The vaginal epithelium, a hormone-sensitive barrier critical for reproductive health, lacks robust in vitro models due to primary tissue scarcity and existing systems’ limitations. Here, we established the first long-term, genetically stable human vaginal epithelial organoids (VEOs) using a tailored Matrigel-based culture medium that preserves the native stratified squamous architecture. Through transcriptomic and functional profiling, we identified progesterone as a key suppressor of immune defense and keratinization. Modeling Chlamydia trachomatis (CT) infection in VEOs recapitulated infection-induced reactive oxygen species (ROS) overproduction, senescence, and inflammation. Progesterone pretreatment significantly reduced ROS and cellular damage, suggesting hormonal modulation of cellular homeostasis. By integrating air-liquid interface (ALI) culture technique and exploring different proportions of Matrigel and collagen composition, we resolved the polarity limitations of three-dimensional (3D) organoids, enabling physiological modeling of infection-induced barrier dysfunction. This study establishes VEOs as a transformative model for dissecting hormone-microbe crosstalk in reproductive health and for accelerating therapeutic development against vaginal infections.

Ovarian cancer (OC) is the leading cause of death among female reproductive tract tumors, and chemotherapy resistance is one of the main reasons for the treatment failure of OC. Many studies showed that abnormal fatty acid synthesis plays an essential role in multiple tumors, whereas, its role in drug resistance of OC remains unclear. Here, we found that the expression of lipid droplets and key lipogenic enzymes were significantly elevated in OC tissues and cells, and high expression of key lipogenic enzymes were associated with poor overall survival rate in OC patients. Interestingly, the expression of lipid droplets and key lipogenic enzymes were further increased in paclitaxel resistant OC cells. Meanwhile, the phosphorylation of AKT participated in fatty acid synthesis of paclitaxel resistant OC cells, and activation/inhibition of AKT could promote/inhibit fatty acid synthesis. Fatostatin could inhibit the proliferation of paclitaxel resistant OC cells via inhibiting AKT/SREBP1 signaling pathway. In paclitaxel resistant OC cells and subcutaneous xenograft tumor models in nude mice, combined treatment with fatostatin and paclitaxel could increase the sensitivity of OC to paclitaxel. This study provides the first evidence that inhibition of fatty acid synthesis might be an effective option to reverse paclitaxel resistance in OC.

Intrauterine adhesion (IUA) is a prevalent gynecological disorder characterized by endometrial fibrosis and compromised regeneration, with a lack of effective clinical treatments. Here, we present a microfluidic biofabrication strategy to engineer vascularized endometrial micro-organoids that recapitulate the cellular complexity and function of native tissue. By co-encapsulating human endometrial stromal cells, epithelial organoids, and endothelial cells (HUVECs) in biocompatible hydrogel microspheres, we created 3D constructs supporting hormone responsiveness, decidualization, and pathological remodeling upon transforming growth factor-βstimulation. Transcriptomic profiling and single-cell sequencing revealed that the presence of endothelial cells alleviated hypoxia-induced inflammation and promoted epithelial homeostasis.In vivotransplantation into a murine IUA model led to improved engraftment, endometrial regeneration, and fertility recovery. This vascularized organoid system offers a scalable and translational platform for endometrial repair and disease modeling, highlighting the promise of biofabrication in reproductive regenerative medicine.

Superficial inguinal lymph node (SILN) metastasis is rare in ovarian cancer, particularly as an isolated presentation without peritoneal dissemination. Here we report a case of solitary SILN metastasis in a patient with high-grade serous carcinoma of ovarian cancer and review previously reported cases from literature. A 58-year-old woman presented with isolated right groin swelling (approximately 4 cm), excisional biopsy suggested ovarian origin but comprehensive imaging and laparoscopy failed to identify a primary intra-abdominal tumor, and postoperative pathology confirmed no evidence of ovarian involvement. Following multidisciplinary consultation, the patient received six cycles of paclitaxel (175 mg/m²) plus carboplatin (AUC-5) chemotherapy (21-day intervals). Remarkably, five years post-treatment, she remains disease-free, highlighting the potential for favorable outcomes even in rare metastatic presentations. This case demonstrates that ovarian cancer is not a disease confined to the intra-peritoneal cavity; SILN metastasis might occur in rare cases possibly via lymphatic and/or hematogenous spread route under specific circumstances. Further investigations related to risk factors and metastatic patterns are warranted to explore the mechanisms and clinical implications of isolated SILN metastasis in ovarian cancer.

