Epigenomics

Identification of lncRNA-Associated ceRNA Network in High-Grade Serous Ovarian Cancer Metastasis

Epigenetic silencing of JAM3 promoted progression in serous ovarian carcinoma through PI3K/AKT pathway

Junctional adhesion molecule 3 (JAM3) is frequently epigenetically silenced in various cancers, but its role in serous ovarian carcinoma (SOC) was unclear. This study evaluated JAM3 expression and methylation in SOC using immunohistochemistry (IHC), bisulfite sequencing PCR (BSP), and quantitative methylation-specific PCR (qMSP). Cell proliferation, apoptosis, migration, and invasion were examined using CCK8, flow cytometry, scratch-wound, and transwell assays. Pathways downstream of JAM3 were explored through RNA sequencing (RNA-seq) and Western Blot analysis, with rescue experiments using AKT inhibitor (MK2206) to validate pathway dependency. Findings revealed that JAM3 expression is significantly reduced in SOC, correlating with advanced clinical stages and poor prognosis. Methylation levels of the JAM3 promoter were higher in SOC samples compared to normal tissues and were linked to increased Ki67 expression and clinical stages. Functionally, overexpressing JAM3 in SOC cells triggered apoptosis and hindered proliferation, migration, and invasion, whereas JAM3 knockdown produced opposite effects. Mechanism analysis demonstrated that JAM3 affects SOC cell proliferation through the PI3K/AKT signaling pathway. Conclusively, JAM3 acts as a tumor suppressor in SOC by modulating the PI3K/AKT pathway. These insights present JAM3 as a promising therapeutic target for SOC diagnosis and treatment.

A novel subtype to predict prognosis and treatment response with DNA driver methylation–transcription in ovarian cancer

Leveraging Epigenetics to Enhance the Efficacy of Cancer-Testis Antigen: A Potential Candidate for Immunotherapy

Ovarian cancer is the most lethal gynecological malignancy in women. The phenotype is characterized by delayed diagnosis, recurrence and drug resistance. Inherent immunogenicity potential, oncogenic function and expression of cancer-testis/germline antigen (CTA) in ovarian cancer render them a potential candidate for immunotherapy. Revolutionary clinical findings indicate that tumor antigen-mediated T-cell and dendritic cell-based immunotherapeutic approaches provide an excellent strategy for targeting tumors. Currently, dendritic cell vaccination for the treatment of B-cell lymphoma and CTA-based T-cell receptor transduced T-cell therapy involving MAGE-A4 and NY-ESO-1 are well documented and shown to be effective. This review highlighted the mechanical aspects of epigenetic drugs that can elicit a CTA-based humoral and cellular immune response and implicate T-cell and dendritic cell-based immunotherapeutic approaches.

Building a Circular RNA Centered Gene Regulation Network Associated with Cervical Squamous Cell Carcinoma

Exosomal MicroRNAs: Novel Players in Cervical Cancer

Cervical cancer ranks fourth for both mortality and morbidity in women globally. Exosomes are considered as extracellular vesicles, secreted continuously by many cells with a size range from 30 to 150 nm. Exosomes can encapsulate microRNAs (miRNAs) and release them for cellular communications. This exosome-induced miRNA transfer is a novel strategy for genetic exchange among cells. This trafficking modality affects many pathological as well as physiological conditions. Moreover, exosomes can protect the miRNAs against harsh environments and keep them very stable. Given that a variety of exosomal miRNAs derived from cervical cancer cells can be targeted to recipient cells and contribute to tumorgenesis, it has been documented that exosomal miRNAs could be applied as diagnostic and therapeutic biomarkers in the treatment of cervical cancer. Herein, we summarize the pathologic and diagnostic roles of exosomal miRNAs in the cervical cancer. Moreover, we highlight the roles of exosomal miRNAs in other cancers.

Evaluation of Six Methylation Markers Derived from Genome-Wide Screens for Detection of Cervical Precancer and Cancer

Prediction of Transcription Factors Binding Events Based on Epigenetic Modifications in Different Human Cells

A systematic review and meta-analysis of the diagnostic effectiveness of human papillomavirus methylation biomarkers for detection of cervical cancer

Targeting TET enzymes in ovarian cancer: epigenetic regulation, chemoresistance, and therapeutic opportunities

The intrinsic and acquired resistance of ovarian cancer to conventional platinum/taxane chemotherapy is approximately 80-85%, with a high recurrence rate, making it one of the most lethal gynecological cancers. Epigenetic dysregulation, a key factor in tumor growth and chemoresistance, includes abnormal DNA methylation and 5-hydroxymethylcytosine (5hmC) loss. The ten-eleven translocation (TET) family of dioxygenases (TET1/TET2/TET3) mediates DNA demethylation, causing oxidation of 5-methylcytosine to 5hmC, potentially altering gene expression due to cancer cell plasticity and impacting treatment responses. This review discusses the multiple effects of TETs in ovarian cancer, highlighting the regulation of epithelial mesenchymal transition (EMT), cancer stem cells (CSCs), and the Wnt/β-catenin and TGF-β signaling pathways by TET enzymes. TET1 plays a dual role, promoting chemoresistance via CSC enrichment and suppressing tumors by replenishing Wnt antagonists. TET2, primarily a tumor suppressor, reduces 5hmC; TET2 loss is associated with poor therapeutic results. Elevated expression of TET3, which controls EMT and miRNA expression, is linked to a worse prognosis. In addition, we reviewed the potential resensitization of resistant tumors to multiple modalities of treatment by reactivating/modulating TET activity and function via cofactors and epigenetic treatment. Regulation of the TET-5hmc axis appears promising to overcome chemoresistance and improve therapeutic outcomes.

PTEN Promoter Methylation And Expression In Endometrial Cancer Tissues

tRF-20-S998LO9D Inhibits Endometrial Carcinoma by Upregulating SESN2

DNA Methylation Markers for Endometrial Cancer Detection in Minimally Invasive Samples: A Systematic Review

Identification of an immune signature to predict poor clinical outcome in cervical cancer

Will methylation assays be part of a full molecular strategy to improve clinical management of cervical neoplasia?

A comprehensive review of m 6 A research in cervical cancer

Cervical cancer (CC) remains one of the most common malignancies among women worldwide, posing a serious threat to women's health. N6-methyladenosine (m

Integrated Bioinformatics And Experimental Validation Reveal The Role Of Jarid2 In Ovarian Cancer

Constructed Competitive Endogenous RNA Network and Patterns of Immune Infiltration Revealing the Prognostic Signature for Cervical Cancer

Fatty Acid Metabolism-Related lncRNA Prognostic Signature for Serous Ovarian Carcinoma

Phytochemicals in Cervical Cancer: An Epigenetic Overview

Cervical cancer is the fourth most common female malignancy worldwide and a complex disease that typically starts with HPV infection. Various genetic and epigenetic alterations are implicated in its development. The current cervical cancer therapies have unsatisfactory outcomes due to their serious adverse effects, necessitating the need for safe, effective preventive and therapeutic modalities. Phytochemicals have been addressed in cervical cancer prevention and treatment, and further understanding the epigenetics of cervical cancer pathogenesis is critical to investigate new preventive and therapeutic modalities. Addressing the epigenetic mechanisms of potential phytochemicals will provide an overview of their use individually or in combination. The primary aim of this review is to highlight the epigenetic effects of the phytochemicals addressed in cervical cancer therapy.

A Systematic Review and Meta-Analysis of Mirnas for the Detection of Cervical Cancer