The inhibitory effect of silencing CDCA3 on migration and proliferation in bladder urothelial carcinoma.
Bladder urothelial carcinoma
CDCA3
Migration
cell cycle
p21
Journal
Cancer cell international
ISSN: 1475-2867
Titre abrégé: Cancer Cell Int
Pays: England
ID NLM: 101139795
Informations de publication
Date de publication:
12 May 2021
12 May 2021
Historique:
received:
05
01
2021
accepted:
30
04
2021
entrez:
13
5
2021
pubmed:
14
5
2021
medline:
14
5
2021
Statut:
epublish
Résumé
CDCA3 is an important component of the E3 ligase complex with SKP1 and CUL1, which could regulate the progress of cell mitosis. CDCA3 has been widely identified as a proto-oncogene in multiple human cancers, however, its role in promoting human bladder urothelial carcinoma has not been fully elucidated. Bioinformatic methods were used to analyze the expression level of CDCA3 in human bladder urothelial carcinoma tissues and the relationship between its expression level and key clinical characteristics. In vitro studies were performed to validate the specific functions of CDCA3 in regulating cell proliferation, cell migration and cell cycle process. Alterations of related proteins was investigated by western blot assays. In vivo studies were constructed to validate whether silencing CDCA3 could inhibit the proliferation rate in mice model. Bioinformatic analysis revealed that CDCA3 was significantly up-regulated in bladder urothelial carcinoma samples and was related to key clinical characteristics, such as tumor grade and metastasis. Moreover, patients who had higher expression level of CDCA3 tend to show a shorter life span. In vitro studies revealed that silencing CDCA3 could impair the migration ability of tumor cells via down-regulating EMT-related proteins such as MMP9 and Vimentin and inhibit tumor cell growth via arresting cells in the G1 cell cycle phase through regulating cell cycle related proteins like p21. In vivo study confirmed that silencing CDCA3 could inhibit the proliferation of bladder urothelial carcinoma cells. CDCA3 is an important oncogene that could strengthen the migration ability of bladder urothelial carcinoma cells and accelerate tumor cell growth via regulating cell cycle progress and is a potential biomarker of bladder urothelial carcinoma.
Sections du résumé
BACKGROUND
BACKGROUND
CDCA3 is an important component of the E3 ligase complex with SKP1 and CUL1, which could regulate the progress of cell mitosis. CDCA3 has been widely identified as a proto-oncogene in multiple human cancers, however, its role in promoting human bladder urothelial carcinoma has not been fully elucidated.
METHODS
METHODS
Bioinformatic methods were used to analyze the expression level of CDCA3 in human bladder urothelial carcinoma tissues and the relationship between its expression level and key clinical characteristics. In vitro studies were performed to validate the specific functions of CDCA3 in regulating cell proliferation, cell migration and cell cycle process. Alterations of related proteins was investigated by western blot assays. In vivo studies were constructed to validate whether silencing CDCA3 could inhibit the proliferation rate in mice model.
RESULTS
RESULTS
Bioinformatic analysis revealed that CDCA3 was significantly up-regulated in bladder urothelial carcinoma samples and was related to key clinical characteristics, such as tumor grade and metastasis. Moreover, patients who had higher expression level of CDCA3 tend to show a shorter life span. In vitro studies revealed that silencing CDCA3 could impair the migration ability of tumor cells via down-regulating EMT-related proteins such as MMP9 and Vimentin and inhibit tumor cell growth via arresting cells in the G1 cell cycle phase through regulating cell cycle related proteins like p21. In vivo study confirmed that silencing CDCA3 could inhibit the proliferation of bladder urothelial carcinoma cells.
CONCLUSIONS
CONCLUSIONS
CDCA3 is an important oncogene that could strengthen the migration ability of bladder urothelial carcinoma cells and accelerate tumor cell growth via regulating cell cycle progress and is a potential biomarker of bladder urothelial carcinoma.
Identifiants
pubmed: 33980246
doi: 10.1186/s12935-021-01969-x
pii: 10.1186/s12935-021-01969-x
pmc: PMC8114508
doi:
Types de publication
Journal Article
Langues
eng
Pagination
257Subventions
Organisme : National Natural Science Foundation of China
ID : 31900902
Organisme : National Natural Science Foundation of China
ID : 81772730
Organisme : Medical Science Advancement Program (Clinical Medicine) of Wuhan University
ID : TFLC2018002
Organisme : Improvement Project for Theranostic Ability on Difficulty Miscellaneous Disease (Tumor) from National Health Commission of China
ID : ZLYNXM202006
Organisme : Science and Technology Department of Hubei Province Key Project
ID : 2018ACA159
Organisme : the research fund from medical Sci-Tech innovation platform of Zhongnan Hospital, Wuhan University
ID : PTXM2021023
Organisme : Non-profit Central Research Institute Fund of Chinese Academy of Medical Sciences
ID : 2020-PT320-004
Organisme : Wuhan Youth Talent Project
ID : WHQG202002
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