Purvalanol A induces apoptosis and reverses cisplatin resistance in ovarian cancer.

Cisplatin (DDP) resistance limits therapeutic efficacy in patients diagnosed with ovarian cancer. Purvalanol A (Pur) is a novel cyclin-dependent kinase (CDK) inhibitor that has been demonstrated to induce apoptosis in various cancer cells. The present study investigated the effect of the combination treatment of Pur and DDP, and the potential anticancer mechanisms in epithelial ovarian cancer (EOC) cells in vitro and in vivo . We found that Pur enhanced the anti-tumor efficacy of cisplatin in EOC cells. The combination of Pur and DDP had more significant effects on apoptosis induction in EOC cells compared with the individual-treatment groups and the control group. We further demonstrated that the combination of Pur and DDP may trigger apoptosis and autophagy in EOC cells by inducing reactive oxygen species (ROS). And the ROS/Akt/mammalian target of rapamycin signaling pathway as a potential mechanism for the initiation of autophagy induced by combination therapy. Similar results were observed in vivo . These results demonstrated that Pur sensitized the response of EOC cells to cisplatin in vitro and in vivo , reversing the resistance to cisplatin in ovarian cancer.

Dimethyl fumarate ameliorates stress urinary incontinence by reversing ECM remodeling via the Nrf2-TGF-ß1/Smad3 pathway in mice.

INTRODUCTION AND HYPOTHESIS: Mechanical trauma and oxidative injury are involved in the pathogenesis of stress urinary incontinence (SUI), and oxidative stress (OS) is considered a potential therapeutic target. The antioxidant properties of dimethyl fumarate (DMF), a potent activator of Nrf2, have been highlighted recently. We therefore predicted that DMF might have therapeutic effects on mechanical trauma-induced SUI. METHODS: The SUI mice model was established by vaginal distension (VD). Leak point pressure (LPP), serum OS biomarkers, cell proliferation and apoptosis, collagen, elastin, matrix metalloproteinases (MMP), Nrf2, the TGF-ß1/Smad3 signaling pathway, and the associated tissue growth factors in the anterior vaginal wall were measured in either wild-type or Nrf2-knockout (Nrf2-/-) female C57BL/6 mice. RESULTS: The results showed that DMF improved the VD-induced LPP reduction, alleviated oxidative injury, stimulated cell proliferation and inhibited apoptosis in the anterior vaginal wall tissue of mice. Moreover, DMF treatment reduced the hydrolysis of ECM proteins by MMP2 and MMP9. The above effects may be mediated by a series of tissue growth factors, including α-SMA, PAI-1, and TIMP-2, with the TGF-ß1/Smad3 signaling pathway as the core regulatory mechanism. In further study, Nrf2-/- mice were used to replicate the SUI model. And the difference is that DMF failed to reactivate the TGF-ß1/Smad3 pathway, nor did it improve LPP. CONCLUSIONS: Dimethyl fumarate can ameliorate urethra closure dysfunction in the VD-induced SUI mice model, and the therapeutic effect of DMF is mediated by the Nrf2-dominated antioxidant system and its downstream TGF-ß1/Smad3 signaling pathway.

Application of estrogen for the treatment of stress urinary incontinence in mice.

BACKGROUND: Stress urinary incontinence (SUI) is a pervasive health tissue among women, which seriously affects the quality of life. The etiology of SUI is complex and diverse in women, with past studies having demonstrated that estrogen deficiency plays an important role in pelvic floor muscle atrophy and urethral degeneration. We comprehensively investigated the effects of estrogen in the treatment of SUI in female mice at cellular and animal levels. METHODS: L929 fibroblasts mechanical injury model was established by four-point bending device, and SUI mouse model was established by vaginal dilation method commonly used to simulate labor injury. After estrogen treatment, the expressions of Collagen I, Collagen III, Elastin, TIMP-1, TIMP-2, MMP-2, and MMP-9 were detected, the leak point pressure (LPP) and abdominal leak point pressure (ALPP) of mice in each group were detected, and both the effect of estrogen on extracellular matrix remodeling of mouse urethra and anterior vaginal wall was observed from the histological level. RESULTS: The results revealed that an appropriate amount of estrogen can promote the expression of Collagen I, Collagen III, Elastin, TIMP-1, and TIMP-2, decrease the expression of MMP-2 and MMP-9, and maintain the dynamic balance of MMPs/TIMPs at both cellular and animal levels. Meanwhile, we determined that estrogen can increase the LPP and ALPP values of SUI mice. The collagen fibers' content in the mice treated with estrogen was significantly greater than in the control group mice. CONCLUSIONS: The estrogen may alleviate the symptoms of SUI by reconstituting ECM, thus laying a solid foundation for further exploration of estrogen therapy.

