Evidence map›Paper›PMID 40414964›Full record

ArticleBiology direct2025

LDHA-mediated YAP lactylation promotes the tumor progression of hepatocellular carcinoma by inducing YAP dephosphorylation and activation.

Xiaoyong Wei, Long Zou, Yanqing Huang, Chuan Qiu, Guang Cheng, Ye Chen, Jun Rao

Abstract read
In one paragraph

Article in Biology direct, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

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  9. Crosstalk BetweenCancers · 2026
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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

7 authors.

Xiaoyong WeiHepatobiliary Surgery, The Second Affiliated Hospital of Nanchang Medical College, Jiangxi Cancer Hospital, Jiangxi Clinical Research Center for Cancer, Nanchang, Jiangxi, 330029, China.ORCID 0000-0002-5089-778X
Long ZouHepatobiliary Surgery, The Second Affiliated Hospital of Nanchang Medical College, Jiangxi Cancer Hospital, Jiangxi Clinical Research Center for Cancer, Nanchang, Jiangxi, 330029, China.
Yanqing HuangThe Medical College of Nanchang University, Nanchang, Jiangxi, 330006, China.
Chuan QiuThe Medical College of Nanchang University, Nanchang, Jiangxi, 330006, China.
Guang ChengHepatobiliary Surgery, The Second Affiliated Hospital of Nanchang Medical College, Jiangxi Cancer Hospital, Jiangxi Clinical Research Center for Cancer, Nanchang, Jiangxi, 330029, China.
Ye ChenHepatobiliary Surgery, The Second Affiliated Hospital of Nanchang Medical College, Jiangxi Cancer Hospital, Jiangxi Clinical Research Center for Cancer, Nanchang, Jiangxi, 330029, China.
Jun RaoJiangxi Cancer Hospital, The Second Affiliated Hospital of Nanchang Medical College, Jiangxi Clinical Research Center for Cancer, Nanchang, Jiangxi, 330029, China. raojun1986@126.com.

Funding

National Natural Science Foundation of China NO: 82360512Science and Technology project of Jiangxi provincial health commission NO: 202210052the "Five-level Progressive" talent cultivation project of Jiangxi Cancer Hospital & Institute No. WCDJ2024JQ03; WCDJ2024JQ02the Natural Science Foundation of Jiangxi NO: 20224BAB206056
6 · The paper itself

Abstract

backgroundHepatocellular carcinoma (HCC) is among the deadliest cancers globally. Yes-Associated Protein (YAP), a Hippo pathway effector, crucially regulates cell proliferation and apoptosis. Recent research has implicated YAP's role in HCC progression, but the mechanisms are unclear. This study aims to clarify YAP's function in HCC, emphasizing its regulation of key pathways and targets.

resultsGene knockout and overexpression models were established in nude mice and cell lines of HCC cells to investigate YAP's impact on tumorigenesis. Additionally, functional assays and molecular biology techniques were employed to identify YAP's regulatory networks. The study demonstrates that LDHA-regulated lactate production promotes YAP activation and malignant phenotypes in HCC. Overexpression of LDHA in HepG2 and Huh7 cells increased lactate levels and activated the YAP pathway, enhancing cell proliferation, migration, and invasion. Lactate treatment also promoted these malignant phenotypes by inhibiting YAP phosphorylation at Ser127. In a xenograft model, lactate accelerated tumor growth through YAP activation. YAP lactylation at K102 antagonized its Ser127 phosphorylation, further promoting malignant progression.

conclusionsThis study highlights the significance of YAP in HCC pathogenesis, providing insights into potential therapeutic targets for HCC management.

Indexed as

Adaptor Proteins, Signal TransducingCarcinoma, HepatocellularLiver NeoplasmsL-Lactate DehydrogenaseTranscription FactorsAnimalsCell Cycle ProteinsCell Line, TumorCell ProliferationDisease ProgressionHumansMiceMice, Inbred BALB CMice, NudePhosphorylationYAP-Signaling ProteinsAdaptor Proteins, Signal TransducingCell Cycle ProteinsLDHA protein, humanL-Lactate DehydrogenaseTranscription FactorsYAP1 protein, humanYAP-Signaling ProteinsHCCLactylationPhosphorylationPoor prognosisYAP

Identifiers

PMID40414964
PMCPMC12105199

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.