Background. Ovarian cancer is the most fatal gynecological malignancy. Owing to its insidious onset, rapid development, and poor prognosis, ovarian cancer is the fifth most common cause of death in women. Although immunotherapy-related drugs, such as Olaparib, can alleviate ovarian cancer progression, there are no remarkable breakthroughs for its effective treatment. It is considered that the transformation of normal cells to cancerous ones involves “recoding” of certain metabolic pathways. Diacylglycerol O-acyltransferase 1 (DGAT1) can synthesize triglycerides by transferring acyl-CoA to diacylglycerol, which plays a key role in lipid synthesis. However, the role of DGAT1 in ovarian cancer is not yet elucidated. Materials and Methods. We analyzed the correlation between DGAT1 and ovarian cancer staging, grading, vascular invasion, and prognosis by collating the information of ovarian cancer specimens from The Cancer Genome Atlas (TCGA) database. Furthermore, the effects of DGAT1 expression on proliferation, migration, invasion, and tumor growth were studied using ovarian cancer cell lines. GSEA was used to analyze the KEGG pathways and biological function enriched because of DGAT1 expression in ovarian cancer. Results. The expression of DGAT1 was elevated in advanced ( ), poorly differentiated ( ), and vascular invaded ( ) ovarian cancer specimens. Prognosis among patients with high expression of DGAT1 was poor. After DGAT1 expression was interfered, proliferation, migration, invasion, colony forming, and tumor growth of ovarian cancer cells were inhibited. In addition, GSEA showed that DGAT1 may be involved in the immune process. Conclusion. DGAT1 expression is associated with the clinical phenotype of ovarian cancer. We suggest that DGAT1 has potential implications in the treatment of ovarian cancer.

Background: Serum 25 (OH) D levels are associated with various diseases, including cancers, but inconsistencies exist for female-specific malignancies. This study is aimed to explore the real relationship between serum 25 (OH) D levels and incidence rates of female specific cancers in premenopausal women by a large-scale prospective cohort study.Study design: We analyzed data from 51,286 UK Biobank participants using Cox regression models to explore associations. Subgroup analyses were based on vitamin D supplementation, alcohol, smoking, BMI, diabetes, sleep, and outdoor exposure. Categorical variables were described by frequencies and compared with chi-squared tests.Results: During a median follow-up of 13.8 years, all cancer incidence was 5.1% (n = 2,614), with ovarian cancer at 0.3% (n = 176), breast cancer at 4.4% (n = 2,232), and uterine body cancer at 0.5% (n = 235). Low serum 25 (OH) D (50 nmol/L) was linked to increased risks of ovarian (HR: 1.457, 95% CI: 1.047–2.027) and uterine body cancer (HR: 1.372, 95% CI: 1.023–1.841). Each 10 nmol/L increase in 25 (OH) D reduced ovarian cancer risk (HR: 0.904, 95% CI: 0.835–0.979). Alcohol use and sleep <6 h were risk factors for ovarian and uterine cancer in those with low 25 (OH) D levels.Conclusion: Maintaining adequate serum 25 (OH) D levels is essential for overall health, reducing the risk of ovarian cancer, and potentially lowering susceptibility to uterine corpus cancer.

