Evidence map›Paper›PMID 42767098›Full record

ArticleTranslational oncology2026

GMPS drives pancreatic cancer progression via suppressing DNA damage, STING activation and cellular senescence.

Yangyi Li, Zifeng Zhang, Dingru Li, Cong Zhou, Yueyue Chen, Chunbin Zhu, Jianhui Yang, Rong Tang, Wei Wang, Xianjun Yu and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

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

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Yangyi LiDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China; Department of Oncology, Shanghai Medical College of Fudan University, Shanghai, 200032, China. Electronic address: liyangyi@fudanpci.org.
Zifeng ZhangShanghai Pancreatic Cancer Institute, Shanghai, 200032, China; Shanghai Key Laboratory of Precision Medicine for Pancreatic Cancer, Shanghai, 200032, China. Electronic address: zhangzifeng@fudanpci.org.
Dingru LiDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China; Pancreatic Center Institute, Fudan University, Shanghai, 200032, China. Electronic address: lidingru@fudanpci.org.
Cong ZhouDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China; Department of Oncology, Shanghai Medical College of Fudan University, Shanghai, 200032, China. Electronic address: zhoucong@fudanpci.org.
Yueyue ChenDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China; Department of Oncology, Shanghai Medical College of Fudan University, Shanghai, 200032, China. Electronic address: chenyueyue@fudanpci.org.
Chunbin ZhuShanghai Pancreatic Cancer Institute, Shanghai, 200032, China; Shanghai Key Laboratory of Precision Medicine for Pancreatic Cancer, Shanghai, 200032, China. Electronic address: zhuchunbin@fudanpci.org.
Jianhui YangShanghai Pancreatic Cancer Institute, Shanghai, 200032, China; Shanghai Key Laboratory of Precision Medicine for Pancreatic Cancer, Shanghai, 200032, China. Electronic address: yangjianhui@fudanpci.org.
Rong TangDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China; Pancreatic Center Institute, Fudan University, Shanghai, 200032, China. Electronic address: tangrong@fudanpci.org.
Wei WangDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China; Department of Oncology, Shanghai Medical College of Fudan University, Shanghai, 200032, China. Electronic address: wangwei@fudanpci.org.
Xianjun YuShanghai Pancreatic Cancer Institute, Shanghai, 200032, China; Shanghai Key Laboratory of Precision Medicine for Pancreatic Cancer, Shanghai, 200032, China; Pancreatic Center Institute, Fudan University, Shanghai, 200032, China. Electronic address: yuxianjun@fudan.edu.cn.
Jin XuDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China; Department of Oncology, Shanghai Medical College of Fudan University, Shanghai, 200032, China. Electronic address: xujin@fudanpci.org.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPancreatic ductal adenocarcinoma (PDAC) is an extremely aggressive malignancy with scarce viable treatment targets. Metabolic rewiring is a typical characteristic of PDAC, but the roles of many metabolic enzymes remain poorly defined.

methodsWe integrated DepMap and TCGA data to screen metabolic genes essential for PDAC proliferation and poor prognosis. Expression patterns were validated by immunohistochemistry and western blotting in 97 PDAC tissues and multiple cell lines. Genetic manipulation experiments in PDAC cell lines, organoids, and a patient‑derived xenograft model were performed to assess proliferation and tumor growth. RNA sequencing, proteomics, flow cytometry, SA-β-gal staining, and immunofluorescence were used to investigate underlying mechanisms.

resultsAmong 2752 metabolic genes, GMPS had the highest hazard ratio and its high expression correlated with worse prognosis. GMPS-high tumors showed increased mutation frequencies of KRAS and TP53, while GMPS-low tumors had higher immune infiltration and drug sensitivity. GMPS protein was elevated in PDAC tissues and cell lines (MIA PaCa-2, Capan-1). GMPS knockdown reduced colony formation, proliferation, organoid growth, and PDX tumor growth, whereas overexpression promoted organoid expansion. Mechanistically, GMPS knockdown induced DNA damage (γH2AX⁺ cells), G1 phase arrest, cellular senescence (upregulation of IL6, MMP2, p21, and increased SA-β-gal staining), and activated the STING-TBK1 pathway.

conclusionsGMPS drives PDAC proliferation by suppressing senescence and STING signaling. GMPS is a promising therapeutic target and prognostic biomarker in PDAC.

Indexed as

Cellular senescenceGMPSPancreatic cancerSTING signaling

Identifiers

PMID42767098
PMCPMC13626766

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