Evidence map›Paper›PMID 42045183›Full record

ArticleCell death & disease2026

Lactic acid promotes metastasis of papillary thyroid carcinoma by enhancing CPT1A lactylation.

Mingjian Zhao, Haifeng Han, Min Sun, Ruowen Li, Huimin Chen, Fangyu Liu, Chengxu Miao, Yongkang Wu, Xiaojia Shi, Mengting Wu and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

14 authors.

Mingjian Zhao *Department of General Surgery, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250012, China.
Haifeng Han *Department of General Surgery, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250012, China.
Min Sun *Department of General Surgery, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250012, China.
Ruowen LiDepartment of General Surgery, Nanjing Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, 210002, China.
Huimin ChenThe Ninth Medical Center of the Chinese PLA General Hospital, Beijing, 100020, China.
Fangyu LiuDepartment of General Surgery, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250012, China.
Chengxu MiaoDepartment of General Surgery, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250012, China.
Yongkang WuDepartment of Cell Biology, School of Basic Medical Sciences, Cheeloo Medical College of Medicine, Shandong University, Jinan, 250012, China.
Xiaojia ShiDepartment of Cell Biology, School of Basic Medical Sciences, Cheeloo Medical College of Medicine, Shandong University, Jinan, 250012, China.
Mengting WuDepartment of Cell Biology, School of Basic Medical Sciences, Cheeloo Medical College of Medicine, Shandong University, Jinan, 250012, China.
Gabriele MaterazziDepartment of Surgical, Medical, and Molecular Pathology and Critical Area, University of Pisa, 56124, Pisa, Italy.
Paolo MiccoliDepartment of Surgical, Medical, and Molecular Pathology and Critical Area, University of Pisa, 56124, Pisa, Italy.
Jinghui LuDepartment of General Surgery, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250012, China. 201262005933@email.sdu.edu.cn.
Xuetian YueDepartment of Cell Biology, School of Basic Medical Sciences, Cheeloo Medical College of Medicine, Shandong University, Jinan, 250012, China. yuexu@sdu.edu.cn.ORCID http://orcid.org/0000-0001-5561-4964

Funding

Ministry of Health of China | Wu Jieping Medical Foundation 6010125122National Natural Science Foundation of China (National Science Foundation of China) 81600617Natural Science Foundation of Shandong Province (Shandong Provincial Natural Science Foundation) ZR2021LZL003
6 · The paper itself

Abstract

Papillary thyroid carcinoma (PTC), the most prevalent thyroid malignancy, exhibits aggressive behavior in subsets with metastasis. Despite advances in risk stratification, biomarkers predicting metastatic potential remain limited. Here, we identify lactate as a critical driver of PTC metastasis through lactylation of carnitine palmitoyltransferase 1 A (CPT1A), the rate-limiting enzyme in fatty acid β-oxidation (FAO). Multi-omics profiling of 27 paired PTC tissues revealed elevated lactate levels and FAO activation, corroborated by TCGA data. Functional assays demonstrated that exogenous lactate enhances PTC cell migration via CPT1A-dependent FAO. Mechanistically, lactate upregulated CPT1A transcription by promoting histone H3K18 lactylation (H3K18la), simultaneously stabilized CPT1A protein via lactylation of CPT1A at K180/K285 to suppress its ubiquitin-proteasomal degradation. Genetic or pharmacological inhibition of CPT1A abolished lactate-driven migration and FAO activity. In vivo, lactylation-deficient CPT1A mutants (K180R/K285R) attenuated lung metastasis and subcutaneous tumor growth in nude mice. This study reveals that lactate-CPT1A axis synergistically amplifies FAO to fuel PTC progression, suggesting CPT1A lactylation as a therapeutic vulnerability for metabolic intervention.

Indexed as

Carnitine O-PalmitoyltransferaseLactic AcidThyroid Cancer, PapillaryThyroid NeoplasmsAnimalsCell Line, TumorCell MovementHumansMiceMice, NudeNeoplasm MetastasisCarnitine O-PalmitoyltransferaseCPT1A protein, humanLactic Acid

Identifiers

PMID42045183
PMCPMC13254147

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Registered trials

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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.