BackgroundAdenomyosis is frequently associated with abnormal uterine bleeding (AUB) and anemia. In the setting of arterial stenosis or hypercoagulability, AUB may precipitate ischemic stroke. However, the optimal management strategy remains unclear.MethodsIn accordance with PRISMA 2020, we systematically searched PubMed, Web of Science, CNKI, and Wanfang from inception to November 20, 2024, without language restrictions. Eligible studies were human case reports or case series that described adenomyosis-associated ischemic stroke with extractable data on management and outcomes. Data extraction was performed independently by two reviewers, and risk of bias was assessed using the JBI tool. A descriptive synthesis was conducted, and Fisher’s exact tests were applied where appropriate.ResultsEighteen studies involving 24 patients fulfilled the inclusion criteria. Among these patients, 66.7% experienced stroke onset during menstruation, 85.7% presented with anemia, and more than 95% showed elevated CA125 and D-dimer levels. Stroke recurrence occurred in 55.6% of patients who received conservative management, compared with 0% of those who underwent hysterectomy (Fisher’s exact p ≈ 0.005). In menstruation-related cases managed conservatively, the recurrence rate reached 83.3%.ConclusionCurrent evidence indicates that rapid uterine hemostasis may facilitate timely initiation of antithrombotic therapy and thereby reduce recurrence risk in adenomyosis-associated stroke. Surgical management, particularly hysterectomy, appears more effective than conservative therapy in carefully selected high-risk patients. Larger prospective studies are needed to confirm these findings and to refine management strategies.

Recently, the global incidence of endometrial cancer is increasing. Endocrine therapy offers advantages in the management of this malignancy due to its broad applicability and favorable tolerability profile. Although conventional endocrine treatments, including progesterone, gonadotropin-releasing hormone agonists and aromatase inhibitors demonstrate efficacy in endometrial cancer, their long-term utility is limited by adverse effects such as drug resistance and disease recurrence with prolonged treatment. Novel endocrine therapeutic agents, including selective estrogen receptor modulators, selective estrogen receptor degraders, epigenetic-targeted therapies, mTOR inhibitors, cyclin-dependent kinase inhibitors, and metformin, remain in preclinical development or clinical trials. Inspiringly, the preliminary findings suggest these emerging agents may positively impact survival outcomes in endometrial cancer patients. This review examines the mechanisms, methodologies, and efficacy of both traditional and novel endocrine therapeutic approaches for endometrial cancer.

