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Integration of Bioinformatics Approaches and Experimental Validations to Understand the Role of Notch Signaling in Ovarian Cancer
Published on: January 12, 2020
CNOT7 modulates biological functions of ovarian cancer cells via AKT signaling pathway
Jiangtao Yu1, Xiaoli Hu1, Xiuxiu Chen1
1Department of Gynecology, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325027, People's Republic of China.
Aims:
CNOT7 plays an important role in many biological processes, providing attractive opportunities for the treatment of malignant tumors. However, the functions and mechanism of CNOT7 in ovarian cancer (OC) have not been elucidated. The purpose of this study was to assess the role of CNOT7 in OC.
Materials And Methods:
SKOV3 and A2780 cells were chosen as the cell lines for the experiments of this manuscript via the analysis of the expression of CNOT7 protein and the mRNA level in ovarian surface epithelium (OSE) cells, SKOV3, HO8910 and A2780 cells. The expression of CNOT7 was detected by western blot assays and RT-PCR in A2780 and SKOV3 cells. The MTT assays, colony formation assays and EdU assays were used to measure cell proliferation when CNOT7 was knocked down or overexpressed in A2780 and SKOV3 cells. Furthermore, cell migration and invasion ability were achieved from transwell assays. Cell cycle and apoptosis rate after small interference RNA-CNOT7 (siRNA-CNOT7) were detected by flow cytometry assays. Finally, the cell proliferation, migration and invasion ability were detected when A2780 and SKOV3 cells with CNOT7 overexpression were treated with LY294002.
Key Findings:
The expression of CNOT7 protein in OC cells, including SKOV3, HO8910 and A2780 cells were significantly higher than that in OSE cells (P < 0.05). The mRNA level of CNOT7 in HO8910 and A2780 cells were significantly higher than that in OSE cells (P < 0.01). However, the mRNA level of CNOT7 in SKOV3 cells was no significant difference compared with OSE cells (P > 0.05). The results suggested that knockdown of CNOT7 could inhibit the cell proliferation, migration and invasion ability in A2780 and SKOV3 cells, and increase cell apoptosis and autophagy. The expression of apoptosis-related molecules (PARP, Caspase3 and Caspase9) and autophagy-related protein (LC3B) were up-regulated after CNOT7 knockdown, while the expression of cycle-related protein (CDK6) and the anti-apoptotic gene (Bcl2) were downregulated. Meanwhile, the opposite results were observed when CNOT7 was overexpressed in A2780 and SKOV3 cells. It is worth noting that the effect of CNOT7 overexpression in A2780 and SKOV3 cells could be partially or completely eliminated by treatment with AKT inhibitor LY294002.
Significance:
CNOT7 has a carcinogenic effect in OC, and the carcinogenic effect may be achieved via the AKT signaling pathway.
Insights
CNOT7 promotes ovarian cancer (OC) progression by enhancing cell proliferation, migration, and invasion. Inhibiting CNOT7 or targeting the AKT pathway may offer new therapeutic strategies for OC treatment.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- CNOT7 is implicated in various biological processes and presents potential as a therapeutic target for malignant tumors.
- The specific role and mechanism of CNOT7 in ovarian cancer (OC) remain largely uncharacterized.
Purpose of the Study:
- To investigate the function and mechanism of CNOT7 in ovarian cancer (OC).
Main Methods:
- CNOT7 expression was analyzed in OC cell lines (SKOV3, HO8910, A2780) and ovarian surface epithelium (OSE) cells using Western blot and RT-PCR.
- Cell proliferation, migration, invasion, cell cycle, and apoptosis were assessed following CNOT7 knockdown or overexpression.
- The impact of AKT inhibitor LY294002 on CNOT7-overexpressing cells was evaluated.
Main Results:
- CNOT7 expression was significantly elevated in OC cells compared to OSE cells.
- CNOT7 knockdown inhibited OC cell proliferation, migration, and invasion, while promoting apoptosis and autophagy.
- CNOT7 overexpression yielded opposite effects, and these effects were partially or fully reversed by LY294002, indicating involvement of the AKT pathway.
Conclusions:
- CNOT7 exhibits a carcinogenic role in ovarian cancer.
- The carcinogenic effects of CNOT7 in OC are likely mediated through the AKT signaling pathway.
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