CCNI2 promotes pancreatic cancer through PI3K/AKT signaling pathway

Authors

  • Bingyang Hu Department of Hepatobiliary Surgery, the First Medical Center, Chinese PLA General Hospital, Chinese PLA Medical School, Haidian District, Beijing City, China
  • Wenzhi Zhang Department of Hepatobiliary Surgery, the First Medical Center, Chinese PLA General Hospital, Chinese PLA Medical School, Haidian District, Beijing City, China
  • Changsheng Zhang Department of General Surgery, Kaifeng Central Hospital, Longting District, Kaifeng City, Henan Province, China
  • Chonghui Li Department of Hepatobiliary Surgery, the First Medical Center, Chinese PLA General Hospital, Chinese PLA Medical School, Haidian District, Beijing City, China
  • Ning Zhang Department of Hepatobiliary Surgery, the First Medical Center, Chinese PLA General Hospital, Chinese PLA Medical School, Haidian District, Beijing City, China
  • Ke Pan Department of Hepatobiliary Surgery, the First Medical Center, Chinese PLA General Hospital, Chinese PLA Medical School, Haidian District, Beijing City, China
  • Xinlan Ge Department of Hepatobiliary Surgery, the First Medical Center, Chinese PLA General Hospital, Chinese PLA Medical School, Haidian District, Beijing City, China
  • Tao Wan Department of Hepatobiliary Surgery, the First Medical Center, Chinese PLA General Hospital, Chinese PLA Medical School, Haidian District, Beijing City, China

DOI:

https://doi.org/10.17305/bb.2023.9337

Keywords:

Pancreatic cancer, cyclin I-like protein (CCNI2), prognosis, phenotype

Abstract

Globally, pancreatic cancer is recognized as one of the deadliest malignancies that lacks effective targeted therapies. This study aims to explore the role of cyclin I-like protein (CCNI2), a homolog of cyclin I (CCNI), in the progression of pancreatic cancer, thereby providing a theoretical basis for its treatment. Firstly, the expression of CCNI2 in pancreatic cancer tissues was determined through immunohistochemical staining. The biological role of CCNI2 in pancreatic cancer cells was further assessed using both in vitro and in vivo loss/gain-of-function assays. Our data revealed that CCNI2 expression was abnormally elevated in pancreatic cancer, and clinically, increased CCNI2 expression generally correlated with reduced overall survival. Functionally, CCNI2 contributed to the malignant progression of pancreatic cancer by promoting the proliferation and migration of tumor cells. Consistently, in vivo experiments verified that CCNI2 knockdown impaired the tumorigenic ability of pancreatic cancer cells. Moreover, the addition of phosphatidylinositol 3-kinase (PI3K) inhibitors could partially reverse the promoting effect of CCNI2 on the malignant phenotypes of pancreatic cancer cells. CCNI2 promoted pancreatic cancer through PI3K/protein kinase B (AKT) signaling pathway, indicating its potential as a prognostic marker and therapeutic target for pancreatic cancer.

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CCNI2 promotes pancreatic cancer through PI3K/AKT signaling pathway

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Published

11-03-2024

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Section

Molecular Biology

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How to Cite

1.
CCNI2 promotes pancreatic cancer through PI3K/AKT signaling pathway. Biomol Biomed [Internet]. 2024 Mar. 11 [cited 2024 Apr. 18];24(2):323–336. Available from: https://bjbms.org/ojs/index.php/bjbms/article/view/9337