Journal
Identification of an Anoikis-associated LncRNA Signature to Predict the Clinical Prognosis and Immune Function of Patients with Endometrial Cancer
Potential mechanism of RRM2 for promoting Cervical Cancer based on weighted gene co-expression network analysis
Cervical cancer is the most common gynecologic malignant tumor, with a high incidence in 50-55-year-olds. This study aims to investigate the potential molecular mechanism of RRM2 for promoting the development of cervical cancer based on The Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO). RRM2 was found to be significant upregulated in cervical tissue (
The natural compound n-butylidenephthalide suppresses type II ovarian cancer cell growth by inducing ferroptosis
Type II high-grade serous ovarian cancer (HGSOC) accounts for 80% of all ovarian cancers. Tumor metastasis and chemotherapy resistance are predominantly caused by cancer stem cells (CSCs). n-butylidenephthalide (BP) has showed promise as an anti-tumor drug in a variety of malignancies. The purpose of this study was to examine the ferroptosis influence of BP on HGSOC. CSCs were isolated from the HGSOC cell lines KURAMOCHI and OVSAHO by employing the CSC marker ALDH. The study assessed cell survival, proliferation, IC
Targeted inhibition of integrin αVβ3 induces cytotoxicity and suppresses migration ability in ovarian cancer cells and tumor spheroids
Ovarian cancer is a gynecological malignancy that has poor prognosis and high lethality. Integrin αVβ3 is highly expressed in solid cancer cells, including ovarian cancer, and is important in proliferation and cell migration. In this study, we performed two-dimensional (2D) and three‑dimensional (3D) cell culture systems to investigate the potential of integrin αVβ3 as a therapeutic target for ovarian cancer. Inhibition of integrin αVβ3 by
Survival rates of patients who undergo minimally invasive surgery for endometrial cancer with cervical involvement
Prognostic Value of Circulating Lymphocyte Subsets in Cervical Cancer Following Postoperative Radiotherapy
Study of long-term effects of pelvic radiotherapy on the function of bone marrow in recurrent cervical cancer patients
The Value of Texture Analysis of Multi-parameter MRI Images in Distinguishing Benign and Malignant Lesions of O-RADS MRI 4 Lesions
Proguanil synergistically sensitizes ovarian cancer cells to olaparib by increasing DNA damage and inducing apoptosis
Ovarian cancer is the second leading cause of cancer-related deaths in women, with low five-year survival rates. Therefore, it is essential to seek new treatment options. Olaparib, a PARP inhibitor, has benefited many ovarian cancer patients, but olaparib is much less effective as a single agent in 50% of patients with high grade severe tumors. Proguanil, which was originally developed as an anti-malarial drug, has gained attention due to its anti-tumor effects. Here, we evaluated the anti-tumor effect of the combination of olaparib and proguanil on ovarian cancer cells, aimed to develop a potential medical option for treating ovarian cancer patients. We examined the effect on proliferation by MTT and colony formation assays, while cell migration was measured by the transwell assay. The effect on apoptosis was measured by flow cytometry and AO/EB staining assays. Western blotting was used to detect protein expression levels in cells treated with olaparib and/or proguanil. In addition, the synergistic effect of these two drugs is calculated by CompuSyn software. The combination of olaparib and proguanil significantly increased growth suppression and apoptosis in ovarian cancer cells, compared to either single agent alone. Furthermore, results showed that the combination of olaparib and proguanil synergistically increased olaparib-induced apoptosis and DNA damage and reduced the efficiency of DNA homologous recombination repair. Our findings indicate that combination of olaparib with proguanil will be a novel potential administration route for treating ovarian cancer patients.
