Evidence map›Paper›PMID 39741303›Full record

ArticleJournal of translational medicine2024

YWHAG promotes bladder cancer metastasis by regulating TMOD3 to activate ERK1/2 and JNK phosphorylation in the MAPK pathway.

Tai Tian, Shiming He, Han Hao, Bao Guan, Yanqing Gong, Jian Fan, Zhenpeng Zhu, Wenzhi Gao, Yucai Wu, Ninghan Feng and 3 more

Abstract read
In one paragraph

Article in Journal of translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
–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

7 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. SYT8 as a potential prognostic biomarker and therapeutic predictor in colorectal cancer: insights from multi-cohort transcriptomic analyses.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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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

13 authors.

Tai Tian *Department of Urology, Peking University First Hospital, Beijing Key Laboratory of Urogenital Diseases (Male) Molecular Diagnosis and Treatment Center, Beijing, 100034, China.
Shiming He *Department of Urology, Peking University First Hospital, Beijing Key Laboratory of Urogenital Diseases (Male) Molecular Diagnosis and Treatment Center, Beijing, 100034, China.
Han Hao *Department of Urology, Peking University First Hospital, Beijing Key Laboratory of Urogenital Diseases (Male) Molecular Diagnosis and Treatment Center, Beijing, 100034, China.
Bao Guan *Department of Urology, Peking University First Hospital, Beijing Key Laboratory of Urogenital Diseases (Male) Molecular Diagnosis and Treatment Center, Beijing, 100034, China.
Yanqing GongDepartment of Urology, Peking University First Hospital, Beijing Key Laboratory of Urogenital Diseases (Male) Molecular Diagnosis and Treatment Center, Beijing, 100034, China.
Jian FanDepartment of Urology, Peking University First Hospital, Beijing Key Laboratory of Urogenital Diseases (Male) Molecular Diagnosis and Treatment Center, Beijing, 100034, China.
Zhenpeng ZhuDepartment of Urology, Peking University First Hospital, Beijing Key Laboratory of Urogenital Diseases (Male) Molecular Diagnosis and Treatment Center, Beijing, 100034, China.
Wenzhi GaoDepartment of Urology, Peking University First Hospital, Beijing Key Laboratory of Urogenital Diseases (Male) Molecular Diagnosis and Treatment Center, Beijing, 100034, China.
Yucai WuDepartment of Urology, Peking University First Hospital, Beijing Key Laboratory of Urogenital Diseases (Male) Molecular Diagnosis and Treatment Center, Beijing, 100034, China.
Ninghan FengDepartment of Urology, The Affiliated Wuxi No. 2 People's Hospital of Nanjing Medical University, Wuxi, 214002, China. n.feng@njmu.edu.cn.
Aixiang WangDepartment of Urology, Peking University First Hospital, Beijing Key Laboratory of Urogenital Diseases (Male) Molecular Diagnosis and Treatment Center, Beijing, 100034, China. wax20030826@126.com.
Yuexian GuoDepartment of Urology, The Third Hospital of Hebei Medical University, Shijiazhuang, 050051, China. Guoyuexian@aliyun.com.
Xuesong LiDepartment of Urology, Peking University First Hospital, Beijing Key Laboratory of Urogenital Diseases (Male) Molecular Diagnosis and Treatment Center, Beijing, 100034, China. pineneedle@sina.com.

Funding

National High Level Hospital Clinical Research Funding (Interdisciplinary Research Project of Peking University First Hospital) 2024IR30The Central Government's Guidance Fund for Local Science and Technology Development 236Z7710GThe National Natural Science Foundation of China 82273350
6 · The paper itself

Abstract

objectiveThis study aims to investigate the molecular mechanisms by which YWHAG (Tyrosine 3-Monooxygenase/Tryptophan 5-Monooxygenase Activation Protein Gamma) promotes metastasis in bladder cancer. Specifically, it seeks to elucidate the role of YWHAG in driving cancer cell invasion and its potential as a prognostic marker for bladder cancer progression.

methodsThe expression pattern of YWHAG in both primary and metastatic bladder cancer tissues was analyzed using immunohistochemistry (IHC) to determine its correlation with clinical stage and prognosis in bladder cancer patients. The functional role of YWHAG in bladder cancer progression was examined through a series of in vitro and in vivo experiments. Transcriptome sequencing was employed to identify the key signaling pathways regulated by YWHAG. The interaction between YWHAG and TMOD3 (Tropomodulin 3) was confirmed through pull-down assays coupled with mass spectrometry, co-immunoprecipitation (Co-IP), and cell immunofluorescence studies. Finally, TMOD3 knockdown experiments were conducted to verify whether the pro-metastatic effects of YWHAG in bladder cancer are mediated through TMOD3.

resultsYWHAG expression was significantly elevated in metastatic bladder cancer tissues compared to primary tumor tissues, and its expression positively correlated with advanced clinical stages and poor prognosis in patients. In vitro and in vivo experiments demonstrated that YWHAG knockdown significantly reduced the invasive, metastatic, and colonization capabilities of bladder cancer cells. Transcriptome analysis revealed that YWHAG knockdown markedly inhibited the phosphorylation of ERK1/2 (extracellular signal-related kinases 1 and 2) and JNK (JUN N-terminal kinases), key components of the MAPK (mitogen-activated protein kinase) signaling pathway. Mechanistically, YWHAG was found to promote bladder cancer cell invasion and metastasis by regulating TMOD3, which subsequently activates the MAPK pathway.

conclusionYWHAG upregulates TMOD3 expression, leading to the activation of ERK1/2 phosphorylation in the MAPK pathway, thereby promoting the invasion and metastasis of bladder cancer cells.

Indexed as

MAP Kinase Signaling SystemNeoplasm MetastasisUrinary Bladder NeoplasmsAnimalsCell Line, TumorCell MovementFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMice, NudeMiddle AgedNeoplasm InvasivenessPhosphorylationPrognosisBladder cancerMAPK signaling pathwayTMOD3Tumor metastasisYWHAG

Identifiers

PMID39741303
PMCPMC11687020

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.