Evidence map›Paper›PMID 37905340›Full record

ArticleActa biochimica et biophysica Sinica2024

RP11-495P10.1 promotes HCC cell proliferation by regulating reprogramming of glucose metabolism and acetylation of the NR4A3 promoter via the PDK1/PDH axis.

Chi Liu, Jie Shi, Zhengyuan Jiang, Shan Jiang, Yuan Wu, Dongqian Peng, Jiebing Tang, Linchi Guo

Open access · diamondAbstract read
In one paragraph

Article in Acta biochimica et biophysica Sinica, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.0field-weighted citation impact, top 21% of its field
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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Hepatocyte nuclear factor 4-Alpha: a key regulator in liver carcinogenesis.Cellular oncology (Dordrecht, Netherlands) · 2025
    Review
  3. 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

8 authors at 3 institutions in 1 country.

Chi LiuDepartment of Biochemistry & Molecular Biology, Harbin Medical University, Harbin 150000, China.
Jie ShiDepartment of Biochemistry & Molecular Biology, Harbin Medical University, Harbin 150000, China.
Zhengyuan JiangDepartment of Biochemistry & Molecular Biology, Harbin Medical University, Harbin 150000, China.
Shan JiangDepartment of Biochemistry & Molecular Biology, Harbin Medical University, Harbin 150000, China.
Yuan WuGeneral Medicine, People's Hospital of Ningxia Hui Autonomous Region, Yinchuan 750000, China.
Dongqian PengGeneral Medicine, People's Hospital of Ningxia Hui Autonomous Region, Yinchuan 750000, China.
Jiebing TangDepartment of Gastrointestinal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin 150086, China.
Linchi GuoGeneral Medicine, People's Hospital of Ningxia Hui Autonomous Region, Yinchuan 750000, China.
Harbin Medical University · CNSecond Hospital of Yichang · CNThe Fourth People's Hospital of Ningxia Hui Autonomous Region · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The incidence and related death of hepatocellular carcinoma (HCC) have increased over the past decades. However, the molecular mechanisms underlying HCC pathogenesis are not fully understood. Long noncoding RNA (lncRNA) RP11-495P10.1 has been proven to be closely associated with the progression of prostate cancer, but its role and specific mechanism in HCC are still unknown. Here, we identify that RP11-495P10.1 is highly expressed in HCC tissues and cells and contributes to the proliferation of HCC cells. Moreover, this study demonstrates that RP11-495P10.1 affects the proliferation of HCC by negatively regulating the expression of nuclear receptor subfamily 4 group a member 3 (NR4A3). Glycometabolism reprogramming is one of the main characteristics of tumor cells. In this study, we discover that RP11-495P10.1 regulates glycometabolism reprogramming by changing the expression of pyruvate dehydrogenase kinase 1 (PDK1) and pyruvate dehydrogenase (PDH), thus contributing to the proliferation of HCC cells. Furthermore, knockdown of RP11-495P10.1 increases enrichment of H3K27Ac in the promoter of NR4A3 by promoting the activity of PDH and the production of acetyl-CoA, which leads to the increased transcription of NR4A3. Altogether, RP11-495P10.1 promotes HCC cell proliferation by regulating the reprogramming of glucose metabolism and acetylation of the NR4A3 promoter via the PDK1/PDH axis, which provides an lncRNA-oriented therapeutic strategy for the diagnosis and treatment of HCC.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsReceptors, SteroidRNA, Long NoncodingAcetylationCell Line, TumorCell ProliferationDNA-Binding ProteinsGene Expression Regulation, NeoplasticGlucoseHumansMalePyruvate Dehydrogenase Acetyl-Transferring KinasePyruvate Dehydrogenase ComplexReceptors, Thyroid HormoneDNA-Binding ProteinsGlucoseNR4A3 protein, humanPDK1 protein, humanPyruvate Dehydrogenase Acetyl-Transferring KinasePyruvate Dehydrogenase ComplexReceptors, SteroidReceptors, Thyroid HormoneRNA, Long NoncodingglycometabolismHCCNR4A3PDK1RP11-495P10.1

Identifiers

PMID37905340
PMCPMC10875365
OpenAlexW4387061257

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LicenceCC BY
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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.