The early surgical period in robotic radical hysterectomy is related to the recurrence after surgery in stage IB cervical cancer
Sesamin inhibits cervical cancer cell proliferation by promoting p53/PTEN-mediated apoptosis
The relationships of genetic polymorphisms of the long noncoding RNA growth arrest-specific transcript 5 with uterine cervical cancer
The purposes of the investigation were to examine the implications of long noncoding RNA growth arrest-specific transcript 5 (GAS5) in progression and clinicopathological factors of uterine cervical cancer, and patient survival in Taiwan. Genotypic distributions of two GAS5 genetic variants rs145204276 and rs55829688 were detected in 208 patients including 111 patients with invasive cancer, 97 with precancerous lesions as well as 307 control women using real-time polymerase chain reaction. It explored that patients with cervical precancerous lesion had lower rate of AGGCA deletion (Del) in both alleles (Del/Del) of GAS5 rs145204276 as compared with control women. Patients with invasive cancer did not exhibit higher rate of Del/Del. Meanwhile, there were no different genotypic distributions in rs55829688 among patients with cervical invasive cancer and those with precancerous lesions as well as control women. Moreover, cervical cancer patients with Ins (insertion, AGGCA)/Del and Del/Del (-/-) in GAS5 rs55829688 tended to have poorer hazard ratio (HR) of 5 years survival. In addition, lymph node metastasis status exerted the most significantly predictive of 5 years survival rate. Conclusively, GAS5 polymorphism rs145204276 is probably applicable to predict 5 years survival HR of cervical cancer patients. However, the mechanism elucidating the methylation status and transcription function of rs145204276 in uterine cervical cancer needs to be delineated for its unique implication in uterine cervical cancer.
Association of Human Papillomavirus Type 16 Long Control Region Variations with Cervical Cancer in a Han Chinese Population
Investigation of metastasis-associated in colon cancer-1 genetic variants in the development and clinicopathologcial characteristics of uterine cervical cancer in Taiwanese women
The objectives of this study were to define the associations among single nucleotide polymorphisms (SNPs) of metastasis-associated in colon cancer-1 (
Impact of pentraxin 3 genetic variants on uterine cervical cancer clinicopathologic characteristics
The aims of this study were to investigate the relationships among
The impact of Aurora kinase A genetic polymorphisms on cervical cancer progression and clinicopathologic characteristics
The aims of this study were to explore the involvement of Aurora kinase A (AURKA) gene single nucleotide polymorphisms (SNPs) in uterine cervical cancer that has not yet been investigated. One hundred and six patients with cervical invasive cancer and 94 patients with precancerous lesions, and 302 Taiwanese female individuals were included. AURKA SNPs rs2273535, rs6024836, rs2064863 and rs1047972 were analyzed for genotypic distributions using real-time polymerase chain reaction. There were no statistically significant differences in the genetic frequencies of AURKA SNPs among patients with invasive cancer and those with precancerous lesions of uterine cervix and control women. There were no associations among AURKA SNPs and clinicopathologcal variables and recurrence and survival events. However, in a multivariate analysis, cervical cancer patients with adenocarcinoma (HR: 3.18, 95% CI: 1.23-8.23; p=0.017) and larger tumor (HR: 5.61, 95% CI: 2.10-14.95; p=0.001) had poorer recurrence-free survival. In conclusion, tumor size and pelvic lymph node status rather than AURKA SNPs were the most obvious independent parameter that could significantly predict 5 years survival rate in Taiwanese women with cervical cancer.
Comparison of two types of the triple incision technique in the treatment of patients with locally advanced vulvar cancer
Identification and Validation of Prognostic Markers for Endometriosis-Associated Ovarian Cancer
The lower incidence of endometrial cancer after sodium-glucose cotransporter 2 inhibitors administration in type 2 diabetes mellitus population: a nationwide cohort study
The Sodium-glucose co-transporter 2 (SGLT2) inhibitor is an anti-glycemic agent that frequently used in type 2 diabetes mellitus (T2DM) with antioxidant effects. Endometrial cancer (EC) is a common gynecological malignancy that correlates with oxidative stress. The aim in the present study is to survey the potential association between the SGLT2 inhibitor administration and the incidence of EC by the application of the National Health Insurance Research Database (NHIRD) of Taiwan. A retrospective cohort study was directed and the T2DM participants were divided into the SGLT2 inhibitors users and non-SGLT2 inhibitors users. After matching, a total of 163,668 and 327,336 participants were included into the SGLT2 inhibitors and control groups, respectively. The primary outcome is regarded as the development of EC according to the diagnostic, image, and procedure codes. Cox proportional hazard regression was employed to generate the adjusted hazard ratio (aHR) and 95% confidence interval (CI) of EC between the two groups. There were 422 and 876 EC events observed in the SGLT2 inhibitors and control groups, respectively. The SGLT2 inhibitors group demonstrated a significantly lower incidence of EC formation compared to the control groups (aHR: 0.87, 95% CI: 0.76-0.99). In the subgroup analysis, the correlation between SGLT2 inhibitor administration and lower rate of EC existed in the T2DM individuals with aged under 60. Moreover, the association between SGLT2 inhibitor administration and lower EC incidence only presented in the T2DM population with SGLT2 inhibitor administration under one year (aHR: 0.58, 95% CI: 0.45-0.73). In conclusion, the administration of SGLT2 inhibitors correlates to lower incidence of EC in T2DM population.