Mechanical Stretching induces the apoptosis of parametrial ligament Fibroblasts via the Actin Cytoskeleton/Nr4a1 signalling pathway.

The anatomical positions of pelvic floor organs are maintained mainly by ligaments and muscles. Long-term excessive mechanical tension stimulation of pelvic floor tissue beyond the endurance of ligaments or muscles will lead to the occurrence of pelvic organ prolapse (POP). In addition, cytoskeletal reconstitution is a key process by which cells respond to mechanical stimulation. The aim of the present study was to investigate the protective effect of actin cytoskeleton to resist mechanical stretching (MS)-induced apoptosis in parametrial ligament fibroblasts (PLFs) and the underlying mechanisms. MS provided by a four­point bending device could significantly induce apoptosis of PLFs from non-POP patients, which exhibited an apoptosis rate close to that of PLFs from POP patients, and the apoptosis rate was higher following latrunculin A (Lat-A, a potent inhibitor of actin) treatment. In addition, Nr4a1 and Bax expression was increased while Bcl-2 and caspase-3 expression was clearly decreased after treatment with MS and Lat-A. However, the apoptosis induced by MS was reduced when the expression of Nr4a1 was downregulated by siRNA. These outcomes reveal a novel mechanism that links the actin cytoskeleton and apoptosis in PLFs by Nr4a1; this mechanism will provide insight into the clinical diagnosis and treatment of POP.

Knockdown of Hypoxia-Inducible Factor 1α (HIF-1α) Promotes Autophagy and Inhibits Phosphatidylinositol 3-Kinase (PI3K)/AKT/Mammalian Target of Rapamycin (mTOR) Signaling Pathway in Ovarian Cancer Cells.

BACKGROUND Ovarian cancer has the highest mortality rate among all female genital tumors because of its insidious onset and drug resistance. Hypoxia-inducible factor 1alpha (HIF-1alpha), one of the best-studied oncogenes, plays an important part in tumor adaptation to microenvironmental hypoxia and was found to be overexpressed in several malignancies, including ovarian cancer. Previous studies found that the effect of HIF-1alpha on cancers may be correlated with autophagy and some signaling pathways, such as PI3K/AKT/mTOR, in several tumors. However, the function and potential mechanism have not been clearly defined. MATERIAL AND METHODS The expression of HIF-1alpha in ovarian cancer tissues were detected by immunohistochemistry. HIF-1alpha was knocked down by siRNA transfection. Cell viability was examined by CCK8 and colony formation assay. Apoptosis and autophagy were detected with flow cytometry, transmission electron microscopy, and laser scanning confocal microscopy, respectively. The proteins related to autophagy and PI3K/AKT/mTOR were detected through Western blot analysis. RESULTS HIF-1alpha was expressed at higher levels in epithelial or metastatic ovarian cancer tissue than in normal fallopian tube tissue. When HIF-1alpha was knocked down by siRNA in A2780 and SKOV3 cells, the viability of ovarian cancer cells was weakened, but the apoptosis and autophagy were strengthened. Accordingly, autophagosome formation increased and the expression of autophagy-related proteins LC3 and P62 increased in HIF-1alpha knockdown cells. The PI3K/Akt/mTOR signaling pathway was also found to be inactivated in HIF-1alpha knockdown cells. CONCLUSIONS These findings show that knockdown of HIF-1alpha promoted autophagy and inhibited the PI3K/AKT/mTOR signaling pathway in ovarian cancer cells.

Therapeutic Effects of Punicalagin Against Ovarian Carcinoma Cells in Association With ß-Catenin Signaling Inhibition.

