TY - JOUR
AU - Zou, Xiaoping
AU - Nie, Shuang
AU - Cao, Jing
AU - Shi, Mengyue
AU - Schuck, Kathleen
AU - Shi, Zhao
AU - Zhang, Lingling
AU - Li, Hongzhen
AU - Sun, Yifeng
AU - Fang, Chao
AU - Hu, Jingxiong
AU - Niu, Yiqi
AU - Yu, Yuanyuan
AU - Zhang, Zhiheng
AU - Li, Chao
AU - Hu, Mingyue
AU - Wang, Lei
AU - Jiang, Kuirong
AU - Lu, Zipeng
AU - Akkan, Jan
AU - Raulefs, Susanne
AU - Kahlert, Christoph
AU - Roth, Susanne
AU - Herr, Ingrid
AU - Wan, Yuan
AU - Mihaljevic, Andre
AU - Qian, Xuetian
AU - Zhang, Qi
AU - Wang, Maggie Haitian
AU - Kleeff, Jörg
AU - Friess, Helmut
AU - Gu, Zuguang
AU - Michalski, Christoph W
AU - Shen, Shanshan
AU - Kong, Bo
TI - ALDH1A3 promotes aggressive basal-like pancreatic cancer through an AP-1/RUNX2 enhancer network.
JO - Oncogene
VL - nn
SN - 0950-9232
CY - London
PB - Springer Nature
M1 - DKFZ-2025-01662
SP - nn
PY - 2025
N1 - epub
AB - The basal-like transcriptional subtype of pancreatic ductal adenocarcinoma (PDAC) is linked to therapy resistance and poor prognosis. The cancer stem cell marker aldehyde dehydrogenase 1A3 (ALDH1A3) is a critical enzyme in acetaldehyde metabolism, but the interconnection to the basal-like subtype is poorly understood. Here, we identified ALDH1A3 as a key gene, which correlates with reduced survival and increased tumor growth. Functional studies revealed interaction of ALDH1A3 with genes like FAM3C, MCC, PMEPA1, and IRS2, forming a network driving PDAC progression. Chromatin profiling showed that ALDH1A3 affects acetylation of histone 3, mediating AP-1 activity, particularly via FOS family members, activating oncogenic pathways such as MAPK and TNF signaling. RUNX2 emerged as a therapeutic target within this network, as its knockdown disrupted MAPK signaling and reduced tumor growth. These findings emphasize the role of ALDH1A3 in linking nuclear metabolic-epigenetic programming in basal-like PDAC, highlighting it as a promising therapeutic target for novel treatment strategies.
LB - PUB:(DE-HGF)16
C6 - pmid:40781158
DO - DOI:10.1038/s41388-025-03530-w
UR - https://inrepo02.dkfz.de/record/303449
ER -