Enhanced Diagnostic Efficiency of Endometrial Carcinogenesis and Progression in Women with Abnormal Uterine Bleeding through Peripheral Blood Cytokine Testing: A Multicenter Retrospective Cohort Study
Molecular mechanisms and Biological Functions of Autophagy in Endometrial Diseases
Autophagy is a highly conserved cellular process crucial for maintaining cellular homeostasis by degrading damaged organelles and misfolded proteins. Emerging evidence highlights its pivotal role in endometrial diseases, including endometriosis, endometritis, and endometrial cancer, where dysregulated autophagy contributes to pathogenesis through mechanisms such as altered hormone signaling, inflammation, and metabolic reprogramming. In this review, we comprehensively summarize the molecular machinery of autophagy, its regulatory networks, and its dual roles in endometrial physiology and pathology. Furthermore, we discuss the molecular mechanisms underlying autophagy in endometrial diseases, and the therapeutic potential of targeting autophagy pathways. By integrating recent advances, this review provides insights into autophagy's complex interplay with endometrial diseases and its implications for future research and therapeutic applications.
Development and validation of a prediction model for recurrence based on ProMisE molecular classifier and immune-inflammatory- nutritional score in endometrial carcinoma: a retrospective multiple-center study
Human Epididymis Protein 4 Predicted Concurrent Intermediate-high-risk Endometrial Cancer and Eligibility of Fertility-sparing Treatment for Patients Diagnosed with Endometrial Atypical Hyperplasia Before Surgery
Causal Relationship between Gut Microbiota and Endometrial Cancer: A Two-Sample Mendelian Randomization Study
Several relevant reports have shown that changes in the composition of the gut microbiota are related to the pathogenesis of endometrial cancer (EC). However, the causal effect of the gut microbiota on EC remains unknown. A two-sample Mendelian randomization (MR) study was used to assess the causal effects of the gut microbiota on EC, EC with endometrioid histologies and EC with non-endometrioid histologies. The genetic statistics of the gut microbiota, including 18,340 participants, were acquired from the MiBioGen database. The summary statistics of EC, EC with endometrioid histologies and EC with non-endometrioid histologies were obtained from the publicly available Genome-wide Association Study (GWAS) database. Suitable single nucleotide polymorphisms (SNPs) were selected as instrumental variables (IVs) (
Nutritional index in relation to prognosis of endometrial cancer
A metabolic-inflammatory-nutritional score (MINS) is associated with lymph node metastasis and prognostic stratification for endometrial cancer patients
Identification of lncRNAs associated with uterine corpus endometrial cancer prognosis based on the competing endogenous RNA network
Uterine Corpus Endometrial Carcinoma (UCEC) is one of the major malignant tumors of the female reproductive system. However, there are limitations in the currently available diagnostic approaches for UCEC. Long non-coding RNAs (lncRNAs) play important roles in regulating biological processes as competitive endogenous RNA (ceRNA) in tumors. To study the potential of lncRNAs as non-invasive diagnostic tumor markers, RNA-sequencing dataset of UCEC patients from The Cancer Genome Atlas was used to identify differentially expressed genes. A lncRNA-miRNA-mRNA ceRNA network was constructed by differentially expressed lncRNAs, miRNAs and miRNAs. Pathway enrichment and functional analysis for the mRNAs in the constructed ceRNA network provide the direction of future research for UCEC by demonstrating the most affected processes and pathways. Seven potential lncRNA biomarkers (C20orf56, LOC100144604, LOC100190940, LOC151534, LOC727677, FLJ35390, LOC158572) were validated in UCEC patients by quantitative real-time PCR. Notably, LOC100190940 and LOC158572 were identified as novel RNA molecules with unknown functions. Receiver operating characteristic (ROC) curve analysis demonstrated that the combined 7 lncRNAs had a high diagnostic value for UCEC patients with area under curve (AUC) of 0.941 (95% CI: 0.875-0.947). Our study highlights the potential of the validated 7 lncRNAs panel as diagnostic biomarkers in UCEC, providing new insights into the UCEC pathogenesis.
