SBSN drives bladder cancer metastasis via EGFR/SRC/STAT3 signalling.

Animals Antigens, Differentiation / metabolism Cell Line, Tumor Cell Movement ErbB Receptors / genetics Gene Expression Regulation, Neoplastic Mice Neoplasm Metastasis Prognosis Proto-Oncogene Proteins pp60(c-src) / metabolism Signal Transduction Urinary Bladder Neoplasms / pathology src-Family Kinases / metabolism

Journal

British journal of cancer
ISSN: 1532-1827
Titre abrégé: Br J Cancer
Pays: England
ID NLM: 0370635

Informations de publication

Date de publication:
07 2022
Historique:
received: 15 11 2021
accepted: 11 03 2022
revised: 25 02 2022
pubmed: 29 4 2022
medline: 22 7 2022
entrez: 28 4 2022
Statut: ppublish

Résumé

Patients with metastatic bladder cancer have very poor prognosis and predictive biomarkers are urgently needed for early clinical detection and intervention. In this study, we evaluate the effect and mechanism of Suprabasin (SBSN) on bladder cancer metastasis. A tissue array was used to detect SBSN expression by immunohistochemistry. A tumour-bearing mouse model was used for metastasis evaluation in vivo. Transwell and wound-healing assays were used for in vitro evaluation of migration and invasion. Comprehensive molecular screening was achieved by western blotting, immunofluorescence, luciferase reporter assay, and ELISA. SBSN was found markedly overexpressed in bladder cancer, and indicated poor prognosis of patients. SBSN promoted invasion and metastasis of bladder cancer cells both in vivo and in vitro. The secreted SBSN exhibited identical biological function and regulation in bladder cancer metastasis, and the interaction of secreted SBSN and EGFR could play an essential role in activating the signalling in which SBSN enhanced the phosphorylation of EGFR and SRC kinase, followed with phosphorylation and nuclear location of STAT3. Our findings highlight that SBSN, and secreted SBSN, promote bladder cancer metastasis through activation of EGFR/SRC/STAT3 pathway and identify SBSN as a potential diagnostic and therapeutic target for bladder cancer.

Sections du résumé

BACKGROUND
Patients with metastatic bladder cancer have very poor prognosis and predictive biomarkers are urgently needed for early clinical detection and intervention. In this study, we evaluate the effect and mechanism of Suprabasin (SBSN) on bladder cancer metastasis.
METHODS
A tissue array was used to detect SBSN expression by immunohistochemistry. A tumour-bearing mouse model was used for metastasis evaluation in vivo. Transwell and wound-healing assays were used for in vitro evaluation of migration and invasion. Comprehensive molecular screening was achieved by western blotting, immunofluorescence, luciferase reporter assay, and ELISA.
RESULTS
SBSN was found markedly overexpressed in bladder cancer, and indicated poor prognosis of patients. SBSN promoted invasion and metastasis of bladder cancer cells both in vivo and in vitro. The secreted SBSN exhibited identical biological function and regulation in bladder cancer metastasis, and the interaction of secreted SBSN and EGFR could play an essential role in activating the signalling in which SBSN enhanced the phosphorylation of EGFR and SRC kinase, followed with phosphorylation and nuclear location of STAT3.
CONCLUSIONS
Our findings highlight that SBSN, and secreted SBSN, promote bladder cancer metastasis through activation of EGFR/SRC/STAT3 pathway and identify SBSN as a potential diagnostic and therapeutic target for bladder cancer.

Identifiants

DOI: 10.1038/s41416-022-01794-7 PMID: 35484216 PMC: PMC9296541
pubmed: 35484216
doi: 10.1038/s41416-022-01794-7
pii: 10.1038/s41416-022-01794-7
pmc: PMC9296541
doi:

Substances chimiques

Antigens, Differentiation 0
suprabasin protein, mouse 0
ErbB Receptors EC 2.7.10.1
Proto-Oncogene Proteins pp60(c-src) EC 2.7.10.2
src-Family Kinases EC 2.7.10.2

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

211-222

Informations de copyright

© 2022. The Author(s), under exclusive licence to Springer Nature Limited.

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Auteurs

Zhongqiu Zhou (Z)

Affiliated Cancer Hospital & Institute of Guangzhou Medical University, 510095, Guangzhou, China.
Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, School of Basic Medical Science, Guangzhou Medical University, 511436, Guangzhou, China.
Meishan Women and Children's Hospital, Alliance Hospital of West China Second University Hospital, Sichuan University, 620000, Meishan, China.

Zhuojun Zhang (Z)

Affiliated Cancer Hospital & Institute of Guangzhou Medical University, 510095, Guangzhou, China.
Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, School of Basic Medical Science, Guangzhou Medical University, 511436, Guangzhou, China.

Han Chen (H)

Affiliated Cancer Hospital & Institute of Guangzhou Medical University, 510095, Guangzhou, China.
Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, School of Basic Medical Science, Guangzhou Medical University, 511436, Guangzhou, China.

Wenhao Bao (W)

Affiliated Cancer Hospital & Institute of Guangzhou Medical University, 510095, Guangzhou, China.
Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, School of Basic Medical Science, Guangzhou Medical University, 511436, Guangzhou, China.

