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Evaluating the Angiogenetic Properties of Ovarian Cancer Stem-Like Cells using the Three-Dimensional Co-Culture System, NICO-1
Published on: December 5, 2020
Targeting cleavage and polyadenylation specific factor 1 via shRNA inhibits cell proliferation in human ovarian
Beiguang Zhang1, Ying Liu, Donghui Liu
1Department of Intervention Therapy, Jilin Cancer Hospital, Changchun, Jilin, China.
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.
Insights
Cleavage and polyadenylation specificity factor 1 (CPSF1) is overexpressed in ovarian cancer. Depleting CPSF1 inhibits cancer cell growth, proliferation, and survival, suggesting it
Area of Science:
- Molecular Biology
- Oncology
- Biochemistry
Background:
- Cleavage and polyadenylation specificity factor 1 (CPSF1) is crucial for pre-mRNA 3'-end formation.
- The role of CPSF1 in ovarian cancer pathogenesis is not well understood.
- Ovarian cancer remains a significant global health challenge requiring novel therapeutic targets.
Purpose of the Study:
- To investigate the expression levels of CPSF1 in ovarian cancer tissues.
- To elucidate the functional role of CPSF1 in ovarian cancer cell behavior.
- To assess the potential of CPSF1 as a therapeutic target for ovarian cancer.
Main Methods:
- Analysis of CPSF1 mRNA expression using the Oncomine Cancer Microarray database.
- Loss-of-function studies utilizing CCK-8, colony formation, and flow cytometry assays.
- Assessment of apoptosis-related proteins (cleaved caspase-3, PARP) and cell cycle regulators (CDK4/cyclin D1) following CPSF1 knockdown.
Main Results:
- CPSF1 mRNA was significantly overexpressed in ovarian cancer tissues compared to normal tissues.
- CPSF1 depletion led to reduced cell viability, impaired colony formation, G0/G1 cell cycle arrest, and increased apoptosis in ovarian cancer cell lines (SKOV-3, OVCAR-3).
- Knockdown of CPSF1 resulted in elevated cleaved caspase-3 and PARP, and decreased CDK4/cyclin D1 expression.
Conclusions:
- CPSF1 promotes ovarian cancer cell growth and proliferation in vitro.
- The findings suggest CPSF1 plays a oncogenic role in ovarian cancer.
- CPSF1 represents a potential therapeutic target for human ovarian cancer treatment.
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