Evidence map›Paper›PMID 37078828›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2023

Elevated Nuclear PHGDH Synergistically Functions with cMyc to Reshape the Immune Microenvironment of Liver Cancer.

Hongwen Zhu, Hua Yu, Hu Zhou, Wencheng Zhu, Xiongjun Wang

Open access · goldAbstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

22 citing papers in PubMed, 26 citations in OpenAlex.

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  11. PHGDH drives 5-FU chemoresistance in colorectal cancer through the Hedgehog signaling.Journal of experimental & clinical cancer research : CR · 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

5 authors at 2 institutions in 1 country.

Hongwen ZhuCAS Key Laboratory of Receptor Research, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
Hua YuPrecise Genome Engineering Center, School of Life Sciences, Guangzhou University, Guangzhou, 510006, China.
Hu ZhouCAS Key Laboratory of Receptor Research, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
Wencheng ZhuInstitute of Neuroscience, State Key Laboratory of Neuroscience, CAS Center for Excellence in Brain Science and Intelligence Technology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200031, China.
Xiongjun WangPrecise Genome Engineering Center, School of Life Sciences, Guangzhou University, Guangzhou, 510006, China.ORCID 0000-0003-3946-5748
Chinese Academy of Sciences · CNGuangzhou University · CN

Funding

Guangdong Natural Science Foundation of Guangdong Province of China 2021B1515020016National Key Research and Development Program of China 2020YFA0509000National Science Foundation of China 82103511National Science Foundation of China 82272174Program of Shanghai Young Academic Research Leader from the Science and Technology Commission of Shanghai Municipality 20XD1424900Shanghai Municipal Science and Technology Major ProjectYangfan Project of Shanghai Science and Technology Commission 20YF1457300Youth Innovation Promotion Association CAS 2022285
6 · The paper itself

Abstract

Herein, we observed that nuclear localization of phosphoglycerate dehydrogenase (PHGDH) is associated with poor prognosis in liver cancer, and Phgdh is required for liver cancer progression in a mouse model. Unexpectedly, impairment of Phgdh enzyme activity exerts a slight effect in a liver cancer model. In liver cancer cells, the aspartate kinase-chorismate mutase-tyrA prephenate dehydrogenase (ACT) domain of PHGDH binds nuclear cMyc to form a transactivation axis, PHGDH/p300/cMyc/AF9, which drives chemokine CXCL1 and IL8 gene expression. Then, CXCL1 and IL8 promote neutrophil recruitment and enhance tumor-associated macrophage (TAM) filtration in the liver, thereby advancing liver cancer. Forced cytosolic localization of PHGDH or destruction of the PHGDH/cMyc interaction abolishes the oncogenic function of nuclear PHGDH. Depletion of neutrophils by neutralizing antibodies greatly hampers TAM filtration. These findings reveal a nonmetabolic role of PHGDH with altered cellular localization and suggest a promising drug target for liver cancer therapy by targeting the nonmetabolic region of PHGDH.

Indexed as

Liver NeoplasmsPhosphoglycerate DehydrogenaseAnimalsCell Line, TumorInterleukin-8MiceTumor MicroenvironmentInterleukin-8Phosphoglycerate DehydrogenasecMycCXCL1/IL8liver cancerneutrophilnuclear PHGDH

Identifiers

PMID37078828
PMCPMC10265107
OpenAlexW4366463507

What OpenQuestion holds

Textmetadata
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.