Calreticulin exposure induced by anticancer drugs is associated with the p53 signaling pathway in colorectal cancer cells

Biochem Biophys Res Commun. 2024 Nov 12:733:150665. doi: 10.1016/j.bbrc.2024.150665. Epub 2024 Sep 5.

Abstract

Immunogenic cell death (ICD) enhances immunogenicity and activates antitumor immune responses. ICD induction by anticancer drugs may be effective against microsatellite-stable colorectal cancers (CRCs) that are less responsive to immune checkpoint inhibitors. Calreticulin (CRT) is crucial in ICD, promoting dendritic cell phagocytosis and initiating antitumor immunity. This study investigated CRT exposure mechanisms in four CRC cell lines and three human CRC organoids. Flow cytometry and immunofluorescence showed that oxaliplatin and 5-fluorouracil caused CRT exposure in all models. Despite CRT's association with endoplasmic reticulum stress, Western blot analysis showed no increase in this stress. These findings suggest alternative pathways. RNA sequencing identified enrichment of p53 signaling pathway genes, including TP53I3, TP53INP1, and YPEL3, which were confirmed by RT-qPCR. These results suggest that the p53 signaling pathway plays an important role in CRT exposure induced by anticancer drugs.

Keywords: Calreticulin; Immunogenic cell death; Organoid; p53.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents* / pharmacology
  • Calreticulin* / genetics
  • Calreticulin* / metabolism
  • Cell Line, Tumor
  • Colorectal Neoplasms* / drug therapy
  • Colorectal Neoplasms* / metabolism
  • Colorectal Neoplasms* / pathology
  • Endoplasmic Reticulum Stress / drug effects
  • Fluorouracil / pharmacology
  • Humans
  • Immunogenic Cell Death / drug effects
  • Oxaliplatin / pharmacology
  • Signal Transduction* / drug effects
  • Tumor Suppressor Protein p53* / metabolism

Substances

  • Calreticulin
  • Tumor Suppressor Protein p53
  • Antineoplastic Agents
  • TP53 protein, human
  • Oxaliplatin
  • CALR protein, human
  • Fluorouracil