Evidence map›Paper›PMID 34601505›Full record

ArticleOncogene2021

USP29 coordinates MYC and HIF1α stabilization to promote tumor metabolism and progression.

Rongfu Tu, Wenqian Kang, Mengjie Yang, Liyuan Wang, Qing Bao, Zhi Chen, Yang Dong, Jingchao Wang, Jue Jiang, Hudan Liu and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
2.6field-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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

  1. Pooled it
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  11. Hypoxia-driven angiogenesis and metabolic reprogramming in vascular tumors.Frontiers in cell and developmental 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 1 institution in 1 country.

Rongfu Tu *Department of Urology, Zhongnan Hospital of Wuhan University, 430071, Wuhan, China.
Wenqian Kang *Department of Urology, Zhongnan Hospital of Wuhan University, 430071, Wuhan, China.ORCID http://orcid.org/0000-0002-1275-9175
Mengjie YangFrontier Science Center for Immunology and Metabolism, Medical Research Institute, Wuhan University, 430071, Wuhan, China.
Liyuan WangFrontier Science Center for Immunology and Metabolism, Medical Research Institute, Wuhan University, 430071, Wuhan, China.
Qing BaoFrontier Science Center for Immunology and Metabolism, Medical Research Institute, Wuhan University, 430071, Wuhan, China.
Zhi ChenFrontier Science Center for Immunology and Metabolism, Medical Research Institute, Wuhan University, 430071, Wuhan, China.
Yang DongFrontier Science Center for Immunology and Metabolism, Medical Research Institute, Wuhan University, 430071, Wuhan, China.
Jingchao WangFrontier Science Center for Immunology and Metabolism, Medical Research Institute, Wuhan University, 430071, Wuhan, China.
Jue JiangFrontier Science Center for Immunology and Metabolism, Medical Research Institute, Wuhan University, 430071, Wuhan, China.
Hudan LiuFrontier Science Center for Immunology and Metabolism, Medical Research Institute, Wuhan University, 430071, Wuhan, China.ORCID http://orcid.org/0000-0003-1362-6048
Guoliang QingDepartment of Urology, Zhongnan Hospital of Wuhan University, 430071, Wuhan, China. qingguoliang@whu.edu.cn.ORCID http://orcid.org/0000-0002-7892-2860
Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor cells must rewire cellular metabolism to satisfy the demands of unbridled growth and proliferation. How these metabolic processes are integrated to fuel cancer cell growth remains largely unknown. Deciphering the regulatory mechanisms is vital to develop targeted strategies for tumor-selective therapies. We herein performed an unbiased and functional siRNA screen against 96 deubiquitinases, which play indispensable roles in cancer and are emerging as therapeutic targets, and identified USP29 as a top candidate essential for metabolic reprogramming that support biosynthesis and survival in tumor cells. Integrated metabolic flux analysis and molecular investigation reveal that USP29 directly deubiquitinates and stabilizes MYC and HIF1α, two master regulators of metabolic reprogramming, enabling adaptive response of tumor cells in both normoxia and hypoxia. Systemic knockout of Usp29 depleted MYC and HIF1α in MYC-driven neuroblastoma and B cell lymphoma, inhibited critical metabolic targets and significantly prolonged survival of tumor-bearing mice. Strikingly, mice homozygous null for the Usp29 gene are viable, fertile, and display no gross phenotypic abnormalities. Altogether, these results demonstrate that USP29 selectively coordinates MYC and HIF1α to integrate metabolic processes critical for cancer cell growth, and therapeutic targeting of USP29, a potentially targetable enzyme, could create a unique vulnerability given deregulation of MYC and HIF1α frequently occurs in human cancers.

Indexed as

A549 CellsAnimalsCell Line, TumorDisease ProgressionGene Expression Regulation, NeoplasticGene Knockout TechniquesHumansHypoxia-Inducible Factor 1, alpha SubunitLymphoma, B-CellMiceNeoplasm TransplantationNeuroblastomaProto-Oncogene Proteins c-mycRNA, Small InterferingTumor HypoxiaUbiquitinationHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitMYC protein, humanProto-Oncogene Proteins c-mycRNA, Small InterferingUbiquitin-Specific ProteasesUSP29 protein, human

Identifiers

PMID34601505
OpenAlexW3202035860

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.