Introduction: Reproductive endocrine disorders (RED), including polycystic ovary syndrome (PCOS), endometriosis (EMs), and female infertility (FI), significantly affect women’s health globally, with varying prevalence across different regions. These conditions can be addressed through medication, surgical interventions, and lifestyle modifications. However, the limited understanding of RED’s etiology and the substantial economic burden of its treatment highlight the importance of investigating its pathogenesis. Metabolites play a critical role in metabolic processes and are potentially linked to the development of RED. Despite existing studies suggesting correlations between metabolites and RED, conclusive evidence remains scarce, primarily due to the observational nature of these studies, which are prone to confounding factors.Methods: This study utilized Mendelian Randomization (MR) to explore the causal relationship between metabolites and RED, leveraging genetic variants associated with metabolite levels as instrumental variables to minimize confounding and reverse causality. Data were obtained from the Metabolomics GWAS Server and the IEU OpenGWAS project. Instrumental variables were selected based on their association with the human gut microbiota composition, and the GWAS summary statistics for metabolites, PCOS, EMs, and FI were analyzed. The MR-Egger regression and random-effects inverse-variance weighted (IVW) methods were employed to validate the causal relationship. Cochran’s Q test was employed to evaluate heterogeneity, sensitivity analysis was performed using leave-one-out analysis, and for pleiotropy analysis, the intercept term of MR-Egger’s method was investigated.Results: The MR analysis revealed significant associations between various metabolites and RED conditions. For instance, a positive association was found between 1-palmitoylglycerophosphocholine and PCOS, while a negative association was noted between phenylacetate and FI. The study identified several metabolites associated with an increased risk and others with protective effects against PCOS, EMs, and FI. These findings highlight the complex interplay between metabolites and RED, suggesting potential pathways through which these conditions could be influenced or treated.Conclusion: This MR study provides valuable insights into the causal relationship between metabolites and female reproductive endocrine disorders, suggesting that metabolic alterations play a significant role in the pathogenesis of PCOS, EMs, and FI, and offering a foundation for future research and therapeutic development.

Regulator of G protein signaling 1 (RGS1) is known to be highly expressed in various tumors, but its specific effects and regulatory mechanism in ovarian cancer (OC) progression are not well understood. To delve into the tumor biology, a predictive risk model for OC was developed, incorporating RGS1, PRKG2, CD24, and ABCB1, with RGS1 exhibiting the strongest correlation. The model’s reliability and validity were confirmed through Kaplan-Meier analysis, receiver operating characteristic (ROC) curve, and principal component analysis (PCA). The risk score was validated as an independent indicator of overall survival, and a nomogram model was created to predict overall survival. Moreover, RGS1 expression was found to be up-regulated and associated with a poor prognosis in OC. Functional studies revealed that deleting RGS1 inhibited OC cell proliferation both in vitro and in vivo, while overexpression of RGS1 enhanced cell proliferation. Additionally, blocking the NF-kB pathway was shown to impede RGS1-induced proliferation, and overexpression of p65 partially reversed the effects of RGS1 deletion, promoting the tumorigenic properties of OC cells. These findings suggest that RGS1 could be a valuable biomarker for predicting prognosis and a potential novel therapeutic target for OC treatment.

Ovarian cancer remains a significant cause of morbidity and mortality in women worldwide. Olaparib, a poly ADP-ribose polymerase (PARP) inhibitor, has been shown in studies to increase the time that people with cancer do not get worse. However, reports have indicated rare adverse effects, like myelodysplastic syndrome (MDS). In this report, we highlight the case of a 42-year-old female patient who was diagnosed with ovarian endometrioid carcinoma, FIGO Stage IIB. Following surgery and chemotherapy, the patient commenced maintenance therapy with Olaparib. After two years, she experienced abnormal blood test results, which ultimately led to a diagnosis of myelodysplastic syndrome (MDS), confirmed through a bone marrow biopsy. Despite initial obstacles, the patient underwent stem cell transplantation as a treatment for MDS. After undergoing stem cell transplantation, the patient experienced a notable improvement in their condition. Upon reevaluation, the transplantation proved successful as it resolved the abnormalities related to MDS. Furthermore, the ovarian cancer status showed a positive response, with no signs of disease progression during the follow-up period. This particular case emphasizes the importance of being vigilant for uncommon adverse effects, such as MDS, in ovarian cancer patients undergoing Olaparib maintenance therapy. Early diagnosis and treatment, which may include stem cell transplantation, can lead to favorable results, not only in managing MDS but also in possibly slowing down the progression of ovarian cancer that is causing it. Additional research is necessary to understand the risk factors and the most effective management approaches for these complications in this specific group of patients.