Aims/Background Accurate identification of lymph node metastasis is critical for optimising surgical strategies in early-stage cervical cancer. This study aimed to analyse multiple clinicopathological factors which are potentially associated with lymph node metastasis to guide personalised lymphadenectomy decisions. Methods This retrospective cohort study included 266 patients with early-stage cervical cancer (International Federation of Gynecology and Obstetrics [FIGO] stage IA1 to IIA2) who underwent surgical treatment at Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, between 1 December 2014 and 31 December 2019. Patients were followed up every 3 months for the first 2 years, every 6 months for the next 3 years, and annually thereafter. The presence of lymph node metastasis was included as the primary outcome, while the associated factors as secondary outcomes. The univariate and multivariate logistic regression were performed to identify risk factors associated with lymph node metastasis. Results The mean age of the study participants (n = 266) was 44.26 years (standard deviation [SD] = 10.19), and the median follow-up duration was 48.7 months (range 12-72 months). Lymph node metastasis was observed in 15.41% of patients. The metastatic rates increased with advancing FIGO stage: IA1 and IA2 (0%), IB1 (13.44%), IB2 (15.00%), IIA1 (23.33%), and IIA2 (66.67%). Univariate analysis identified FIGO stage (p < 0.001), depth of stromal invasion (p < 0.001), tumour size (p = 0.017), parametrial invasion (p < 0.001), and lymphovascular space invasion (LVSI) (p < 0.001) as significantly associated risk factors for lymph node metastasis. Multivariate analysis identified tumour size ≥4 cm (adjusted odds ratio [OR]: 3.857; 95% confidence interval [CI]: 1.530-9.728; p = 0.004), FIGO stage II (adjusted OR: 8.247; 95% CI: 3.171-21.455; p < 0.001), LVSI (adjusted OR: 2.974; 95% CI: 1.344-6.632; p = 0.008), and parametrial invasion (adjusted OR: 5.585; 95% CI: 1.900-16.415; p = 0.002) as independent risk factors for nodal metastasis. Conclusion This study identifies several key clinicopathological factors associated with lymph node metastasis in early-stage cervical cancer. These findings underscore the importance of meticulous preoperative risk assessment and offer an evidence-based foundation for tailored surgical planning to improve patient outcomes.

Polysaccharides of Cistanche deserticola Ma (CDPS), with high safety and low toxicity have been reported to possess anti-inflammatory, immunomodulatory, antioxidant, anti-aging, anti-osteoporosis, antidepressant, intestinal flora regulatory and hepatoprotective properties. Nevertheless, the effects of CDPS on inflammatory bowel disease (IBD) and its underlying mechanisms have never been reported. To estimate its therapeutic potential on IBD, the extracted CDPS were characterized via utilizing a series of chemical, spectroscopic, and instrumental analyses, and the protective effects and mechanisms of CDPS in colitis mice was investigated. Our results indicated that CDPS were identified as acidic heteropolysaccharides. CDPS alleviated dextran sodium sulfate-induced IBD mice characterized by decreasing disease activity index, improving colon length and body weight, restoring histopathological lesions, inhibiting the expression of pro-inflammatory cytokine (IL-6, IL-1β, TNF-α) and MPO activity, elevating the expression of anti-inflammatory cytokine (IL-10) in colon tissue. The findings manifested CDPS could mitigate the inflammation of colon. Simultaneously, CDPS inhibited the expression of genes and proteins associated with SRC/EGFR/PI3K/AKT signaling pathways, and reduced the diversity and abundance of harmful gut microbiota, including Helicobacter, Bacteroides and Colidextribacter, while descending the relative abundance of Lachnospiraceae_NK4A136_group at genus level. In summary, this work elucidated that CDPS alleviates IBD symptoms via mitigating the inflammation of colon, and modulating intestinal microbiota and SRC/EGFR/PI3K/AKT signaling pathways. It underscores the promise of CDPS as a functional food ingredient or preventive drugs for IBD.

GANT61 induced autophagy via the AKT pathway and promoted the accumulation of lipid droplets in both cell lines. The molecular mechanism behind this lipid accumulation appears to involve the mediation of SREBP1. Furthermore, the combination of GANT61 with CQ/Fatostatin significantly inhibited the proliferation and clonogenicity of SKOV3 and SKOV3PTX cells.

