Evidence map›Paper›PMID 37092319›Full record

ArticleThe EMBO journal2023

Glutamate dehydrogenase1 supports HIF-1α stability to promote colorectal tumorigenesis under hypoxia.

Kunhua Hu, Yufeng Ding, Hongwen Zhu, Xiaoqian Jing, Weiling He, Hua Yu, Xiongjun Wang

Open access · greenAbstract read
In one paragraph

Article in The EMBO journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

15 citing papers in PubMed, 13 citations in OpenAlex.

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  11. The role of acetylation and deacetylation in cancer metabolism.Clinical and translational medicine · 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

7 authors at 4 institutions in 1 country.

Kunhua Hu *Guangdong Key Laboratory of Liver Disease Research, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.ORCID 0000-0001-9422-7828
Yufeng Ding *School of Life Sciences, Precise Genome Engineering Center, Guangzhou University, Guangzhou, China.ORCID 0009-0003-5803-2777
Hongwen Zhu *Department of Analytical Chemistry and CAS Key Laboratory of Receptor Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China.ORCID 0000-0002-2116-4245
Xiaoqian Jing *Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Weiling HeThe First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.
Hua YuSchool of Life Sciences, Precise Genome Engineering Center, Guangzhou University, Guangzhou, China.ORCID 0000-0003-0411-1085
Xiongjun WangSchool of Life Sciences, Precise Genome Engineering Center, Guangzhou University, Guangzhou, China.ORCID 0000-0003-3946-5748
Guangzhou University · CNSun Yat-sen University · CNChinese Academy of Sciences · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor cells surviving hypoxic stress acquire the ability to drive cancer progression. To explore the contribution of dehydrogenases to the low oxygen concentration response, we used siRNAs targeting 163 dehydrogenase-coding genes and discovered that glutamate dehydrogenase 1 (GDH1) plays a critical role in regulating colorectal cancer (CRC) cell survival under hypoxia. We observed that GDH1 deficiency had an inhibitory effect on CRC occurrence and impaired hypoxia-inducible factor 1-alpha (HIF-1α) stability even under hypoxia. Mechanistically, hypoxia triggered p300 recruitment to GDH1, promoting its acetylation at K503 and K527. GDH1 acetylation at K527 induced the formation of a GDH1 complex with EGLN1/HIF-1α; in contrast, GDH1 acetylation at K503 reinforced its affinity for α-ketoglutarate (αKG), and glutamate production. In line with this view, αKG is a product of GDH1 under normoxia, but hypoxia stimulation reversed GDH1 enzyme activity and αKG consumption by the EGLN1/HIF-1α complex, increasing HIF-1α stability and promoting CRC progression. Clinically, hypoxia-modulated GDH1 AcK503/527 can be used as a biomarker of CRC progression and is a potential target for CRC treatment.

Indexed as

Colorectal NeoplasmsGlutamic AcidCarcinogenesisCell HypoxiaCell Line, TumorCell Transformation, NeoplasticHumansHypoxiaHypoxia-Inducible Factor 1, alpha SubunitGlutamic AcidHypoxia-Inducible Factor 1, alpha Subunitacetylationcolorectal cancerGDH1HIF1αα-ketoglutarate

Identifiers

PMID37092319
PMCPMC10267683
OpenAlexW4366821906

What OpenQuestion holds

Textmetadata
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.