SNHG3/hsa-miR-455-5p Axis-mediated High Expression of MTHFD2 Correlates with Tumor Immune Infiltration and Endometrial Carcinoma Progression
Prognostic value of pretreatment systemic inflammatory markers in patients with stage I endometrial cancer
Anticancer peptide Q7 suppresses the growth and migration of human endometrial cancer by inhibiting DHCR24 expression and modulating the AKT-mediated pathway
Endometrial cancer is one of the most common malignancy affecting women in developed countries. Resection uterus or lesion area is usually the first option for a simple and efficient therapy. Therefore, it is necessary to find a new therapeutic drug to reduce surgery areas to preserve fertility. Anticancer peptides (ACP) are bioactive amino acids with lower toxicity and higher specificity than chemical drugs. This study is to address an ACP, herein named Q7, which could downregulate 24-Dehydrocholesterol Reductase (DHCR24) to disrupt lipid rafts formation, and sequentially affect the AKT signal pathway of HEC-1-A cells to suppress their tumorigenicity such as proliferation and migration. Moreover, lipo-PEI-PEG-complex (LPPC) was used to enhance Q7 anticancer activity
Minimally invasive surgery for patients with advanced stage endometrial cancer
Prognostic significance of histological grade in low-risk endometrial cancer
FBXO17 Inhibits the Wnt/β-Catenin Pathway and Proliferation of Ishikawa Cells
Uterine corpus endometrial carcinoma (UCEC) is one of the most common types of cancer in women, and the incidence is rapidly increasing. Studies have shown that various signaling pathways serve crucial roles in the tumorigenesis of UCEC, amongst which the Wnt/β-catenin pathway is of great interest due to its crucial role in cell proliferation and the huge potential as a therapeutic target. In the present study, it was shown that FBXO17, which is a member of the F-box family, is abnormally downregulated in UCEC tissues compared with non-tumor endometrial tissues, and this was significantly associated with the clinical histological grade, as well as the abnormal proliferation of the UCEC cell line, Ishikawa, both
Promoter Methylation-mediated Silencing of the MiR-192-5p Promotes Endometrial Cancer Progression by Targeting ALX1
Preoperative neutrophil-to-lymphocyte, platelet-to-lymphocyte and monocyte-to-lymphocyte ratio as a prognostic factor in non-endometrioid endometrial cancer
Prediction of lymphovascular space invasion in patients with endometrial cancer
Gene Mutations and Related Molecular Events in Distant Metastasis of Cervical Cancer: A Review
Cervical cancer, a serious gynecological malignancy, often leads to poor patient prognosis due to distant metastasis. The metastasis mechanism is not fully understood. This study explores the link between gene mutations and distant metastasis in cervical cancer.
Identification of Key Genes via Integrated Multi-Omics and Machine Learning Uncovers Tumor Biological Features and Prognostic Biomarkers in Uterine Leiomyosarcoma
Uterine leiomyosarcoma (ULMS) is a rare, aggressive uterine malignancy with high misdiagnosis rates, poor prognosis, and limited molecular biomarkers. Its pathogenesis, links between specific genes and the tumor immune microenvironment (TIME), and applications of machine learning (ML) and Mendelian randomization (MR) remain understudied. Multi-cohort data (4 GEO datasets, TCGA-SARC, single-cell sequencing) were integrated. Differentially expressed genes (DEGs) and WGCNA-derived key modules identified "InteGenes". 113 ML algorithms were compared to build a diagnostic model (top: GBM, core genes = "Mgenes"). CIBERSORT analyzed TIME; MR explored Mgenes-ULMS causal links. 96 InteGenes enriched in cell cycle/p53/DNA repair pathways. The GBM model had training AUC = 1 and validation accuracy 92.3-100%; 36 Mgenes (e.g., TRIP13, AUC = 0.972) showed diagnostic value. Mgenes correlated with TIME (upregulated Mgenes ↔ M2 TAMs/Tregs; downregulated ↔ effector cells). MR found no genetic causality between Mgenes and ULMS. InteGenes reflect ULMS pathogenesis; the GBM model and Mgenes are promising diagnostic tools. Mgenes modulate ULMS's TIME, offering immunotherapeutic targets. This study advances ULMS molecular/immune understanding for translational research.