Background: Uterine cystic adenomyosis (CA) is a unique form of adenomyosis with a single or fused lumen of the cystic space exceeding a diameter of 1 cm that typically results in progressively worsening dysmenorrhea. In most cases, the prognosis and pregnancy outcomes of CA remained unclear, and therefore further studies are warranted. Case Description: A 19-year-old woman was admitted for irregular vaginal bleeding that lasted for more than one month. Transabdominal B-ultrasound examination revealed a hypoechoic nodule measuring approximately 4.8 cm x 3.9 cm x 4.9 cm that is situated on the posterior wall of the uterus, in close proximity to the uterine fundus. The preoperative diagnosis was concluded as a pelvic mass with a cancer antigen 125 (CA125) level of 51.48 U/mL. She accepted a laparoscopic myomectomy and the CA lesion crossing the myometrium was removed. During operation, dense adhesions were found among a portion of the colorectum, omentum, uterus and bilateral adnexal areas. A cystic mass of approximately 7.0 cm x 5.0 cm x 4.0 cm was visible in the posterior wall of the uterus, and a sinus of approximately 1.0 cm in diameter was found to be connected to the uterine cavity at the lower posterior wall of the uterus, and the cystic wall was attached to the endometrium. Based on the classification criteria of MUSCLE (myometrial location, uterine site, structure, contents, level, endometrial or inner lining), the current case is classified as an A1-B1 mixed type. Following surgery, GnRH-a consolidation therapy was applied for 3 months. Such treatment relieved her symptoms and improved her quality of life while preserving her reproductive function. Conclusions: This is the first reported case of an A1-B1 mixed type CA that was successfully treated by laparoscopic surgery supplemented with GnRH-a consolidation therapy.

Endometrial injury is a prevalent gynecological condition that poses a significant threat to fertility and women's health. While the current reported endometrial organoids demonstrate potential in remodeling endometrial functions, they often lack the complexity and physiological relevance of in vivo tissue. Here, we introduce a vascularized triple-cellular endometrial complex integrating endometrial epithelial organoids, stromal cells, and endothelial cells within a microfluidic chip with a composite hydrogel comprising Matrigel and fibrin. This novel endometrial complex exhibits robust growth and endometrial repair capabilities in an immunodeficient mouse model of endometrial damage, significantly improving pregnancy rates. Single-cell RNA sequencing revealed bidirectional cellular paracrine crosstalk between epithelial, stromal, and endothelial cells in the vascularized endometrial complex. Endothelial cells secrete BMP6 and Galectin-9, which enhance mitochondrial function and promote epithelial cell proliferation. Conversely, epithelial and stromal cells secrete WNT7A and WNT5A, respectively, to stimulate angiogenesis and vascular network formation of endothelial cells. These findings reveal the paracrine interactions that underpin the superior regenerative properties of the vascularized triple-cellular endometrial complex, offering a potential therapeutic strategy for endometrial repair and a valuable in vitro model for endometrial pathophysiological studies.

For low-frequency source localization with a small-aperture acoustic array, we propose a high-resolution localization algorithm based on complex Wishart prior. The algorithm, named Wishart-CSM-SBL, employs vectorized cross-spectral matrix (CSM) preprocessing and performs parameter updating within the sparse Bayesian learning (SBL) framework. Existing SBL algorithms struggle to capture the complex correlations between nonadjacent columns of the dictionary set in small-aperture, low-frequency scenarios, often resulting in failed signal recovery. To solve this problem, the Wishart-CSM-SBL algorithm introduces the complex Wishart distribution and develops novel priors for sparse signal and noise. Specifically, the sparse signal is characterized by a two-layer prior model comprising complex Gaussian and complex Wishart distributions. By capturing the intricate correlations among the columns of the dictionary set, this modeling approach significantly improves the accuracy and robustness of sparse recovery. The complex Wishart distribution is employed to represent the noise with an unknown structure, addressing the performance degradation in existing algorithms that assume noise with uniform variance. This is achieved by accounting for noise in-homogeneity and correlation. In addition, a 2-D off-grid solution is extended to eliminate localization errors caused by coarse grid division. Finally, simulations verify that the algorithm outperforms existing algorithms for small-aperture arrays and low-frequency source scenarios.

