Abstract |
Cleavage and polyadenylation specificity factor 1 (CPSF1), a member of CPSF complex, has been reported to play a key role in pre-mRNA 3'-end formation, but its possible role in ovarian cancer remains unclear. In the present study, we found the mRNA level of CPSF1 was overexpressed in ovarian cancer tissues using Oncomine Cancer Microarray database. Then the loss-of-function assays, including CCK-8, colony formation and flow cytometry assays, were performed to determine the effects of CPSF1 on cell viability, proliferation, cell cycle and apoptosis of human ovarian cancer cell lines (SKOV-3 and OVCAR-3). The results indicated that depletion of CPSF1 suppressed cell viability, impaired colony formation ability, induced cell cycle arrest at G0/G1 phase and promoted cell apoptosis in ovarian cancer cells. Furthermore, knockdown of CPSF1 upregulated the expression of cleaved caspase-3 and PARP and downregulated CDK4/ cyclin D1 expression. These data suggested that CPSF1 could promote ovarian cancer cell growth and proliferation in vitro and its depletion might serve as a potential therapeutic target for human ovarian cancer.
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Authors | Beiguang Zhang, Ying Liu, Donghui Liu, Lei Yang |
Journal | Journal of biosciences
(J Biosci)
Vol. 42
Issue 3
Pg. 417-425
(Sep 2017)
ISSN: 0973-7138 [Electronic] India |
PMID | 29358555
(Publication Type: Journal Article)
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Chemical References |
- CCND1 protein, human
- Cleavage And Polyadenylation Specificity Factor
- RNA, Small Interfering
- Cyclin D1
- Poly(ADP-ribose) Polymerases
- CDK4 protein, human
- Cyclin-Dependent Kinase 4
- CASP3 protein, human
- Caspase 3
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Topics |
- Apoptosis
(genetics)
- Caspase 3
(genetics, metabolism)
- Cell Line, Tumor
- Cell Movement
- Cell Proliferation
- Cleavage And Polyadenylation Specificity Factor
(antagonists & inhibitors, genetics, metabolism)
- Cyclin D1
(genetics, metabolism)
- Cyclin-Dependent Kinase 4
(genetics, metabolism)
- Epithelial Cells
(metabolism, pathology)
- Female
- G1 Phase Cell Cycle Checkpoints
(genetics)
- Gene Expression Regulation, Neoplastic
- Humans
- Ovary
(metabolism, pathology)
- Poly(ADP-ribose) Polymerases
(genetics, metabolism)
- RNA, Small Interfering
(genetics, metabolism)
- Signal Transduction
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