Evidence map›Paper›PMID 33686769›Full record

ArticleCancer science2021

OTUB1 facilitates bladder cancer progression by stabilizing ATF6 in response to endoplasmic reticulum stress.

Hui-Hui Zhang, Chao Li, Jian-Wei Ren, Lian Liu, Xue-Hua Du, Jie Gao, Tao Liu, Shang-Ze Li

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 6% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Research progress of DUB enzyme in breast cancer.Clinical and experimental medicine · 2025
    Review
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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

8 authors at 4 institutions in 1 country.

Hui-Hui ZhangDepartment of Laboratory Medicine, Hunan Normal University School of Medicine, Changsha, China.ORCID https://orcid.org/0000-0001-7691-5651
Chao LiHubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, Wuhan, China.
Jian-Wei RenTibet University Medical College, Lhasa, China.
Lian LiuDepartment of Laboratory Medicine, Hunan Normal University School of Medicine, Changsha, China.
Xue-Hua DuHubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, Wuhan, China.
Jie GaoHubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, Wuhan, China.
Tao LiuDepartment of Urology, Zhongnan Hospital of Wuhan University, Wuhan, China.
Shang-Ze LiDepartment of Laboratory Medicine, Hunan Normal University School of Medicine, Changsha, China.
Wuhan University · CNHunan Normal University · CNChongqing University · CNTibet University · CN

Funding

National Natural Science Foundation of China 81602450National Natural Science Foundation of China 81902844Natural Science Foundation of Hunan ProvinceResearch Foundation of Education Bureau of Hunan Province 16B161
6 · The paper itself

Abstract

The unfolded protein response (UPR) plays an important role in carcinogenesis, but the functional role and mechanism of UPR-associated bladder carcinogenesis remain to be characterized. Upon UPR activation, ATF6α is activated to upregulate the transcription of UPR target genes. Although the mechanism of ATF6 activation has been studied extensively, the negative regulation of ATF6 stabilization is not well understood. Here, we report that the deubiquitinase otubain 1 (OTUB1) facilitates bladder cancer progression by stabilizing ATF6 in response to endoplasmic reticulum stress. OTUB1 expression is raised in bladder cancer patients. Genetic ablation of OTUB1 markedly inhibited bladder cancer cell proliferation, viability, and migration both in vitro and in vivo. Mechanistically, luciferase pathway screening showed that ATF6 signaling was clearly activated compared with other pathways. OTUB1 was found to activate ATF6 signaling by inhibiting its ubiquitylation, thereby remodeling the stressed cells through transcriptional regulation. Our results show that high OTUB1 expression promotes bladder cancer progression by stabilizing ATF6 and that OTUB1 is a potential therapeutic target in bladder cancer.

Indexed as

Endoplasmic Reticulum StressActivating Transcription Factor 6AnimalsCell Line, TumorCell MovementCell ProliferationCysteine EndopeptidasesDeubiquitinating EnzymesDisease ProgressionGene Expression Regulation, NeoplasticHumansMicePrognosisSignal TransductionUnfolded Protein ResponseUrinary Bladder NeoplasmsActivating Transcription Factor 6ATF6 protein, humanCysteine EndopeptidasesDeubiquitinating EnzymesOTUB1 protein, humanATF6bladder cancerdeubiquitinationOTUB1UPR

Identifiers

PMID33686769
PMCPMC8177800
OpenAlexW3135840509

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.