HHEX-PRKAR2B axis-mediated PKA activation drives glucose metabolism-dependent progression of pancreatic ductal adenocarcinoma.

Junxiang Wen, Qiuchen Li, Shuxiang Xu, Wenjun Lu, Fei Wu, Jiatao Lou, Lin Wang

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Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

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7 authors.

Junxiang WenDepartment of Laboratory Medicine, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, China.

Qiuchen LiDepartment of Laboratory Medicine, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, China.

Shuxiang XuDepartment of Laboratory Medicine, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, China.

Wenjun LuDepartment of Laboratory Medicine, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, China.

Fei WuDepartment of Laboratory Medicine, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, China.

Jiatao LouDepartment of Laboratory Medicine, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, China.

Lin WangDepartment of Laboratory Medicine, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

By virtue of its function as a key metabolic regulator, malignant transformation in the pancreas not only confers high aggressiveness but also disrupts systemic metabolism. However, the causal relationship between metabolic reprogramming and the progression of pancreatic ductal adenocarcinoma (PDAC) remains incompletely understood. This study identifies aberrant protein kinase A (PKA) activation in PDAC, correlating with poor prognosis. Mechanistically, downregulation of the transcription factor hematopoietically expressed homeobox (HHEX) represses protein kinase cAMP-dependent type II regulatory subunit beta (PRKAR2B), relieving inhibition on PKA catalytic activity. A high-glucose microenvironment promotes cAMP production, further activating PKA, which then enhances glycolysis via specific upregulation of hexokinase 2 (HK2).

Indexed as

CancerHuman metabolismMolecular interaction

Identifiers

PMID41704777

DOI10.1016/j.isci.2026.114691

PMCPMC12907050

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