In one paragraphArticle in EMBO reports, 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
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 registryThe 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 literatureWho cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
4 · The recordCorrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what moneyAuthors and funding
11 authors.
Jiamin Chen *Department of Pathology and Institute of Molecular Pathology, The First Affiliated Hospital, The MOE Basic Research and Innovation Center for the Targeted Therapeutics of Solid Tumors, Jiangxi Medical College, Nanchang University, Nanchang, China.ORCID 0009-0008-5425-0175 Mingyue Zhao *Medical Research Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, China.ORCID 0000-0002-5173-9820 Guanxu Ji *Oncology Department, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.ORCID 0000-0002-0384-2890 Kecheng LiuMedical Research Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, China.
Shengqi ShenDepartment of Pathology and Institute of Molecular Pathology, The First Affiliated Hospital, The MOE Basic Research and Innovation Center for the Targeted Therapeutics of Solid Tumors, Jiangxi Medical College, Nanchang University, Nanchang, China.
Shi-Ting LiMedical Research Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, China.
Jin CaiMedical Research Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, China.ORCID 0009-0006-8427-7075 Linchong SunMedical Research Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, China.
Jin LiOncology Department, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China. JL@gzlab.ac.cn.ORCID 0009-0005-5915-1019 Ping GaoDepartment of Pathology and Institute of Molecular Pathology, The First Affiliated Hospital, The MOE Basic Research and Innovation Center for the Targeted Therapeutics of Solid Tumors, Jiangxi Medical College, Nanchang University, Nanchang, China. pgao2@ustc.edu.cn.ORCID 0000-0002-6930-7989 Tong ZhangDepartment of Pathology and Institute of Molecular Pathology, The First Affiliated Hospital, The MOE Basic Research and Innovation Center for the Targeted Therapeutics of Solid Tumors, Jiangxi Medical College, Nanchang University, Nanchang, China. tzhang11@mail.ustc.edu.cn.ORCID 0009-0007-7343-4175 Funding
MOST | National Natural Science Foundation of China (NSFC) 82130087MOST | National Natural Science Foundation of China (NSFC) 82303213MOST | National Natural Science Foundation of China (NSFC) 82341013MOST | National Natural Science Foundation of China (NSFC) 92357301Tianfu Jincheng Laboratory No. TFJCPI20250001
6 · The paper itselfAbstract
Metabolic reprogramming, including enhanced glycolysis and altered fatty acid metabolism, supports the proliferation of cancer cells under hypoxic stress. However, the mechanism underlying the regulation of cholesterol metabolism under hypoxic stress remains incompletely understood. Here, we report that lactate-induced cholesterol accumulation activates mammalian target of rapamycin complex 1 (mTORC1) signalling under hypoxic conditions, thereby promoting hepatocellular carcinoma (HCC) progression. Mechanistically, lactate upregulates scavenger receptor class B type 1 (SCARB1) expression by increasing histone H3 lysine 18 lactylation (H3K18la), leading to increased cholesterol levels. We further demonstrate that SCARB1-mediated cholesterol uptake is essential for the activation of mTORC1, which promotes tumour growth by preventing excessive autophagy in HCC cells. Importantly, analysis of clinical HCC samples reveals a positive correlation between H3K18la expression and SCARB1 expression. Taken together, these findings provide novel insights into hypoxia-driven metabolic reprogramming and reveal a previously unrecognized connection between lactate and cholesterol metabolism, suggesting a potential innovative cancer therapy for HCC.
Indexed as
AutophagyCarcinoma, HepatocellularCholesterolLactic AcidLiver NeoplasmsScavenger Receptors, Class BAnimalsCell Line, TumorCell ProliferationDisease ProgressionGene Expression Regulation, NeoplasticHistonesHumansMechanistic Target of Rapamycin Complex 1Metabolic ReprogrammingMiceCholesterolHistonesLactic AcidMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesSCARB1 protein, humanScavenger Receptors, Class BTOR Serine-Threonine Kinases
Identifiers
PMID42265306
PMCPMC13400630
What OpenQuestion holds
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LicenceCC BY
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