancreatic Neoplasms* / metabolism
  • Phosphatidylinositol 3-Kinases / genetics
  • Phosphatidylinositol 3-Kinases / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism
  • Signal Transduction

Substances

  • Glycoproteins
  • Hypoxia-Inducible Factor 1, alpha Subunit
  • Deoxycytidine
  • teleocalcin
  • Proto-Oncogene Proteins c-akt
  • Gemcitabine