Evidence map›Paper›PMID 42910221›Full record

ArticleInternational journal of biological sciences2026

OLFM4 promotes intrahepatic cholangiocarcinoma progression through a PKM2-glycolysis-histone lactylation feedback loop.

Shuochen Liu, Kai Cao, Changan Chen, Xiao Xu, Jijun Shan, Chang Li, Ruixiang Chen, Yananlan Chen, Jiang Chang, Wangjie Jiang and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of biological sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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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

14 authors.

Shuochen LiuDepartment of Hepatobiliary Surgery, The First Affiliated Hospital with Nanjing Medical University; Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences; NHC Key Laboratory of Living Donor Liver Transplantation, Nanjing Medical University, Nanjing, Jiangsu Province, China.
Kai CaoDepartment of Hepatobiliary Surgery, The First Affiliated Hospital with Nanjing Medical University; Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences; NHC Key Laboratory of Living Donor Liver Transplantation, Nanjing Medical University, Nanjing, Jiangsu Province, China.
Changan ChenDepartment of Hepatobiliary Surgery, The First Affiliated Hospital with Nanjing Medical University; Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences; NHC Key Laboratory of Living Donor Liver Transplantation, Nanjing Medical University, Nanjing, Jiangsu Province, China.
Xiao XuDepartment of Hepatobiliary Surgery, The First Affiliated Hospital with Nanjing Medical University; Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences; NHC Key Laboratory of Living Donor Liver Transplantation, Nanjing Medical University, Nanjing, Jiangsu Province, China.
Jijun ShanDepartment of Hepatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
Chang LiDepartment of Hepatobiliary Surgery, The First Affiliated Hospital with Nanjing Medical University; Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences; NHC Key Laboratory of Living Donor Liver Transplantation, Nanjing Medical University, Nanjing, Jiangsu Province, China.
Ruixiang ChenDepartment of Hepatobiliary Surgery, The First Affiliated Hospital with Nanjing Medical University; Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences; NHC Key Laboratory of Living Donor Liver Transplantation, Nanjing Medical University, Nanjing, Jiangsu Province, China.
Yananlan ChenDepartment of Hepatobiliary Surgery, The First Affiliated Hospital with Nanjing Medical University; Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences; NHC Key Laboratory of Living Donor Liver Transplantation, Nanjing Medical University, Nanjing, Jiangsu Province, China.
Jiang ChangDepartment of Hepatobiliary Surgery, The First Affiliated Hospital with Nanjing Medical University; Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences; NHC Key Laboratory of Living Donor Liver Transplantation, Nanjing Medical University, Nanjing, Jiangsu Province, China.
Wangjie JiangDepartment of Hepatobiliary Surgery, The First Affiliated Hospital with Nanjing Medical University; Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences; NHC Key Laboratory of Living Donor Liver Transplantation, Nanjing Medical University, Nanjing, Jiangsu Province, China.
Yaodong ZhangDepartment of Hepatobiliary Surgery, The First Affiliated Hospital with Nanjing Medical University; Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences; NHC Key Laboratory of Living Donor Liver Transplantation, Nanjing Medical University, Nanjing, Jiangsu Province, China.
Dong WangDepartment of Hepatobiliary Surgery, The First Affiliated Hospital with Nanjing Medical University; Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences; NHC Key Laboratory of Living Donor Liver Transplantation, Nanjing Medical University, Nanjing, Jiangsu Province, China.
Changxian LiDepartment of Hepatobiliary Surgery, The First Affiliated Hospital with Nanjing Medical University; Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences; NHC Key Laboratory of Living Donor Liver Transplantation, Nanjing Medical University, Nanjing, Jiangsu Province, China.
Xiangcheng LiDepartment of Hepatobiliary Surgery, The First Affiliated Hospital with Nanjing Medical University; Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences; NHC Key Laboratory of Living Donor Liver Transplantation, Nanjing Medical University, Nanjing, Jiangsu Province, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic reprogramming is increasingly recognized as a key characteristic of intrahepatic cholangiocarcinoma (ICC) initiation and progression. Among these metabolic alterations, glycolysis is central for supporting tumor growth. Elucidating the precise molecular mechanisms of glycolysis in ICC is critical for developing precision therapies. Here, comprehensive integrative analyses revealed that olfactomedin 4 (OLFM4) is upregulated in ICC specimens and is associated with adverse patient outcomes. Mechanistically, OLFM4 promotes ICC progression by recruiting ubiquitin specific peptidase 10 (USP10) to stabilize pyruvate kinase M2 (PKM2). This interaction enhances glycolysis and lactate production, thereby elevating histone lactylation, with a prominent impact on H3K18 lactylation (H3K18la). Consequently, H3K18la positively regulates OLFM4 transcription, establishing a positive glycolysis-histone lactylation feedback loop. Notably, tiliroside, a candidate pharmacological inhibitor of OLFM4, demonstrated antitumor efficacy in ICC. Collectively, these findings support targeting OLFM4 as a promising therapeutic strategy for ICC management.

Indexed as

Bile Duct NeoplasmsCarrier ProteinsCholangiocarcinomaGranulocyte Colony-Stimulating FactorHistonesMembrane ProteinsThyroid HormonesAnimalsCell Line, TumorGlycolysisHumansMiceThyroid Hormone-Binding ProteinsCarrier ProteinsGranulocyte Colony-Stimulating FactorHistonesMembrane ProteinsOLFM4 protein, humanThyroid Hormone-Binding ProteinsThyroid Hormonesglycolysishistone lactylationintrahepatic cholangiocarcinomaOLFM4PKM2

Identifiers

PMID42910221
PMCPMC13685613

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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.