AIM: The aim of this study was to investigate the effects of punicalagin, a polyphenol isolated from Punica granatum, on human A2780 ovarian cancer cells in vitro. METHODS: The viability of human A2780 ovarian cells was evaluated using Cell Counting Kit-8 assay. Cell cycle was detected with flow cytometry analysis. The protein expression levels of Bcl-2, Bax, ß-catenin, cyclin D1, survivin, tissue inhibitor of metalloproteinase (TIMP)-2, and TIMP-3 were measured using Western blot analysis. Matrix metalloproteinase (MMP)-2 and MMP-9 activity was determined with gelatin zymography. Wound healing assay was used to determine cell migration. RESULTS: Punicalagin inhibited the cell viability of A2780 cells in a dose- and time-dependent manner, and the cell cycle of A2780 cells was arrested in G1/S phase transition. The treatment also induced apoptosis as shown by the up-regulation of Bax and down-regulation of Bcl-2. On the other hand, punicalagin treatment increased the expressions of TIMP-2 and TIMP-3, decreased the activities of MMP-2 and MMP-9, and inhibited cell migration. In addition, the ß-catenin pathway was suppressed as shown by the down-regulations of ß-catenin and its downstream factors including cyclin D1 and survivin. CONCLUSIONS: Punicalagin may have cancer-chemopreventive as well as cancer-chemotherapeutic effects against human ovarian cancer in humans through the inhibition of ß-catenin signaling pathway.

Transvaginal genital fistula repair with insertion of Foley catheter via fistula tract.

AIM: Genital fistula is one of the most devastating injuries in women. Despite advances in medical care, it continues to be a distressing problem, and the success rate of repair surgery is still limited. We herein describe our experience with the surgical approach using Foley catheter to repair genital fistula after gynecological surgery. METHODS: We retrospectively reviewed 29 patients who had received genital fistula repair surgery with Foley catheter between October 2011 and December 2013. Based on traditional transvaginal genital fistula repair surgery, we inserted a Foley catheter into the bladder or intestine through the fistula opening. As a result, the fistula opening could be tracked, which allows for a clear view to improve fistula repair. All 29 patients were followed up at 1, 4, and 12 weeks postoperatively. RESULTS: Of the 29 patients, 28 had successful surgical outcome (96.55% success rate). The mean operative time was 85 ± 8.1 min. The mean blood loss was 109 ± 23.4 mL. No intraoperative complications were observed. The mean postoperative hospitalization time was 10 ± 2.8 days. The follow-up rate was 100%. CONCLUSIONS: Repair of transvaginal genital fistula using Foley catheter had a high success rate, short operative time, minimal blood loss, low morbidity and short hospital stay. Therefore, this approach is minimally invasive and effective.

Clinical efficacy of add-back therapy in treatment of endometriosis: a meta-analysis.

OBJECTIVE: A meta-analysis was conducted to determine the effectiveness of using gonadotropin-releasing hormone analogues (GnRH-a), both with and without hormonal add-back therapy, for the management of endometriosis. METHODS: Cochrane library, Ovid (Embase) and Pubmed databases were searched between the years 1998 and 2013 for published, prospective, randomised controlled trials (RCT) that assessed the effectiveness of "add-back" therapy for EMs treatment. The meta-analysis was performed using RevMan V5.0. The main outcome measures were as follows: lumbar spine bone mineral density (BMD) immediately after treatment and after 6 months of follow-up; femoral neck BMD; serum estradiol levels; changes in the Kupperman index score; the pelvic pain score, including dysmenorrhoea and dyspareunia; and pelvic tenderness. RESULTS: A total of 13 RCT, including 945 participants, were identified. The evidence suggested that "add-back" therapy was more effective for symptom relief than GnRH-a alone. BMD was significantly different when comparing "add-back" therapy to GnRH-a alone, both immediately after treatment and at 6 months. The "add-back" therapy increased serum oestrogen and did not reduce the efficacy of GnRH-a for treating dysmenorrhoea and dyspareunia. A variety of add-back regimens had a same effect for the treatment of endometriosis. CONCLUSIONS: "Add-back" therapy, based on the GnRH-a dose, does not reduce the efficacy of using GNRH-a for the management of endometriosis. "Add-back" therapy reduced the occurrence of side effects that can occur with GnRH-a therapy alone, such as osteoporosis and menopausal syndrome. There were no statistically significant differences when comparing the effectiveness of a variety of "add-back" regimens to each other.

[Effect of mechanical stress on human parametrial ligament fibroblasts apoptosis].

