ABSTRACT: Background: Endometrialcyst of ovary (EMC) may develop into endometriosis-associated ovarian cancer over time (EAOC). EAOC pathogenesis is unknown. This study investigated the likely mechanism of EAOC publishing related with orthotopic endometrial, searched for a feasible biomarker using RNA sequencing, and examined the molecular function of this biomarker in ectopic endometrial cells from EAOC and EMC patients. Methods: RNA sequencing was performed on 5 EAOC and 4 EMC tissue samples. Differential expression analysis employed RNA-seq data. To identify biomarkers, differential genes were used in PPI network design, GO pathway enrichment, and GSEA pathway enrichment. Immunohistochemical staining revealed FOS expression in various endometrium. Lv-FOS was utilized to up-regulate FOS in hEnSCs, and cell counting kit-8 (CCK-8), colony formation assay, and scratch assay were performed to assess cell viability, proliferation, and migration. Western blot showed protein expression alterations. Results: 249 genes were differently expressed, including FOS. Pathway enrichment study demonstrated that MAPK, AP-1, ERK, and other signaling pathways were involved in EMC-to-EAOC conversion. FOS upregulation in hEnSCs increased cell viability, proliferation, and migration. Western blot results showed that FOS, CDK4, cyclinD1, P21, and invasion-related proteins p-stat3, MMP2, and MMP9 were up- or down-regulated, respectively. Conclusion: Mitosis and cell cycle affect EMC to EAOC progression. FOS expression, a novel biomarker, promotes EMC transition into EAOC and endometrial cell proliferation, invasion, and migration. Keywords: FOS, endometrialcyst of ovary, endometriosis-associated ovarian cancer, biomarker
