FAM111B knockdown attenuates tumorigenesis of ovarian cancer via the down regulation of MYC

Abstract Background Ovarian cancer, a prevalent malignancy with the highest fatality rate among gynecological cancers, continues to face challenges in the development of effective targeted therapy approaches. While the FAM111B gene has been implicated in various cancer types, its specific role in ovarian cancer remains poorly understood. Methods The ES2 and A2780 ovarian cell lines were used to explore the cellular proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) in FAM111B knockdown experiments. The mouse tumor model was constructed to investigate the impact of FAM111B silencing in vivo. Tissue microarray was used to explore the prognostic value of different FAM111B expression level. Western blotting assay, MYC overexpression rescue experiments, protein transcriptomics and bioinformatics analysis were employed to explore the downstream molecular mechanism of FAM111B. Results The in vitro experiments indicated that the inhibition of FAM111B resulted in decreased cellular proliferation, migration, invasion, and EMT in ovarian cancer cell lines. The suppression of FAM111B resulted in the suppression of tumor growth in a mouse xenograft model. Immunohistochemistry analyses conducted on tissue-microarray samples obtained from patients with serous ovarian cancer indicated that elevated levels of FAM111B expression were associated with unfavorable prognostic outcomes. The silencing of FAM111B mechanistically suppressed MYC expression, with subsequent MYC overexpression reversing the phenotypic suppression caused by FAM111B silencing. Additionally, protein transcriptomics analysis indicated that FAM111B is implicated in genetic information processing via the MYC pathway, underscoring its central role in ovarian cancer tumorigenesis. Conclusions These findings suggest that FAM111B may serve as a novel biomarker and potential therapeutic target for ovarian cancer.