Overexpression of FOS enhances the malignant potential of eutopic endometrial stromal cells in patients with endometriosis‑associated ovarian cancer.

Endometrial cysts of the ovary (EMC) may develop into endometriosis (EM)‑associated ovarian cancer over time (EAOC), but the pathogenesis of this disease has not been determined. In the present study, RNA sequencing was used to identify a feasible biomarker, and the molecular function of this biomarker in eutopic endometrial cells from EAOC and EMC patients was evaluated to explore the potential mechanism related to EAOC and orthotopic endometrial tissue. RNA sequencing was performed on 5 EAOC and 4 EMC tissue samples, and differential expression analysis was performed. To identify biomarkers, differentially expressed genes were subjected to protein‑protein interaction network design, Gene Ontology pathway enrichment, and Gene Set Enrichment Analysis pathway enrichment. The expression of FOS in the endometrium was detected via immunohistochemical staining. Lv‑FOS was utilized to upregulate FOS in human endometrial stromal cells (hEnSCs), and Cell Counting Kit‑8, colony formation and scratch assays were performed to assess cell viability, proliferation and migration, respectively. Western blotting was used to determine protein expression. In total, 249 genes, including FOS, were differentially expressed. Pathway enrichment analysis demonstrated that the MAPK, AP‑1, ERK and other signaling pathways were involved in the EMC‑to‑EAOC conversion. FOS upregulation in hEnSCs increased cell viability, proliferation and migration. Western blot results revealed that after FOS expression was inhibited, P21 expression was upregulated, and CDK4, Cyclin D1, p‑Stat3, MMP2 and MMP9 expression was downregulated. In conclusion, mitosis and the cell cycle were found to affect the progression of EMC to EAOC. The expression of FOS, a novel biomarker, was identified to enhance the malignant potential of eutopic endometrial stromal cells in patients with EM‑associated ovarian cancer.