BackgroundAdenomyosis is often associated with abnormal uterine bleeding (AUB), which can lead to anemia. Recurrent bleeding, especially in the presence of cerebral infarction risk, may exacerbate the likelihood of cerebral infarction through a hypercoagulable state. Although the relationship between adenomyosis and ischemic stroke is less frequently explored, controlling AUB and maintaining antithrombotic therapy remain clinical challenges. This report presents the application of endometrial ablation in a patient with adenomyosis, AUB, and cerebral infarction.MethodsWe report a case of a 50-year-old female patient who developed acute ischemic stroke due to adenomyosis-related AUB. During the acute phase, the patient underwent endometrial ablation, successfully controlling the bleeding while continuing antiplatelet therapy.ResultsAfter endometrial ablation, the patient's abnormal uterine bleeding was effectively controlled, with no recurrence of cerebral infarction. At a 37-month follow-up, the patient had no further vaginal bleeding or recurrence of cerebral infarction.ConclusionThis case is the first to report the use of endometrial ablation in a patient with adenomyosis and cerebral infarction, demonstrating the potential of this procedure in emergency hemostasis and maintaining antithrombotic therapy. Endometrial ablation is an effective, minimally invasive treatment with a quick recovery, making it a viable option for patients who cannot tolerate major surgery.

Ovarian cancer (OC) is a highly heterogeneous malignancy influenced by germline genetic factors, with BRCA1/2 mutations being well-established risk factors. Germline double heterozygosity (GDH), particularly involving rare combinations, remains poorly understood. This study presents the first report of BRCA1/BRIP1 GDH in a case of Chinese OC patients and compares their clinical characteristics and treatment responses to a patient with BRCA1/BRCA2 GDH. The BRCA1/BRIP1 GDH patient is a 46-year-old female diagnosed with advanced ovarian adenocarcinoma at clinical stage FIGO IVB, exhibited severe chemotherapy-induced toxicity and postoperative complications, including chylous leakage. In contrast, the BRCA1/BRCA2 GDH patient is a 44-year-old female with high-grade serous ovarian cancer at clinical stage FIGO IIIC, tolerated chemotherapy well. Both patients experienced clinical benefit from Olaparib maintenance therapy. Genetic testing confirmed pathogenic variants in both cases, revealing distinct clinical trajectories influenced by different GDH profiles. Our findings suggest that different GDH combinations may influence chemotherapy tolerance and therapeutic effectiveness in OC. BRCA1/BRIP1 GDH patients may require personalized dose adjustments to mitigate toxicity and optimize efficacy. This study underscores the clinical significance of GDH heterogeneity and the importance of comprehensive genetic testing for guiding individualized treatment strategies. Future research should focus on expanding sample sizes and conducting in-depth functional analyses to further clarify the clinical implications of different GDH types, ultimately refining treatment approaches for GDH-associated OC.

PURPOSE:It is widely accepted that there is a strong relationship between iron levels and cancer. This study aimed to investigate the relationship between serum ferritin levels and the severity and prognosis of gynecological malignant tumors. METHODS:This retrospective study included patients with gynecological malignant tumors at Sir Run Run Shaw Hospital in the Department of Obstetrics and Gynecology from January 2013 to June 2019. Patients were grouped according to their serum ferritin level: low (< 13 μg/L), normal (13-150 μg/L), and high (> 150 μg/L). Correlation analyses were performed between serum ferritin level and other factors. Cox univariable and multivariable analysis and Kaplan-Meier survival curves were used to assess the impact of ferritin on survival in patients with gynecologic tumors. RESULTS:The 402 total patients were divided into a low (n= 37), normal (n= 182), and high (n= 183) ferritin level group. Correlation analyses were performed that WBC, MCV, CRP, CA125, and CA153 were significantly positively correlated with serum ferritin level. The Kaplan-Meier survival curves revealed that of the three groups analyzed, the high serum ferritin level group had a significantly shorter survival time versus the normal and low serum ferritin level groups (log-rank P= 0.003). Univariable Cox regression analysis identified that patients with high serum ferritin levels had a significant correlation with risk of death compared to the patients with lower and normal serum ferritin levels. Serum ferritin was not found to be significant (HR = 0.792, 95% CI: 0.351-1.787, P= 0.574) in the multivariable Cox analysis. CONCLUSION:Although this study did not find serum ferritin to be a significant independent prognosis indicator in gynecological malignant tumors, this study did identify that gynecological malignant tumor patients with high serum ferritin levels have significantly less survival time than patients with low or normal serum ferritin levels.