OBJECTIVE: To explore the possible mechanism of mechanical factors in the pathogenesis of pelvic organ prolapse (POP). METHODS: The experiment material were uterosacral ligament and cardinal ligament- derived fibroblast from 10 patients who received total hysterectomy due to benign disease except POP. Fibroblast were cultured after collagenase digestion and identified by morphology and immocytochemical methods. Fibroblasts of 4-8 generations were stretched by four-point bending system for 0µ (0 mm), 1 333 µ (1 mm), 2 666 µ (2 mm), 5 333 µ (4 mm) strain, using 0 mm strain as the control group. Parameters was set to a frequency of 0.1 Hz, 4 hours. Cell apoptosis was tested by flow cytometry. RESULTS: Mechanical strain increased cell apoptosis [0 µ: (7.4 ± 1.5)%, 1 333 µ: (8.7 ± 2.2)%, 2 666 µ: (19.4 ± 3.4)%, 5333 µ: (50.9 ± 6.6)%, respectively]. Cell apoptosis rate was significantly higher under strong mechanical strain (2 666 µ and 5 333 µ versus 0 µ, all P < 0.05). CONCLUSION: Increased mechanical stress loading on human parametrial ligament fibroblasts could raise the rate of apoptosis.

[Investigation of social support for inpatients with occupational diseases].

OBJECTIVE: To investigate and analyze the social support for inpatients with occupational diseases and to provide reference and basis for relevant medical and nursing interventions. METHODS: The social support rating scale (SSRS) was used to investigate the social support for 95 inpatients with occupational diseases. RESULTS: The total SSRS score of these patients was significantly lower than the national norm (32.5±9.31 vs 34.56±3.73, P < 0.05). The social support was mainly from the family, but medical staff and spiritual support were the main source and type of social support that are expected. CONCLUSION: Patients with occupational diseases have gained little social support, in both economic and spiritual aspects. In clinical practice, the patient's demand for knowledge of diseases and spiritual needs should be satisfied, and appropriate social support should be provided.

Ferrostatin-1 alleviates the damage of C2C12 myoblast and mouse pelvic floor muscle induced by mechanical trauma.

Ferroptosis is a special form of regulated cell death, which is reported to play an important role in a variety of traumatic diseases by promoting lipid peroxidation and devastating cell membrane structure. Pelvic floor dysfunction (PFD) is a kind of disease affecting the quality and health of many women's lives, which is closely related to the injury of the pelvic floor muscle. Clinical findings have discovered that there is anomalous oxidative damage to the pelvic floor muscle in women with PFD caused by mechanical trauma, but the specific mechanism is still unclear. In this study, we explored the role of ferroptosis-associated oxidative mechanisms in mechanical stretching-induced pelvic floor muscle injury, and whether obesity predisposed pelvic floor muscle to ferroptosis from mechanical injury. Our results, in vitro, showed that mechanical stretch could induce oxidative damage to myoblasts and trigger ferroptosis. In addition, glutathione peroxidase 4 (GPX4) down-regulation and 15-lipoxygenase 1(15LOX-1) up-regulation exhibited the same variational characteristics as ferroptosis, which was much more pronounced in palmitic acid (PA)-treated myoblasts. Furthermore, ferroptosis induced by mechanical stretch could be rescued by ferroptosis inhibitor (ferrostatin-1). More importantly, in vivo, we found that the mitochondria of pelvic floor muscle shrank, which were consistent with the mitochondrial morphology of ferroptosis, and GPX4 and 15LOX-1 showed the same change observed in cells. In conclusion, our data suggest ferroptosis is involved in the injury of the pelvic floor muscle caused by mechanical stretching, and provide a novel insight for PFD therapy.

Bibliometric analysis of studies on stress urinary incontinence surgery.

Background: Stress urinary incontinence (SUI) is characterized by the involuntary leakage of urine during activities that increase abdominal pressure. In recent years, a considerable number of studies on SUI surgery have been published. However, there has been a lack of systematic quantification and comprehensive summarization of these studies. Bibliometrics is a discipline that utilizes measurement methods to quantify scientific literature. Thus, this study utilized publications from the Web of Science (WOS) as a data source and conducted a comprehensive analysis and visualization of studies related to SUI surgery in recent years using bibliometric techniques. Methods: We conducted a search and retrieved information on 988 studies related to SUI surgery in the WOS Core Collection. The data covered ten years from September 7, 2013, to September 7, 2023. We employed VOSviewer software, CiteSpace software, and Bibliometrix for analysis and visualization. Results: Over the ten years, the number of publications exhibited a fluctuating trend, initially decreasing and then increasing. The United States emerged as the leading contributor in terms of both publication volume and quality. The University of Alabama Birmingham ranked as the institution with the highest number of publications, while the International Urogynecology Journal featured the most publications among journals. Conclusions: This paper presents a bibliometric analysis of publications related to SUI surgery from 2013 to 2023. The aim is to offer researchers a concise overview of the field and inspire future research directions.

