KRAS mutation: The booster of pancreatic ductal adenocarcinoma transformation and progression

Zining Zhang; Zining Zhang; Heng Zhang; Heng Zhang; Xiang Liao; Xiang Liao; Hsiang-i Tsai; Hsiang-i Tsai

doi:10.3389/fcell.2023.1147676

Frontiers in Cell and Developmental Biology (Apr 2023)

KRAS mutation: The booster of pancreatic ductal adenocarcinoma transformation and progression

Zining Zhang,
Zining Zhang,
Heng Zhang,
Heng Zhang,
Xiang Liao,
Xiang Liao,
Hsiang-i Tsai,
Hsiang-i Tsai

Affiliations

Zining Zhang: Institute of Medical Imaging and Artificial Intelligence, Jiangsu University, Zhenjiang, China
Zining Zhang: Department of Medical Imaging, The Affiliated Hospital of Jiangsu University, Zhenjiang, China
Heng Zhang: Institute of Medical Imaging and Artificial Intelligence, Jiangsu University, Zhenjiang, China
Heng Zhang: Department of Medical Imaging, The Affiliated Hospital of Jiangsu University, Zhenjiang, China
Xiang Liao: Institute of Medical Imaging and Artificial Intelligence, Jiangsu University, Zhenjiang, China
Xiang Liao: Department of Medical Imaging, The Affiliated Hospital of Jiangsu University, Zhenjiang, China
Hsiang-i Tsai: Institute of Medical Imaging and Artificial Intelligence, Jiangsu University, Zhenjiang, China
Hsiang-i Tsai: Department of Medical Imaging, The Affiliated Hospital of Jiangsu University, Zhenjiang, China

DOI: https://doi.org/10.3389/fcell.2023.1147676
Journal volume & issue: Vol. 11

Abstract

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Pancreatic ductal adenocarcinoma (PDAC) is the most common type of pancreatic cancer. It has a poor response to conventional therapy and has an extremely poor 5-year survival rate. PDAC is driven by multiple oncogene mutations, with the highest mutation frequency being observed in KRAS. The KRAS protein, which binds to GTP, has phosphokinase activity, which further activates downstream effectors. KRAS mutation contributes to cancer cell proliferation, metabolic reprogramming, immune escape, and therapy resistance in PDAC, acting as a critical driver of the disease. Thus, KRAS mutation is positively associated with poorer prognosis in pancreatic cancer patients. This review focus on the KRAS mutation patterns in PDAC, and further emphases its role in signal transduction, metabolic reprogramming, therapy resistance and prognosis, hoping to provide KRAS target therapy strategies for PDAC.

Published in Frontiers in Cell and Developmental Biology

ISSN: 2296-634X (Online)
Publisher: Frontiers Media S.A.
Country of publisher: Switzerland
LCC subjects: Science: Biology (General)
Website: https://www.frontiersin.org/journals/cell-and-developmental-biology

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