BackgroundTo identify key genes associated with cisplatin resistance in ovarian cancer, a comprehensive analysis was conducted on three datasets from the GEO database and through experimental validation.MethodsGene expression profiles were retrieved from the GEO database. DEGs were identified by comparing gene expression profiles between cisplatin-sensitive and resistant ovarian cancer cell lines. The identified genes were further subjected to GO, KEGG, and PPI network analysis. Potential inhibitors of key genes were identified through methods such as LibDock nuclear molecular docking. In vitro assays and RT-qPCR were performed to assess the expression levels of key genes in ovarian cancer cell lines. The sensitivity of cells to chemotherapy and proliferation of key gene knockout cells were evaluated through CCK8 and Clonogenic assays.ResultsResults showed that 12 genes influenced the chemosensitivity of the ovarian cancer cell line SKOV3, and 9 genes were associated with the prognosis and survival outcomes of ovarian cancer patients. RT-qPCR results revealed NDRG1, CYBRD1, MT2A, CNIH3, DPYSL3, and CARMIL1 were upregulated, whereas ERBB4, ANK3, B2M, LRRTM4, EYA4, and SLIT2 were downregulated in cisplatin-resistant cell lines. NDRG1, CYBRD1, and DPYSL3 knock-down significantly inhibited the proliferation of cisplatin-resistant cell line SKOV3. Finally, photofrin, a small-molecule compound targeting CYBRD1, was identified.ConclusionThis study reveals changes in the expression level of some genes associated with cisplatin-resistant ovarian cancer. In addition, a new small molecule compound was identified for the treatment of cisplatin-resistant ovarian cancer.

BACKGROUND:Ovarian cancer is insidious and usually detected in advanced stages of the disease. As the ovaries are pelvic organs, changes in their pelvic fluid metabolites may be associated with ovarian cancer. METHODS:Metabolomic changes in the pelvic fluid were detected using liquid chromatography-tandem mass spectrometry (LC-MS/MS) in patients with ovarian cancer, ovarian cysts and uterine fibroids. Area under the curve (AUC) analysis was used to assess the diagnostic performance of lipid metabolites and blood tumor indices. The Pearson correlation algorithm was used to analyze the correlation between clinical characteristics and lipid metabolites in ovarian cancer patients. RESULTS:There were 24 lipid metabolites significantly changed in the pelvic fluid of ovarian cancer patients (p < 0.05). Palmitoylcarnitine, lipoamide, lipid metabolites, and blood tumor indices (CA15-3 and CA125) showed AUC > 0.8, with palmitoylcarnitine reaching a high of 0.942. In addition, we found that some lipid metabolites were significantly associated with the clinical stage, abdominal water volume, lymphatic metastasis, and recurrence (p < 0.05, r > 0.5). CONCLUSION:Levels of specific lipid metabolites are potential biomarkers of ovarian cancer and may play a key role in the early diagnosis and prognostic assessment of ovarian cancer. SIGNIFICANCE:Our results showed that pelvic metabolites, especially some lipid metabolites, play an important role in the diagnosis of ovarian cancer. Meanwhile, partial lipid metabolites were closely associated with the clinical presentation and prognosis of patients with ovarian cancer. We believe that our study makes a significant contribution to the literature because it provides a potential approach that is more effective for ovarian cancer detection.