Potential Markers to Differentiate Uterine Leiomyosarcomas from Leiomyomas
Uterine leiomyomas (ULM) are the most common benign tumors of the female genitalia, while uterine leiomyosarcomas (ULMS) are rare. The sarcoma is diffuse growth, prone to hematogenous metastasis, and has a poor prognosis. Due to their similar clinical symptoms and morphological features, it is sometimes difficult to distinguish them, and the final diagnosis depends on histological diagnosis. Misdiagnosis of ULM as ULMS will lead to more invasive and extensive surgery when it is not needed, while misdiagnosis of ULMS as ULM may lead to delayed treatment and poor prognosis. This review searched and studied the published articles on ULM and ULMS, and summarized the potential markers for the differential diagnosis of ULMS. These markers will facilitate differential diagnosis and personalized treatment, providing timely diagnosis and potentially better prognosis for patients.
Discovering the abnormalities and functional importance of ferroptosis-related molecules in cervical cancer
Ferroptosis is an iron-dependent nonapoptotic form of cell death that links iron, lipid, and glutathione levels to a variety of disease-related activities. However, the characteristics of ferroptosis in cervical carcinoma (CC) are poorly understood. We acquired raw data on CC cohorts from The Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO) database. Key genes were identified using differential gene expression analysis and intersected for further immune infiltration, transcription regulation, gene set variation analysis (GSVA), gene set enrichment analysis (GSEA), and drug sensitivity analysis. We also used immunohistochemical (IHC) staining to confirm the expression of important genes in cervical cancer tissue and their prognostic relevance. Finally, gene silencing and cell coculture experiments were used to verify the biological functional mechanism and its role in the tumor microenvironment (TME). Through bioinformatics analysis, we discovered that GCH1 and H1.2 are key ferroptosis-related molecules in cervical cancer. GCH1 and H1.2 could act as useful prognostic markers in cervical cancer, and in addition to their connection with the tumor microenvironment, the possible transcriptional regulatory network, hallmark pathways and chemotherapy sensitivity were also clarified. IHC of the tissue microarray (TMA) and immunofluorescence spatial distance evaluation revealed that GCH1 was more highly expressed in cervical cancer tissue than in paracarcinoma tissue. For patients with cervical cancer, higher GCH1 expression corresponded to a lower M2 cell proportion and a higher M1/M2 ratio as well as a greater GCH1-M2 distance. Silencing GCH1 in SiHa cells blocked the cell cycle, promoted apoptosis, and inhibited the migration and invasion abilities of the cells, possibly through the inhibition of the phosphorylated PI3K/AKT/mTOR pathway. Coculture of the cells with macrophages revealed that the silencing of GCH1 led to decreased expression of tumor necrosis factor (TNF), a biomarker of M1 macrophages. In this study, we performed a thorough investigation of ferroptosis-related genes and identified the functional complexity of GCH1 during tumorigenesis in cervical cancer.
PRDX3 Promotes Lymph Node Metastasis in Cervical Cancer by Activating NF-κB Signaling Pathway and Anoikis Resistance
Lymph node metastasis (LNM) confers significant treatment failure and adverse clinical outcomes in cervical cancer (CCa). However, large unknown lies in the mechanisms underlying LNM in CCa. In this study, we discovered that PRDX3 is elevated in CCa with LNM and associates with poor prognosis in CCa patients. Moreover, multivariate logistic analysis revealed that PRDX3 is an independent predictor of LNM in CCa. Functional investigations demonstrated that PRDX3 promotes invasion, lymphangiogenesis, and LNM of CCa. Mechanistically, PRDX3 activates NF-κB signaling pathway and upregulates the downstream pro-metastatic molecules VEGF-C and MMP-9 in CCa cells. Furthermore, PRDX3 could inhibit the anoikis of detached CCa cells by reducing the ROS level and hence promote LNM in CCa. Importantly, genetic inhibition of PRDX3 potently slows LNM of CCa. These findings highlight a novel PRDX3-mediated mechanism of LNM in CCa and recognize PRDX3 as a promising predictive marker and target of clinical intervention for LNM in CCa.