Microneedle systems: cell, exosome, and nucleic acid based strategies.

Cells, exosomes, and nucleic acids play crucial roles in biomedical engineering, holding substantial clinical potential. However, their utility is often hindered by various drawbacks, including cellular immunogenicity, and instability of exosomes and nucleic acids. In recent years, microneedle (MN) technology has revolutionized drug delivery by offering minimal invasiveness and remarkable versatility. MN has emerged as an ideal platform for the extraction, storage, and delivery of these biological components. This review presents a comprehensive overview of the historical progression and recent advances in the field of MN. Specifically, it highlights the current applications of cell-, exosome-, and nucleic acid-based MN systems, while presenting prevailing research challenges. Additionally, the review provides insights into the prospects of MN in this area, aiming to provide new ideas for researchers and facilitate the clinical translation of MN technology.

Collagen type â -loaded methacrylamide hyaluronic acid hydrogel microneedles alleviate stress urinary incontinence in mice: A novel treatment and prevention strategy.

Stress urinary incontinence (SUI), a chronic disease with widespread effects and an overall prevalence of up to 46% in adult women, is associated with a heavy disease burden. The clinical treatment for mild to moderate SUI is conservative, such as electrical stimulation and Kegel exercises, but the therapeutic effect is unsatisfactory, so it is imperative to seek new treatment modalities. Hydrogel microneedles (MNs) have been widely used in transdermal drug delivery because of their minimally invasive and highly biocompatible characteristics. Therefore, for the first time, we combined collagen type I with MN technology for the treatment and prevention of mild to moderate SUI.

Chitin-based hydrogel loaded with bFGF and SDF-1 for inducing endogenous mesenchymal stem cells homing to improve stress urinary incontinence.

Nonoperative treatments for Stress Urinary Incontinence (SUI) represent an ideal treatment method. Mesenchymal stem cell (MSCs) treatment is a new modality, but there is a lack of research in the field of gynecological pelvic floor and no good method to induce internal MSC homing to improve SUI. Herein, we develop an injectable and self-healing hydrogel derived from ß-chitin which consists of an amino group of quaternized ß-chitin (QC) and an aldehyde group of oxidized dextran (OD) between the dynamic Schiff base linkage.it can carry bFGF and SDF-1a and be injected into the vaginal forearm of mice in a non-invasive manner. It provides sling-like physical support to the anterior vaginal wall in the early stages. In the later stage, it slowly releasing factors and promoting the homing of MSCs in vivo, which can improve the local microenvironment, increase collagen deposition, repair the tissue around urethra and finally improve SUI (Scheme 1). This is the first bold attempt in the field of pelvic floor using hydrogel mechanical support combined with MSCs homing and the first application of chitin hydrogel in gynecology. We think the regenerative medicine approach based on bFGF/SDF-1/chitin hydrogel may be an effective non-surgical approach to combat clinical SUI.

Targeting purine metabolism in ovarian cancer.

Purine, an abundant substrate in organisms, is a critical raw material for cell proliferation and an important factor for immune regulation. The purine de novo pathway and salvage pathway are tightly regulated by multiple enzymes, and dysfunction in these enzymes leads to excessive cell proliferation and immune imbalance that result in tumor progression. Maintaining the homeostasis of purine pools is an effective way to control cell growth and tumor evolution, and exploiting purine metabolism to suppress tumors suggests interesting directions for future research. In this review, we describe the process of purine metabolism and summarize the role and potential therapeutic effects of the major purine-metabolizing enzymes in ovarian cancer, including CD39, CD73, adenosine deaminase, adenylate kinase, hypoxanthine guanine phosphoribosyltransferase, inosine monophosphate dehydrogenase, purine nucleoside phosphorylase, dihydrofolate reductase and 5,10-methylenetetrahydrofolate reductase. Purinergic signaling is also described. We then provide an overview of the application of purine antimetabolites, comprising 6-thioguanine, 6-mercaptopurine, methotrexate, fludarabine and clopidogrel. Finally, we discuss the current challenges and future opportunities for targeting purine metabolism in the treatment-relevant cellular mechanisms of ovarian cancer.

