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Research Paper|Volume 13, Issue 4|pp 5607—5620

Calreticulin: a potential diagnostic and therapeutic biomarker in gallbladder cancer

Jianwen Ye1, Lei Qi2, Zhicheng Du1, Long Yu1, Kunlun Chen1, Renfeng Li1, Ruo Feng3, Wenlong Zhai1,4
  • 1Department of Hepatobiliary and Pancreatic Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan Province, China
  • 2Department of Pharmacy, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan Province, China
  • 3Department of Histology and Embryology, Medical College of Zhengzhou University, Zhengzhou 450052, Henan Province, China
  • 4Key Laboratory of Digestive Organ Transplantation of Henan Province, Open and Key Laboratory of Hepatobiliary and Pancreatic Surgery and Digestive Organ Transplantation at Henan Universities, Zhengzhou Key Laboratory of Hepatobiliary and Pancreatic Disease and Organ Transplantation, Zhengzhou 450052, Henan Province, China
* Equal contribution
Received: December 17, 2019Accepted: September 24, 2020Published: February 11, 2021
https://doi.org/10.18632/aging.202488

Copyright: © 2021 Ye et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Recent studies suggested that calreticulin (CRT) has an important role in the progression of various types of cancer. Our previous study suggested that CRT was upregulated and acted as an oncogene in hepatocellular carcinoma. However, the role of CRT in gallbladder cancer (GBC) remains unclear. The expression level of CRT was upregulated in GBC tissues in comparison with adjacent non-tumor tissues and chronic cholecystitis tissues. Moreover, CRT expression was found to be correlated with the tumor size. Knockdown of CRT inhibited cell proliferation, induced apoptosis, arrested cell cycle and resulted in decreased resistance to gemcitabine, which was mediated by the inactivation of the PI3K/Akt pathway. Collectively, the present results suggested a potential role of CRT in GBC progression and provided novel insights into the mechanism underlying the CRT-mediated chemosensitivity in GBC cells.