Evidence map›Paper›PMID 42292413›Full record

ReviewFrontiers in immunology2026

Roles of lactate and lactylation in tumor immune suppression and drug resistance.

Jiaqi Li, Wangji Yang, Tian Xin, Zhaokai Zhou, Xiaoyu Liu, Pei Tang, Junsha An, Bin Ma, Fu Peng

Abstract readReview
In one paragraph

Review in Frontiers in immunology, 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

9 authors.

Jiaqi Li *West China School of Medicine, West China School of Pharmacy, Department of Thyriod and Breast Surgery, West China School of Public Health, West China Fourth Hospital, Sichuan University, Chengdu, China.
Wangji Yang *West China School of Medicine, West China School of Pharmacy, Department of Thyriod and Breast Surgery, West China School of Public Health, West China Fourth Hospital, Sichuan University, Chengdu, China.
Tian XinWest China School of Medicine, West China School of Pharmacy, Department of Thyriod and Breast Surgery, West China School of Public Health, West China Fourth Hospital, Sichuan University, Chengdu, China.
Zhaokai ZhouNational Clinical Research Center for Metabolic Diseases, Department of Urology, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
Xiaoyu LiuWest China School of Medicine, West China School of Pharmacy, Department of Thyriod and Breast Surgery, West China School of Public Health, West China Fourth Hospital, Sichuan University, Chengdu, China.
Pei TangWest China School of Medicine, West China School of Pharmacy, Department of Thyriod and Breast Surgery, West China School of Public Health, West China Fourth Hospital, Sichuan University, Chengdu, China.
Junsha AnWest China School of Medicine, West China School of Pharmacy, Department of Thyriod and Breast Surgery, West China School of Public Health, West China Fourth Hospital, Sichuan University, Chengdu, China.
Bin MaWest China School of Medicine, West China School of Pharmacy, Department of Thyriod and Breast Surgery, West China School of Public Health, West China Fourth Hospital, Sichuan University, Chengdu, China.
Fu PengWest China School of Medicine, West China School of Pharmacy, Department of Thyriod and Breast Surgery, West China School of Public Health, West China Fourth Hospital, Sichuan University, Chengdu, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic reprogramming is a hallmark of cancer, with excessive lactate accumulation driven by aerobic glycolysis profoundly reshaping the tumor microenvironment (TME). Beyond being a metabolic by-product, lactate acts as a signaling metabolite and epigenetic regulator that promotes immune suppression and therapeutic resistance. Lactate-induced acidification impairs immune cell function and reprograms macrophages, T cells, and dendritic cells toward immunosuppressive phenotypes. Moreover, lactate drives lysine lactylation of histone and non-histone proteins, linking metabolic status to transcriptional regulation and oncogenic signaling. Emerging evidence indicates that lactate and lactylation cooperatively enhance tumor survival, invasion, and resistance to chemotherapy, radiotherapy, anti-angiogenic therapy, and immunotherapy. This review summarizes mechanisms of lactate production, transport, and signaling, and discusses therapeutic strategies targeting lactate metabolism, lactylation, and TME acidification, highlighting their potential in precision and combination cancer therapy.

Indexed as

Drug Resistance, NeoplasmLactic AcidNeoplasmsAnimalsHumansMetabolic ReprogrammingSignal TransductionTumor MicroenvironmentLactic Aciddrug resistanceimmune suppressionlactatelactylationtumor microenvironment

Identifiers

PMID42292413
PMCPMC13260245

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.