Evidence map›Paper›PMID 41971017›Full record

ReviewGenes & diseases2026

Lactylation-driven therapeutic resistance in cancer: Mechanisms and therapeutic opportunities.

Wanghao Zhang, Guanglong Huang, Woheng Tang, Jiaxian Li, Jingxian Chen, Yaojiang Feng, Kaichen Li, Can Pan, Shunshen Li, Huayang Zhang and 3 more

Abstract readReview
In one paragraph

Review in Genes & diseases, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Histone deacetylases in cancer metabolic reprogramming.Experimental & molecular medicine · 2026
    Review
  2. Review
  3. Article
  4. Article
  5. Article
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

13 authors.

Wanghao ZhangDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China.
Guanglong HuangDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China.
Woheng TangThe Second Clinical Medical College, Southern Medical University, Guangzhou, Guangdong 510260, China.
Jiaxian LiThe First Clinical Medical College, Southern Medical University, Guangzhou, Guangdong 510515, China.
Jingxian ChenSchool of Public Health, Southern Medical University, Guangzhou, Guangdong 510515, China.
Yaojiang FengThe First Clinical Medical College, Southern Medical University, Guangzhou, Guangdong 510515, China.
Kaichen LiThe First Clinical Medical College, Southern Medical University, Guangzhou, Guangdong 510515, China.
Can PanThe First Clinical Medical College, Southern Medical University, Guangzhou, Guangdong 510515, China.
Shunshen LiThe First Clinical Medical College, Southern Medical University, Guangzhou, Guangdong 510515, China.
Huayang ZhangDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China.
Rongxu YeDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China.
Hao LongDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China.
Guo-Zhong YiDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lactylation, a type of post-translational modification (PTM) of proteins driven by cancer metabolic reprogramming, not only offers new perspectives on the Warburg effect but also has drawn increasing attention due to its critical roles in tumorigenesis and therapeutic resistance. Given its significant potential for precision cancer therapy, this review first integrates recent advancements in lactylation research by systematically summarizing newly identified lactylation writers, readers, and erasers, as well as their involvement in feedback loops and crosstalk with other modifications. Subsequently, we elaborate on how histone and non-histone lactylation contribute to both intrinsic and acquired resistance to radiotherapy, chemotherapy, targeted therapy, and immunotherapy. Key mechanisms encompass maintaining cancer stemness, enhancing DNA damage repair, reprogramming metabolic pathways, inhibiting ferroptosis, and promoting an immunosuppressive tumor microenvironment. Finally, we evaluate preclinical strategies targeting lactylation, including inhibition of lactate metabolic pathways and direct modulation of lactylation-modifying enzymes or lactylated proteins, while critically assessing mechanistic challenges and early-phase clinical trial outcomes. Our analysis establishes a theoretical framework and actionable roadmap for the development of lactylation-based precision therapies in oncology.

Indexed as

LactateLactylationTherapeutic resistanceTumor microenvironmentWarburg effect

Identifiers

PMID41971017
PMCPMC13068659

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.