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Article

Spatiotemporal control of SMARCA5 by a MAPK-RUNX1 axis distinguishes mutant KRAS-driven pancreatic malignancy from tissue regeneration.

Nature cancer - 1 Jan 2026

Han Jing, Lu Xiaoman, Guo Mengmeng, He Ruizhe, Zhuo Meilian, Wang Saisai, Li Yong, Liu Xiangzheng, Zou Di, Wang Jiacheng, Mao Jiangjiao, Chen Qian, Wang Xia, Peng Junya, Xie Wei, David Charles J, Chen Mo

Abstract excerpt

Acute pancreatitis-induced acinar-to-ductal metaplasia involves global chromatin remodeling and contributes to normal tissue regeneration. Oncogenic KRAS hijacks this process to promote PDAC formation. Here we show that regeneration and KRASG12D-driven oncogenesis can be decoupled from tissue regeneration through a chromatin remodeler, SMARCA5. We show that SMARCA5 maintains KRASG12D-dependent chromatin...

Read the complete abstract on PubMed

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Share to Adenosine Triphosphatases
Share to Carcinoma, Pancreatic Ductal

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Chromatin Assembly and Disassembly

Share to Chromosomal Proteins, Non-Histone

Share to Core Binding Factor Alpha 2 Subunit

Share to MAP Kinase Signaling System

Share to Pancreatic Neoplasms

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Source

Identifiers

PMID: 41198969
DOI: 10.1038/s43018-025-01065-3

Genes

SMARCA5
KRAS
RUNX1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

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