Increased expression of TRIP13 drives the tumorigenesis of bladder cancer in association with the EGFR signaling pathway.
ATPases Associated with Diverse Cellular Activities
/ metabolism
Aged
Apoptosis
Biomarkers, Tumor
Carcinogenesis
Cell Cycle
Cell Cycle Proteins
/ metabolism
Cell Line, Tumor
Cell Movement
Cell Proliferation
Cell Transformation, Neoplastic
Computational Biology
ErbB Receptors
/ metabolism
Female
Gene Expression Regulation, Neoplastic
Humans
Lymphatic Metastasis
Male
Middle Aged
Neoplasm Metastasis
RNA, Small Interfering
/ metabolism
Signal Transduction
Treatment Outcome
Urinary Bladder Neoplasms
/ metabolism
Bladder cancer
EGFR
TRIP13
Tumorigenesis
Journal
International journal of biological sciences
ISSN: 1449-2288
Titre abrégé: Int J Biol Sci
Pays: Australia
ID NLM: 101235568
Informations de publication
Date de publication:
2019
2019
Historique:
received:
01
01
2019
accepted:
04
04
2019
entrez:
25
7
2019
pubmed:
25
7
2019
medline:
17
4
2020
Statut:
epublish
Résumé
Thyroid hormone receptor interactor 13 (TRIP13) is a crucial regulator of the spindle apparatus checkpoint and double-stranded break repair. The abnormal expression of TRIP13 was recently found in several human cancers, whereas the role of TRIP13 in the development of bladder cancer (BCa) has not been fully elucidated. Here, we reported that TRIP13 expression was elevated in BCa tissues compared with normal bladder tissues. Notably, the increased expression of TRIP13 was correlated with advanced tumor stage, lymph node metastasis, distant metastasis and reduced survival in BCa patients. Knockdown of TRIP13 in bladder cancer cells suppressed proliferation, induced cell cycle arrest, promoted apoptosis, and impaired cell motility, ultimately inhibiting tumor xenograft growth. Mechanistic investigations revealed that TRIP13 directly bound to epidermal growth factor receptor (EGFR), modulating the EGFR signaling pathway. Furthermore, TRIP13 expression was positively correlated with EGFR expression in BCa specimens, and the high expression of both TRIP13 and EGFR predicted poor survival. Overall, our results underscore the crucial role of TRIP13 in the tumorigenesis of BCa and provide a novel biomarker and therapeutic target for BCa treatment.
Identifiants
pubmed: 31337978
doi: 10.7150/ijbs.32718
pii: ijbsv15p1488
pmc: PMC6643140
doi:
Substances chimiques
Biomarkers, Tumor
0
Cell Cycle Proteins
0
RNA, Small Interfering
0
EGFR protein, human
EC 2.7.10.1
ErbB Receptors
EC 2.7.10.1
ATPases Associated with Diverse Cellular Activities
EC 3.6.4.-
TRIP13 protein, human
EC 3.6.4.-
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1488-1499Déclaration de conflit d'intérêts
Competing Interests: The authors have declared that no competing interest exists.
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