BackgroundOvarian cancer (OC) ranks as the fifth most prevalent neoplasm in women and exhibits an unfavorable prognosis. To improve the OC patient's prognosis, a pioneering risk signature was formulated by amalgamating disulfidptosis-related genes.MethodsA comparative analysis of OC tissues and normal tissues was carried out, and differentially expressed disulfidptosis-related genes (DRGs) were found using the criteria of |log2 (fold change) | > 0.585 and adjusted P-value < 0.05. Subsequently, the TCGA training set was utilized to create a prognostic risk signature, which was validated by employing both the TCGA testing set and the GEO dataset. Moreover, the immune cell infiltration, mutational load, response to chemotherapy, and response to immunotherapy were analyzed. To further validate these findings, QRT-PCR analysis was conducted on ovarian tumor cell lines.ResultsA risk signature was created using fourteen differentially expressed genes (DEGs) associated with disulfidptosis, enabling the classification of ovarian cancer (OC) patients into high-risk group (HRG) and low-risk group (LRG). The HRG exhibited a lower overall survival (OS) compared to the LRG. In addition, the risk score remained an independent predictor even after incorporating clinical factors. Furthermore, the LRG displayed lower stromal, immune, and estimated scores compared to the HRG, suggesting a possible connection between the risk signature, immune cell infiltration, and mutational load. Finally, the QRT-PCR experiments revealed that eight genes were upregulated in the human OC cell line SKOV3 compared with the human normal OC line IOSE80, while six genes were down-regulated.ConclusionsA fourteen-biomarker signature composed of disulfidptosis-related genes could serve as a valuable risk stratification tool in OC, facilitating the identification of patients who may benefit from individualized treatment and follow-up management.

Ovarian cancer develops insidiously and is frequently diagnosed at advanced stages. Screening for ovarian cancer is an effective strategy for reducing mortality. This study aimed to investigate the molecular mechanisms underlying the development of ovarian cancer and identify novel tumor biomarkers for the diagnosis and prognosis of ovarian cancer. Three databases containing gene expression profiles specific to serous ovarian cancer (GSE18520, GSE12470, and GSE26712) were acquired. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes were analyzed for the differentially expressed gene (DEGs). The protein-protein interaction (PPI) network was constructed using the STRING database. The pivotal genes in the PPI network were screened using the Cytoscape software. Survival curve analysis was performed using a Kaplan-Meier Plotter. The cancer genome atlas and Gene Expression Omnibus databases were used to find the relationship between Hub gene and serous ovarian cancer. PCR and immunohistochemistry were used to detect the expression of Hub gene in serous ovarian cancer tissues and cells. Downstream pathways of the candidate tumor marker genes were predicted using Gene Set Enrichment Analysis. In this study, 252 DEGs were screened for pathway enrichment. 20 Hub genes were identified. Survival analysis suggested that Aurka, Bub1b, Cenpf, Cks1b, Kif20a, Mad2l1, Racgap1, and Ube2c were associated with the survival of patients with serous ovarian cancer. MAD2L1 and BUB1B levels were significantly different in serous ovarian cancer at different stages. Finally, Mad2l1 was found to play a role in the cell cycle, oocyte meiosis, and ubiquitin-mediated proteolysis. Meanwhile, Bub1b may play a role in the cell cycle, ubiquitin-mediated proteolysis, and spliceosome processes. Mad2l1 and Bub1b could be used as markers to predict ovarian carcinogenesis and prognosis, providing candidate targets for the diagnosis and treatment of serous ovarian cancer.

Connector enhancer of kinase suppressor of Ras 2 (CNKSR2) is a scaffold protein that mediates mitogen-activated protein kinase pathways. However, the molecular function of CNKSR2 in cervical squamous cell carcinoma (CESC) remains unknown. This study aimed to characterize the role of CNKSR2 in patients with CESC. Immunohistochemistry revealed that the expression of CNKSR2 in CESCs is relatively low compared with that in normal cells. We also explored the gene expression profile of high- and low-CNKSR2 expression in patients with cervical cancer. Furthermore, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed that the expression of CNKSR2 was upregulated in synapse assembly, which was coordinately regulated using the cAMP signaling pathway and calcium signaling pathway. The correlation between CNKSR2 and cancer immune cell infiltration was investigated via single-sample gene set enrichment analysis (ssGSEA). High CNKSR2 expression was associated with better overall survival (OS) and disease-free survival (DFS). Interestingly, high CNKSR2 expression was a good predictor of the survival outcome in cervical cancer patients. Additionally, CNKSR2 expression was strongly correlated with diverse immune cells in CESCs, including NK cells and T cells. These findings suggest that CNKSR2 is correlated with prognosis and immune infiltration, laying the foundation for future studies on the functional role of CNKSR2 in CESC.