The Forkhead box M1 (FOXM1), an important regulator of cell differentiation and proliferation, is overexpressed in a number of aggressive human carcinomas. The purpose of this study was to examine the expression levels of FOXM1 in epithelial ovarian cancer (EOC), to identify the relationship between FOXM1 expression and patient survival, and to investigate the role of FOXM1 in human ovarian cancer development. Immunohistochemical analysis for FOXM1 was performed in a total of 158 ovarian tissue specimens, all with linked clinical outcome data. Kaplan–Meier method and Cox proportional hazards analysis were used to relate FOXM1 expression to clinicopathological variables and to progression-free survival (PFS) and overall survival (OS). In vitro studies were performed to determine the function of FOXM1 in cell proliferation, migration and invasion in EOC cells using pcDNA3.1-FOXM1 and FOXM1 shRNA. Elevated FOXM1 levels were associated with lymph node metastasis (P = 0.009), but not with age, FIGO stage, histological grade and histological type. Patients with high expression of FOXM1 had poorer PFS (P = 0.0001) and OS (P < 0.0001) than patients with low expression of FOXM1. Furthermore, multivariate analyses indicated that FOXM1 positivity was an independent prognostic factor for PFS (P = 0.046) and OS (P = 0.022), respectively. Overexpression of FOXM1 increased expression and activity of matrix metalloproteinase-2 (MMP-2), MMP-9 and vascular endothelial growth factor-A (VEGF-A), and cancer cell proliferation, migration and invasion of HO-8910 cells, whereas knockdown of FOXM1 reduced expression and activity of MMP-2, MMP-9 and VEGF-A, and cancer cell proliferation, migration and invasion of HO-8910 PM cells. Our results suggest that FOXM1 expression is likely to play important roles in EOC development and progression. FOXM1 expression is a potential prognostic factor for PFS and OS, and it could be a novel treatment target in EOC patients.

Carnitine palmitoyltransferase 2 (CPT2) is a rate-limiting enzyme involved in fatty acid β-oxidation (FAO) regulation. Recently, it has been increasingly recognized that lipid metabolism dysregulation is closely implicated in tumorigenesis. However, the involvement of CPT2 in the progression of cancer is still largely unclear, especially in ovarian cancer (OC). In the present study, CPT2 expression and its clinical significance were determined in OC tissues and cells. The biological functions and molecular mechanisms of CPT2 in OC growth and metastasis were determined by in vitro and in vivo assays. We found that CPT2 was frequently down-regulated in primary ovarian serous carcinomas, which is significantly correlated with poor survival of ovarian cancer patients. Functional experiments revealed that CPT2 inhibited OC cell growth and metastasis via suppression of G1/S cell cycle transition and epithelial to mesenchymal transition (EMT), as well as induction of cell apoptosis. Mechanistically, suppression of ROS/NFκB signaling pathway by increasing fatty acid oxidation-derived NADPH production was involved in the anti-tumorigenic functions of CPT2 in OC cells. Altogether, our findings demonstrate that CPT2 functions as a potential tumor suppressor in OC progression. CPT2 may serve as a novel prognostic marker and therapeutic target in OC.

Basigin, which has four isoforms, has been demonstrated to be involved in progression of various human cancers. The aim of this study was to examine the prognostic value of basigin-2 protein expression in epithelial ovarian cancer. Furthermore, the function of basigin-2 in ovarian cancer was further investigated in cell culture models.

Background: Ovarian cancer (OC), as a malignant tumor that seriously endangers the lives and health of women, is renowned for its complex tumor heterogeneity. Multi-omics analysis, as an effective method for distinguishing tumor heterogeneity, can more accurately differentiate the prognostic subtypes with differences among patients with OC. The aim of this study is to explore the prognostic subtypes of OC and analyze the molecular characteristics among the different subtypes.Methods: We utilized 10 clustering algorithms to analyze the multi-omics data of OC patients from The Cancer Genome Atlas (TCGA). After that, we integrated them with ten different machine-learning methods in order to determine high-resolution molecular subgroups and generate machine-learning-driven characteristics that are both resilient and consensus-based. Following the application of multi-omics clustering, we were able to identify two cancer subtypes (CSs) that were associated with the prognosis. Among these, CS2 demonstrated the most positive predictive outcome. Subsequently, five genes that constitute the machine learning (ML)-driven features were screened out by ML algorithms, and these genes possess a powerful predictive ability for prognosis. Subsequently, the function of FXYD Domain-Containing Ion Transport Regulator 6 (FXYD6) in OC was analyzed through gene knockdown and overexpression, and the mechanism by which it affects the functions of OC was explored.Results: Through multi-omics analysis, we ascertained that the high-risk score group exhibits a poorer prognosis and lack of response to immunotherapy. Moreover, this group is more prone to display the “cold tumor” phenotype, with a lower likelihood of benefiting from immunotherapy. FXYD6, being a crucial differential molecule between subtypes, exerts a tumor-promoting effect when knocked down; conversely, its overexpression yields an opposite outcome. Additionally, we discovered that the overexpression of FXYD6 can induce ferroptosis in OC cells, implying that a low level of FXYD6 in OC cells can safeguard them from ferroptosis. Insightful and more precise molecular categorization of OC can be achieved with a thorough examination of multi-omics data. There are significant consequences for clinical practice stemming from the discovery of risk scores since they provide a useful tool for early prognosis prediction as well as the screening of candidates for immunotherapy.

Background: The malignant transformation of endometriosis has garnered widespread attention; however, most cases of malignant transformation occur in ovarian endometriomas, while extraovarian malignant transformation is rare. We present an uncommon instance of extraovarian endometrioid adenocarcinoma originating from the uterosacral ligament(USL) in a 41-year-old female, which emerged from deep infiltrating endometriosis of the uterosacral ligament 4 years after a previous clinical diagnosis of adenomyosis. Case presentation: A 41-year-old woman, presenting with progressively worsening secondary dysmenorrhea for 4 years and dyspareunia for over 1 year, underwent “laparoscopic total hysterectomy, left adnexectomy, right salpingectomy, right ovarian endometrioma cystectomy, bilateral uterosacral ligament DIE lesion resection, anterior rectal resection, rectal DIE lesion resection with end-to-end anastomosis, left ureteral DIE lesion excision, and pelvic adhesiolysis.” Postoperative pathology revealed a well-differentiated endometrioid adenocarcinoma of the uterosacral ligament (FIGO grade 1), arising from malignant transformation of pelvic endometriosis. Subsequently, a completion surgery was performed, consisting of “transabdominal right oophorectomy, pelvic and para-aortic lymphadenectomy, omentectomy, biopsy of an ileal surface lesion, resection of a right pelvic wall peritoneal lesion, and pelvic adhesiolysis.” Postoperative pathological examination revealed a metastatic carcinoma in the right obturator lymph node. The final diagnosis was stage IV according to the FIGO 2009 staging system (FIGO stage IV) pelvic endometriosis-associated malignancy with direct invasion of the rectal wall by the USL adenocarcinoma. The patient underwent six cycles of adjuvant chemotherapy with paclitaxel and carboplatin given every three weeks. Over five years after finishing treatment, there are no signs of recurrence. Conclusion: This paper describes an unusual case where deep infiltrating endometriosis of the uterosacral ligament led to malignant transformation. During long-term treatment and surgery for endometriosis, the potential for malignant transformation and the malignant characteristics of endometriosis should be fully considered. Prompt and thorough surgical intervention is crucial.