IFN-γ inhibits ovarian cancer progression via SOCS1/JAK/STAT signaling pathway
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[1] Department of Gynaecology and Obstetrics, The Second Afliated Hospital of Soochow University, No.1055 sanxiang road, Suzhou 215004, China
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[2] Department of Scientifc Research Management, Zhuhai People’s Hospital (Zhuhai Hospital Afliated With Jinan University), Zhuhai 519000, Guangdong, China
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- Localización: Clinical & translational oncology, ISSN 1699-048X, Vol. 24, Nº. 1 (Enero), 2022, págs. 57-65
- Idioma: inglés
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Resumen
Abstract Purpose Ovarian cancer (OC) is a common malignancy, and IFN-γ, a multifunctional cytokine, is unveiled to impede the multiplication and enhance apoptosis in diverse tumor cells in previous research. Nonetheless, its function and mechanism in OC are blurred.
Methods OC cell lines SKOV3 and OVCAR3 were dealt with diferent concentrations (0–40 ng/ml) of IFN-γ. CCK-8 experiment was utilized to examine cell multiplication; Flow cytometry was executed to detect apoptosis and cell cycle; Wound healing assay was utilized to detect cell migration; and Transwell experiment was implemented to examine cell invasion. qRT-PCR analysis was applied to detect STAT5, STAT3, JAK2 and JAK3 mRNA expression in OC cell lines. Western blot experiment was applied to detect the protein and phosphorylation levels of SOCS1, STAT5 and STAT3.
Results IFN-γ suppressed OC cell multiplication in a concentration-dependent manner. Relative to the control group, IFN-γ restrained OC cell migration, invasion, enhanced apoptosis and prevented cell transformation from G0/G1 to S phase. Further analysis revealed that IFN-γ up-modulated SOCS1 expression and impeded STAT5 and STAT3 protein phosphorylation levels, and knockdown of SOCS1 partially counteracted the inhibitory efect of IFN-γ on STAT5 and STAT3 protein phosphorylation levels.
Conclusion IFN-γ represses OC progression by facilitating SOCS1 to suppress STAT3 and STAT5 protein phosphorylation
