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Review Article | Open Access

GATA6 in pancreatic cancer initiation and progression

Muyuan MaJianhong AnTingting Jiang( )Keping Xie( )
Center for Pancreatic Cancer Research, The South China University of Technology School of Medicine, Guangzhou, Guangdong 510006, China

Peer review under responsibility of Chongqing Medical University.

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Abstract

Pancreatic ductal adenocarcinoma (PDA) is a lethal malignancy characterized by insidious onset and lack of effective therapy. The molecular pathogenesis of PDA remains to be understood fully. Transcriptional factor GATA6 is an important transcriptional regulator in normal pancreas development, particularly in the initial specification and differentiation of the pancreas. Recent studies have linked pancreatic malignancy closely to GATA6. Increased levels of GATA6 expression enhance pancreatic cancer cell growth. GATA6 emerges as a lineage-specific oncogenic factor in PDA, augmenting the oncogenic phenotypes of PDA cells upon its overexpression. However, elevated GATA6 levels are correlated with well-differentiated tumors and a more favorable patient prognosis. Experimental evidence in genetic mouse models has revealed a tumor-suppressive role for GATA6. The circumstantial roles of GATA6 in pancreatic tumorigenesis remain to be defined. This review aims to elucidate recent advances in comprehending GATA6, emphasizing its crucial roles in both pancreas physiology and pathology. Special attention will be given to its involvement in PDA pathogenesis, exploring its potential as a novel biomarker and a promising therapeutic target for PDA.

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Genes & Diseases
Article number: 101353
Cite this article:
Ma M, An J, Jiang T, et al. GATA6 in pancreatic cancer initiation and progression. Genes & Diseases, 2025, 12(2): 101353. https://doi.org/10.1016/j.gendis.2024.101353

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Received: 13 November 2023
Revised: 28 March 2024
Accepted: 29 May 2024
Published: 17 June 2024
© 2024 The Authors.

This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

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