Corrigendum: Development and validation of a prognostic nomogram based on DNA methylation-driven genes for patients with ovarian cancer.

[This corrects the article DOI: 10.3389/fgene.2021.675197.].

The anti-HSV-2 effect of alumen: In vitro and in vivo experimental studies.

This study investigated the anti-HSV-2 effect of alumen through in vitro and in vivo experiments. Viable cell counting was employed to assess the toxicity of alumen on Vero cells. The inhibition rate of HSV-2 was defined as the cytopathic effect (CPE) of the cells infected with the virus. Alumen suppositories of different concentrations were vaginally applied to the guinea pigs which were then infected with HSV-2 via a vaginal route. The clinical symptoms were observed and the local virus titer calculated. The results showed that alumen had an in vitro anti-HSV-2 effect by means of antiviral duplication, direct killing of the virus, and antiviral adsorption. Alumen suppositories of different concentrations could reduce or completely inhibit HSV-2 infection in guinea pigs. It was concluded that alumen had an in vitro anti-HSV-2 effect through multiple approaches and it could suppress in vivo vaginal HSV-2 infection of guinea pig to some extent.

Expression of ArfGAP3 in Vaginal Anterior Wall of Patients With Pelvic Floor Organ Prolapse in Pelvic Organ Prolapse and Non-Pelvic Organ Prolapse Patients.

PURPOSE OF INVESTIGATION: The purpose of this study was to study the expression of adenosine diphosphate ribosylation factor GTPase-activating protein 3 (ArfGAP3) in the anterior vaginal wall of patients with pelvic organ prolapse (POP). MATERIALS AND METHODS: From July 2016 to July 2018, the anterior vaginal wall of 31 POP patients (pelvic organ prolapse quantification [POP-Q] II-III [n = 10] and POP-Q IV [n = 21]) with pelvic floor dysfunction-related symptoms who underwent vaginal hysterectomy were enrolled in POP group in the Department of Gynecology of Wuhan University People's Hospital. The anterior vaginal wall of 28 non-POP patients who underwent vaginal hysterectomy was selected as control group. The expression of 3 groups was determined by immunohistochemical staining, Western blotting, and quantitative real-time fluorescence polymerase chain reaction. RESULTS: The expression levels of ArfGAP3 of POP-Q II-III and POP-Q IV groups were lower than the control group (P < 0.05), and there were significant differences between POP-Q II-III and POP-Q IV groups (P < 0.05). CONCLUSIONS: The expression of ArfGAP3 in the anterior vaginal wall of POP patients decreased, which was related to the pathogenesis and clinical grading of POP.

Development and Validation of a Prognostic Nomogram Based on DNA Methylation-Driven Genes for Patients With Ovarian Cancer.

Background: DNA methylation affects the development, progression, and prognosis of various cancers. This study aimed to identify DNA methylated-differentially expressed genes (DEGs) and develop a methylation-driven gene model to evaluate the prognosis of ovarian cancer (OC). Methods: DNA methylation and mRNA expression profiles of OC patients were downloaded from The Cancer Genome Atlas, Genotype-Tissue Expression, and Gene Expression Omnibus databases. We used the R package MethylMix to identify DNA methylation-regulated DEGs and built a prognostic signature using LASSO Cox regression. A quantitative nomogram was then drawn based on the risk score and clinicopathological features. Results: We identified 56 methylation-related DEGs and constructed a prognostic risk signature with four genes according to the LASSO Cox regression algorithm. A higher risk score not only predicted poor prognosis, but also was an independent poor prognostic indicator, which was validated by receiver operating characteristic (ROC) curves and the validation cohort. A nomogram consisting of the risk score, age, FIGO stage, and tumor status was generated to predict 3- and 5-year overall survival (OS) in the training cohort. The joint survival analysis of DNA methylation and mRNA expression demonstrated that the two genes may serve as independent prognostic biomarkers for OS in OC. Conclusion: The established qualitative risk score model was found to be robust for evaluating individualized prognosis of OC and in guiding therapy.