Evidence map›Paper›PMID 38098610›Full record

ArticleMedComm2023

BDH1-mediated LRRC31 regulation dependent on histone lysine β-hydroxybutyrylation to promote lung adenocarcinoma progression.

Jingjing Huang, Lu Liang, Shiyao Jiang, Yueying Liu, Hua He, Xiaoyan Sun, Yi Li, Li Xie, Yongguang Tao, Li Cong and 1 more

Open access · goldAbstract read
In one paragraph

Article in MedComm, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

17 citing papers in PubMed, 17 citations in OpenAlex.

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  12. Ketone body mediated histone β-hydroxybutyrylation is reno-protective.bioRxiv : the preprint server for biology · 2025
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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

11 authors at 2 institutions in 2 countries.

Jingjing HuangThe Key Laboratory of Model Animal and Stem Cell Biology in Hunan Province, Hunan Normal University Changsha Hunan China.
Lu LiangThe Key Laboratory of Model Animal and Stem Cell Biology in Hunan Province, Hunan Normal University Changsha Hunan China.
Shiyao JiangThe Key Laboratory of Model Animal and Stem Cell Biology in Hunan Province, Hunan Normal University Changsha Hunan China.
Yueying LiuThe Key Laboratory of Model Animal and Stem Cell Biology in Hunan Province, Hunan Normal University Changsha Hunan China.
Hua HeThe Key Laboratory of Model Animal and Stem Cell Biology in Hunan Province, Hunan Normal University Changsha Hunan China.
Xiaoyan SunThe Key Laboratory of Model Animal and Stem Cell Biology in Hunan Province, Hunan Normal University Changsha Hunan China.
Yi LiThe Key Laboratory of Model Animal and Stem Cell Biology in Hunan Province, Hunan Normal University Changsha Hunan China.
Li XieDepartment of Head and Neck Surgery Hunan Cancer Hospital, Xiangya School of Medicine, Central South University Changsha Hunan China.
Yongguang TaoDepartment of Pathology Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Xiangya Hospital, School of Basic Medicine, Central South University Changsha Hunan China.ORCID https://orcid.org/0000-0003-2354-5321
Li CongThe Key Laboratory of Model Animal and Stem Cell Biology in Hunan Province, Hunan Normal University Changsha Hunan China.
Yiqun JiangThe Key Laboratory of Model Animal and Stem Cell Biology in Hunan Province, Hunan Normal University Changsha Hunan China.
Hunan Normal University · CNCentral South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung adenocarcinoma (LUAD) is the most common form of lung cancer, with a consistently low 5-year survival rate. Therefore, we aim to identify key genes involved in LUAD progression to pave the way for targeted therapies in the future. BDH1 plays a critical role in the conversion between acetoacetate and β-hydroxybutyrate. The presence of β-hydroxybutyrate is essential for initiating lysine β-hydroxybutyrylation (Kbhb) modifications. Histone Kbhb at the H3K9 site is attributed to transcriptional activation. We unveiled that β-hydroxybutyrate dehydrogenase 1 (BDH1) is not only conspicuously overexpressed in LUAD, but it also modulates the overall intracellular Kbhb modification levels. The RNA sequencing analysis revealed leucine-rich repeat-containing protein 31 (LRRC31) as a downstream target gene regulated by BDH1. Ecologically expressed BDH1 hinders the accumulation of H3K9bhb in the transcription start site of LRRC31, consequently repressing the transcriptional expression of LRRC31. Furthermore, we identified potential BDH1 inhibitors, namely pimozide and crizotinib, which exhibit a synergistic inhibitory effect on the proliferation of LUAD cells exhibiting high expression of BDH1. In summary, this study elucidates the molecular mechanism by which BDH1 mediates LUAD progression through the H3K9bhb/LRRC31 axis and proposes a therapeutic strategy targeting BDH1-high-expressing LUAD, providing a fresh perspective for LUAD treatment.

Indexed as

BDH1H3K9bhbLRRC31lung adenocarcinomaβ‐hydroxybutyrate

Identifiers

PMID38098610
PMCPMC10719427
OpenAlexW4389738633

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.