Evidence map›Paper›PMID 42552465›Full record

ArticleActa pharmacologica Sinica2026

PGK1-driven histone lactylation fuels MDSC-driven immune evasion and tumor progression in triple-negative breast cancer.

Yong-Peng Wang, Wen-Zhen Dang, Zhen-Dan Liu, Bing Li, Huan Xiong, Hudagula Bai, Xiao Li, Shuo Wu, Cheng Luo, Wei-Lie Xiao and 1 more

Abstract read
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In one paragraph

Article in Acta pharmacologica Sinica, 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
–field-weighted citation impact
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.

Yong-Peng Wang *Key Laboratory of Medicinal Chemistry for Natural Resource, Ministry of Education; Yunnan Key Laboratory of Research and Development for Natural Products; School of Pharmacy and School of Chemical Science and Technology, Yunnan University, Kunming, 650500, China.
Wen-Zhen Dang *State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
Zhen-Dan Liu *School of Pharmaceutical Science and Technology, Hangzhou Institute for Advanced Study, University of Chinese Academy of Sciences, Hangzhou, 310024, China.
Bing Li *State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
Huan XiongZhongshan Institute for Drug Discovery, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Zhongshan, 528400, China.
Hudagula BaiChina Pharmaceutical University, Nanjing, 211198, China.
Xiao LiState Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
Shuo WuSchool of Pharmaceutical Science and Technology, Hangzhou Institute for Advanced Study, University of Chinese Academy of Sciences, Hangzhou, 310024, China.
Cheng LuoState Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China. cluo@simm.ac.cn.
Wei-Lie XiaoKey Laboratory of Medicinal Chemistry for Natural Resource, Ministry of Education; Yunnan Key Laboratory of Research and Development for Natural Products; School of Pharmacy and School of Chemical Science and Technology, Yunnan University, Kunming, 650500, China. xiaoweilie@ynu.edu.cn.
Yuan-Yuan ZhangState Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China. zhangyy@simm.ac.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic reprogramming and immune regulation are tightly interconnected processes that critically influence cancer progression. The efficacy of immunotherapy is limited in triple-negative breast cancer (TNBC) by metabolic abnormality and immunosuppressive microenvironment. However, the molecular mechanisms through which these alterations cooperate to drive immune evasion and tumor progression in TNBC remain poorly defined. Through transcriptomic profiling, we identified glycolysis and chemokine signaling as the dominant intersecting metabolic and immune pathways that distinguish TNBC from non-TNBC subtypes. Phosphoglycerate kinase 1 (PGK1) is associated with poor prognosis and with myeloid-derived suppressor cells (MDSCs), acting as a key metabolic node linking metabolic regulation to immune modulation. Functionally, PGK1 knockdown inhibited tumor growth in vitro and in vivo and reduced MDSC recruitment. Notably, PGK1 knockdown exerted a more pronounced antitumor effect under immune surveillance, accompanied by decreased infiltration of both monocytic and polymorphonuclear MDSCs and recovered CD8

Indexed as

chemokineglycolysisMDSCPGK1TNBC

Identifiers

PMID42552465

What OpenQuestion holds

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.