Impact of CD44 genetic variants on clinicopathological characteristics of uterine cervical cancer patients
CD44 genetic variants have been found to be related to various cancers. However, to date, no study has demonstrated the involvement of CD44 polymorphisms in uterine cervical cancer in Taiwanese women. Therefore, we conducted a retrospective study, consecutively recruiting 113 patients with invasive cancer, 92 patients with high-grade cervical intraepithelial neoplasias, and 302 control women to assess the relationships among CD44 polymorphisms, cervical carcinogenesis, and patient survival. Real-time polymerase chain reaction was used to determine the genotypic distributions of six polymorphisms: rs1425802, rs187115, rs713330, rs11821102, rs10836347, and rs13347. The results revealed that women with the mutant homozygous genotype CC exhibited a higher risk of invasive cancer compared to those with the wild homozygous genotype TT [p=0.035; hazard ratio (HR)=10.29, 95% confidence interval (95% CI)=1.18-89.40] and TT/TC [p=0.032; HR=10.66, 95% CI=1.23-92.11] in the CD44 polymorphism rs713330. No significant association was found between CD44 genetic variants and clinicopathological parameters. Among the clinicopathological parameters, only positive pelvic lymph node metastasis (p=0.002; HR=8.57, 95% CI=2.14-34.38) and the AG/GG genotype compared to AA (p=0.014; HR=3.30, 95% CI=1.28-8.49) in CD44 polymorphism rs187115 predicted a higher risk of poor five-year survival, according to multivariate analysis. In conclusion, an important and novel finding revealed that Taiwanese women with the AG/GG genotype in CD44 polymorphism rs187115 exhibited a higher risk of poor five-year survival.
NAT10-mediated RNA acetylation enhances HNRNPUL1 mRNA stability to contribute cervical cancer progression
N4-acetylcytidine (ac4C) is a lately discovered nucleotide modification that has been shown to be closely implicated in cancer. N-acetyltransferase10(NAT10) acts as an enzyme that regulates mRNA acetylation modifications. Currently, the role of NAT10-mediated RNA acetylation modification in cervical cancer remains to be elucidated. On the basis of transcriptome analysis of TCGA and GEO open datasets (GSE52904, GSE29570, GSE122697), NAT10 is upregulated in cervical cancer tissues and correlated with poor prognosis. Knockdown of NAT10 suppressed the cell proliferation, invasion, and migration of cervical cancer cells. The in vivo oncogenic function of NAT10 was also confirmed in xenograft models. Combined RNA-seq and acRIP-seq analysis revealed HNRNPUL1 as the target of NAT10 in cervical cancer. NAT10 positively regulate HNRNPUL1 expression by promoting ac4C modification and stability of HNRNPUL1 mRNA. Furthermore, depletion of HNRNPUL1 suppressed the cell division, invasion, and migration of cervical cancer. HNRNPUL1 overexpression partially restored cellular function in cervical cancer cells with NAT10 knockdown. Thus, this study demonstrates that NAT10 contributes to cervical cancer progression by enhancing HNRNPUL1 mRNA stability via ac4C modification, and NAT10-ac4C-HNRNPUL1 axis might be a potential target for cervical cancer therapy.
Multi‐omics analysis of tumor mutational burden combined with prognostic assessment in epithelial ovarian cancer based on TCGA database
CHD1L promotes EOC cell invasiveness and metastasis via the regulation of METAP2
Chromodomain helicase DNA binding protein 1-like (CHD1L) gene has been proposed to play an oncogenic role in human hepatocellular carcinoma. Previously we reported that CHD1L overexpression is significantly associated with the metastasis proceeding of epithelial ovarian cancer (EOC), and may predict a poor prognosis in EOC patients. However, the potential oncogenic mechanisms by which CHD1L acts in EOC remain unclear. To elucidate the oncogenic function of CHD1L, we carried out a series of
Notch1 Affects Chemo-resistance Through Regulating Epithelial-Mesenchymal Transition (EMT) in Epithelial Ovarian cancer cells
Over-expression of RALYL suppresses the progression of ovarian clear cell carcinoma through inhibiting MAPK and CDH1 signaling pathways
Ferroptosis: A New Promising Target for Ovarian Cancer Therapy
Ferroptosis is a novel kind of regulated cell death distinct from autophagy, apoptosis, and necrosis; it is predominantly caused by the iron-dependent lipid peroxidation. According to studies, numerous conventional signaling pathways and biological processes are implicated in the process of ferroptosis. In recent years, researchers have shown that ferroptosis plays an important role in the genesis, development, and metastasis of malignancies, including ovarian cancer. Several studies have revealed that ferroptosis has synergistic effects with chemotherapy, radiotherapy, and immunotherapy in inhibiting the growth of ovarian cancer cells. This suggests that ferroptosis is important in ovarian cancer treatment and may be a new target. In this review, we summarize the features of ferroptosis, including its underlying basis and function in ovarian cancer, as well as its potential applications in the treatment of ovarian cancer.