Xiangqin Kuang (X)

Affiliated Cancer Hospital & Institute of Guangzhou Medical University, 510095, Guangzhou, China.
Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, School of Basic Medical Science, Guangzhou Medical University, 511436, Guangzhou, China.

Ping Zhou (P)

Affiliated Cancer Hospital & Institute of Guangzhou Medical University, 510095, Guangzhou, China.
Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, School of Basic Medical Science, Guangzhou Medical University, 511436, Guangzhou, China.

Zhiqing Gao (Z)

Affiliated Cancer Hospital & Institute of Guangzhou Medical University, 510095, Guangzhou, China.
Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, School of Basic Medical Science, Guangzhou Medical University, 511436, Guangzhou, China.

Difeng Li (D)

Affiliated Cancer Hospital & Institute of Guangzhou Medical University, 510095, Guangzhou, China.
Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, School of Basic Medical Science, Guangzhou Medical University, 511436, Guangzhou, China.

Xiaoyi Xie (X)

Affiliated Cancer Hospital & Institute of Guangzhou Medical University, 510095, Guangzhou, China.
Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, School of Basic Medical Science, Guangzhou Medical University, 511436, Guangzhou, China.

Chunxiao Yang (C)

Affiliated Cancer Hospital & Institute of Guangzhou Medical University, 510095, Guangzhou, China.
Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, School of Basic Medical Science, Guangzhou Medical University, 511436, Guangzhou, China.

Xuhong Chen (X)

Medical Research Center, Southern University of Science and Technology Hospital, 518055, Shenzhen, China.

Jinyuan Pan (J)

Department of Oncology, Huanggang Central Hospital of Yangtze University, 438000, Huanggang, China.

Ruiming Tang (R)

The Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan People's Hospital, 511518, Guangzhou, China.

Zhengfu Feng (Z)

The Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan People's Hospital, 511518, Guangzhou, China.

Lihuan Zhou (L)

The Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan People's Hospital, 511518, Guangzhou, China.

Lan Wang (L)

Department of Pathogen Biology and Immunology, School of Basic Courses, Guangdong Pharmaceutical University, 510006, Guangzhou, China.

Jianan Yang (J)

Affiliated Cancer Hospital & Institute of Guangzhou Medical University, 510095, Guangzhou, China. yangjianan@gzhmu.edu.cn.
Department of Urologic Oncosurgery, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, 510095, Guangzhou, China. yangjianan@gzhmu.edu.cn.
ORCID: 0000-0002-1369-836X

Lili Jiang (L)

Affiliated Cancer Hospital & Institute of Guangzhou Medical University, 510095, Guangzhou, China. jianglili@gzhmu.edu.cn.
Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, School of Basic Medical Science, Guangzhou Medical University, 511436, Guangzhou, China. jianglili@gzhmu.edu.cn.
ORCID: 0000-0003-2361-5975

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Classifications MeSH

questionsmedicales.fr › Eucaryotes › Animaux › SBSN drives bladder cancer metastasis via...
questionsmedicales.fr › Facteurs biologiques › Marqueurs biologiques › Antigènes de différenciation › SBSN drives bladder cancer metastasis via...
questionsmedicales.fr › Cellules › Cellules cultivées › Cellules cancéreuses en culture › Lignée cellulaire tumorale › SBSN drives bladder cancer metastasis via...
questionsmedicales.fr › Phénomènes physiologiques › Mouvement cellulaire › SBSN drives bladder cancer metastasis via...
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Protéines membranaires › Récepteurs de surface cellulaire › Récepteurs peptidiques › Récepteur facteur croissance › Récepteurs ErbB › SBSN drives bladder cancer metastasis via...
questionsmedicales.fr › Phénomènes génétiques › Régulation de l'expression des gènes › Régulation de l'expression des gènes tumoraux › SBSN drives bladder cancer metastasis via...
questionsmedicales.fr › Eucaryotes › Animaux › Chordés › Vertébrés › Mammifères › Eutheria › Rodentia › Muridae › Murinae › Souris › SBSN drives bladder cancer metastasis via...
questionsmedicales.fr › États, signes et symptômes pathologiques › Processus pathologiques › Processus néoplasiques › Métastase tumorale › SBSN drives bladder cancer metastasis via...
questionsmedicales.fr › Diagnostic › Pronostic › SBSN drives bladder cancer metastasis via...
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Protéines tumorales › Protéines oncogènes › Protéines proto-oncogènes › Protéines proto-oncogènes pp60(c-src) › SBSN drives bladder cancer metastasis via...
questionsmedicales.fr › Phénomènes physiologiques cellulaires › Transduction du signal › SBSN drives bladder cancer metastasis via...
questionsmedicales.fr › Maladies urogénitales › Maladies urologiques › Tumeurs urologiques › Tumeurs de la vessie urinaire › SBSN drives bladder cancer metastasis via...
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Protéines et peptides de signalisation intracellulaire › Protein-tyrosine kinases › src-Family kinases › SBSN drives bladder cancer metastasis via...