Evidence map›Paper›PMID 37833415›Full record

ArticleNature communications2023

USP36 stabilizes nucleolar Snail1 to promote ribosome biogenesis and cancer cell survival upon ribotoxic stress.

Kewei Qin, Shuhan Yu, Yang Liu, Rongtian Guo, Shiya Guo, Junjie Fei, Yuemeng Wang, Kaiyuan Jia, Zhiqiang Xu, Hu Chen and 8 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 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
4.6field-weighted citation impact, top 5% 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, 30 citations in OpenAlex.

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  13. Ribosome-directed cancer therapies: the tip of the iceberg?Trends in pharmacological sciences · 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

18 authors at 2 institutions in 2 countries.

Kewei Qin *Center of Growth, Metabolism and Aging, Key Laboratory of Bio-Resource and Eco-Environment of Ministry of Education, College of Life Sciences, Sichuan University, 610064, Chengdu, China.
Shuhan Yu *Center of Growth, Metabolism and Aging, Key Laboratory of Bio-Resource and Eco-Environment of Ministry of Education, College of Life Sciences, Sichuan University, 610064, Chengdu, China.
Yang LiuCenter of Growth, Metabolism and Aging, Key Laboratory of Bio-Resource and Eco-Environment of Ministry of Education, College of Life Sciences, Sichuan University, 610064, Chengdu, China.
Rongtian GuoCenter of Growth, Metabolism and Aging, Key Laboratory of Bio-Resource and Eco-Environment of Ministry of Education, College of Life Sciences, Sichuan University, 610064, Chengdu, China.
Shiya GuoCenter of Growth, Metabolism and Aging, Key Laboratory of Bio-Resource and Eco-Environment of Ministry of Education, College of Life Sciences, Sichuan University, 610064, Chengdu, China.
Junjie FeiCenter of Growth, Metabolism and Aging, Key Laboratory of Bio-Resource and Eco-Environment of Ministry of Education, College of Life Sciences, Sichuan University, 610064, Chengdu, China.
Yuemeng WangCenter of Growth, Metabolism and Aging, Key Laboratory of Bio-Resource and Eco-Environment of Ministry of Education, College of Life Sciences, Sichuan University, 610064, Chengdu, China.
Kaiyuan JiaCenter of Growth, Metabolism and Aging, Key Laboratory of Bio-Resource and Eco-Environment of Ministry of Education, College of Life Sciences, Sichuan University, 610064, Chengdu, China.
Zhiqiang XuState Key Laboratory of Biotherapy, West China Hospital, Sichuan University, 610041, Chengdu, China.
Hu ChenCenter of Growth, Metabolism and Aging, Key Laboratory of Bio-Resource and Eco-Environment of Ministry of Education, College of Life Sciences, Sichuan University, 610064, Chengdu, China.ORCID http://orcid.org/0000-0001-8136-7442
Fengtian LiCenter of Growth, Metabolism and Aging, Key Laboratory of Bio-Resource and Eco-Environment of Ministry of Education, College of Life Sciences, Sichuan University, 610064, Chengdu, China.ORCID http://orcid.org/0000-0002-7931-7427
Mengmeng NiuCenter of Growth, Metabolism and Aging, Key Laboratory of Bio-Resource and Eco-Environment of Ministry of Education, College of Life Sciences, Sichuan University, 610064, Chengdu, China.ORCID http://orcid.org/0000-0002-0940-4672
Mu-Shui DaiDepartment of Molecular & Medical Genetics, Oregon Health & Science University, Portland, OR, USA.ORCID http://orcid.org/0000-0001-9031-6962
Lunzhi DaiState Key Laboratory of Biotherapy, West China Hospital, Sichuan University, 610041, Chengdu, China.ORCID http://orcid.org/0000-0002-3003-8910
Yang CaoCenter of Growth, Metabolism and Aging, Key Laboratory of Bio-Resource and Eco-Environment of Ministry of Education, College of Life Sciences, Sichuan University, 610064, Chengdu, China.ORCID http://orcid.org/0000-0002-1925-2123
Yujun ZhangCenter of Growth, Metabolism and Aging, Key Laboratory of Bio-Resource and Eco-Environment of Ministry of Education, College of Life Sciences, Sichuan University, 610064, Chengdu, China.
Zhi-Xiong Jim XiaoCenter of Growth, Metabolism and Aging, Key Laboratory of Bio-Resource and Eco-Environment of Ministry of Education, College of Life Sciences, Sichuan University, 610064, Chengdu, China. jimzx@scu.edu.cn.ORCID http://orcid.org/0000-0003-2504-5742
Yong YiCenter of Growth, Metabolism and Aging, Key Laboratory of Bio-Resource and Eco-Environment of Ministry of Education, College of Life Sciences, Sichuan University, 610064, Chengdu, China. yy-yiyong@scu.edu.cn.ORCID http://orcid.org/0000-0003-4664-9692
Sichuan University · CNOregon Health & Science University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor growth requires elevated ribosome biogenesis. Targeting ribosomes is an important strategy for cancer therapy. The ribosome inhibitor, homoharringtonine (HHT), is used for the clinical treatment of leukemia, yet it is ineffective for the treatment of solid tumors, the reasons for which remain unclear. Here we show that Snail1, a key factor in the regulation of epithelial-to-mesenchymal transition, plays a pivotal role in cellular surveillance response upon ribotoxic stress. Mechanistically, ribotoxic stress activates the JNK-USP36 signaling to stabilize Snail1 in the nucleolus, which facilitates ribosome biogenesis and tumor cell survival. Furthermore, we show that HHT activates the JNK-USP36-Snail1 axis in solid tumor cells, but not in leukemia cells, resulting in solid tumor cell resistance to HHT. Importantly, a combination of HHT with the inhibition of the JNK-USP36-Snail1 axis synergistically inhibits solid tumor growth. Together, this study provides a rationale for targeting the JNK-USP36-Snail1 axis in ribosome inhibition-based solid tumor therapy.

Indexed as

LeukemiaNeoplasmsCell NucleolusCell SurvivalHumansRibosomesUbiquitin ThiolesteraseUbiquitin ThiolesteraseUSP36 protein, human

Identifiers

PMID37833415
PMCPMC10575996
OpenAlexW4387608466

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.