Comparison of abdominal and minimally invasive radical hysterectomy in patients with early stage cervical cancer
The aim of this study was to compare survival outcomes of open radical hysterectomy and minimally invasive radical hysterectomy (MIS) in early stage cervical cancer. A retrospective analysis of 148 patients with stage IB1 - IIA2 cervical cancer who underwent either minimally invasive or open radical hysterectomy. Tumor characteristics, recurrence rate, disease-free survival (DFS), and overall survival (OS) were compared according to surgical approach. In total, 110 and 38 patients were assigned to open surgery and MIS groups. After a medical follow-up of 42.1 months, the groups showed similar survival outcomes (recurrence rate, DFS, and OS). However, in patients with tumor size >2 cm, recurrence rate was significantly higher in MIS group (22.5% vs 0%; p=0.008). And in patients with tumor size >2 cm, MIS group showed significantly poorer DFS than open surgery group (p=0.017), although OS was similar between the two groups (p=0.252). In patients with tumor size >2 cm, MIS was associated with higher recurrence rates and poorer DFS than open surgery. However, in patients with tumor size ≤2 cm, MIS did not seem to compromise oncologic outcomes.
Lipopolysaccharide Affects the Proliferation and Glucose Metabolism of Cervical Cancer Cells Through the FRA1/MDM2/p53 Pathway
Previous studies have found that LPS and FRA1 play opposite roles in cervical cancer. In addition, LPS functions by regulating the expression of FRA1 in many disease models, but there is currently no study of their relationship in the energy metabolism of tumor cells. This study, therefore, investigates the effects of LPS on FRA1-mediated glucose metabolism and the possible mechanisms it may have in cervical cancer cells. We constructed FRA1 stable overexpressing/ empty vector cervical cancer cell lines, where glucose consumption, the level of lactic acid production and the expression of energy metabolism related molecules were detected under the stimulation of LPS. At the same time, the changes in proliferation ability of cervical cancer cells were detected. We discovered that LPS promotes glucose consumption, lactic acid production, pentose phosphate bypass, and inhibits aerobic oxidation, by inhibiting the expression of FRA1; and that LPS promotes the growth of cervical cancer cells. Our results indicate that LPS affects the proliferation and glucose metabolism of cervical cancer cells through the FRA1/MDM2/p53 pathway.
Integrating Single-Cell and Bulk RNA Sequencing Data to Explore Sphingolipid Metabolism Molecular Signatures in Ovarian Cancer Prognosis: an Original Study
Effect of tissue inhibitor of metalloproteinases-3 genetics polymorphism on clinicopathological characteristics of uterine cervical cancer patients in Taiwan
Single nucleotide polymorphisms (SNPs) of tissue inhibitor of metalloproteinases-3 (
Gemcitabine and Selected mTOR Inhibitors in Uterine Sarcomas and Carcinosarcoma Cells- an Isobolographic Analysis
Side-Effects on the Renal function of Cytoreductive Surgery with Hyperthermic Intraperitoneal Chemotherapy
High Expression of TBC1 Domain Family Member 22A is Related to Poor Prognosis in Ovarian Serous Cystadenocarcinoma
The associations and roles of microRNA single-nucleotide polymorphisms in cervical cancer
Cervical cancer is one of the fourth most common gynecological malignancies and has been identified as the fourth leading cause of cancer death in women worldwide. MicroRNAs (miRNAs) are single-stranded sequences of noncoding RNAs that are approximately 22-24 nucleotides in length. They modulate posttranscriptional mRNA expression and play critical roles in cervical cancer. Single nucleotide polymorphisms (SNPs) in miRNA genes may alter miRNA expression and maturation and have been associated with various cancers. This review mainly focuses on the roles of SNPs in miRNA genes in the development of cervical cancer and summarizes the research progress of miRNA SNPs in cervical cancer and their molecular regulation mechanisms.
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