Evidence map›Paper›PMID 39401430›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024

The Tumor Suppressor TPD52-Governed Endoplasmic Reticulum Stress is Modulated by APC

Weichao Dan, Yizeng Fan, Yuzhao Wang, Tao Hou, Yi Wei, Bo Liu, Mengxing Li, Jiaqi Chen, Qixiang Fang, Taotao Que and 6 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

9 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
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  8. Review
  9. The Tumor Suppressor TPD52-Governed Endoplasmic Reticulum Stress is Modulated by APCAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
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

16 authors.

Weichao DanDepartment of Urology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, P. R. China.
Yizeng FanDepartment of Urology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, P. R. China.
Yuzhao WangDepartment of Urology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, P. R. China.
Tao HouDepartment of Urology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, P. R. China.
Yi WeiDepartment of Urology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, P. R. China.
Bo LiuDepartment of Urology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, P. R. China.
Mengxing LiDepartment of Urology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, P. R. China.
Jiaqi ChenDepartment of Urology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, P. R. China.
Qixiang FangDepartment of Urology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, P. R. China.
Taotao QueDepartment of Urology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, P. R. China.
Yuzeshi LeiDepartment of Urology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, P. R. China.
Chendong GuoDepartment of Urology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, P. R. China.
Chi WangDepartment of Urology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, P. R. China.
Yang GaoDepartment of Urology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, P. R. China.
Jin ZengDepartment of Urology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, P. R. China.
Lei LiDepartment of Urology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, P. R. China.ORCID 0000-0003-4928-8722

Funding

National Key Research and Development Program of China 2023YFC3404104National Natural Science Foundation of China 81925028National Natural Science Foundation of China 82230097
6 · The paper itself

Abstract

Aberrant regulation of unfolded protein response (UPR)/endoplasmic reticulum (ER) stress pathway is associated with cancer development, metastasis, and relapse, and the UPR signal transducer ATF6 has been proposed as a diagnostic and prognostic marker for many cancers. However, a causal molecular link between ATF6 activation and carcinogenesis is not established. Here, it is found that tumor protein D52 (TPD52) integrates ER stress and UPR signaling with the chaperone machinery by promoting S2P-mediated cleavage of ATF6. Although TPD52 has been generally considered as an oncogene, TPD52 is identified as a novel tumor suppressor in bladder cancer. Significantly, attenuation of the ER stress via depletion of TPD52 facilitated tumorigenesis in a subset of human carcinomas. Furthermore, the APC

Indexed as

Endoplasmic Reticulum StressAnimalsCell Line, TumorDisease Models, AnimalHumansMiceNeoplasm ProteinsSignal TransductionTumor Suppressor ProteinsUnfolded Protein ResponseUrinary Bladder NeoplasmsNeoplasm ProteinsTPD52 protein, humanTumor Suppressor ProteinsATF6Cdc20ER stressTPD52unfolded protein response

Identifiers

PMID39401430
PMCPMC11615746

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.