International Review of Cell and Molecular Biology

Epigenetic regulation via histone modifications in ovarian cancer

Ovarian cancer is a highly heterogeneous and lethal gynecological malignancy, with its progression tightly regulated by both genetic and epigenetic mechanisms. Among the epigenetic regulators, histone modifications-including acetylation, methylation, phosphorylation, ubiquitination, and SUMOylation-have emerged as pivotal modulators of chromatin architecture and gene transcription. These post-translational modifications, governed by specific histone-modifying enzymes, shape the transcriptional landscape of tumor cells and influence key oncogenic processes such as cellular proliferation, invasion, stemness, DNA repair, and chemotherapy resistance. Dysregulation of enzymes such as histone acetyltransferases (HATs), deacetylases (HDACs), methyltransferases (HMTs), demethylases (HDMs), ubiquitin ligases, and SUMO ligases has been implicated in the pathogenesis of ovarian cancer and is associated with adverse clinical outcomes. Importantly, these modifications are reversible, rendering them tractable therapeutic targets. This review provides a comprehensive synthesis of the major classes of histone modifications and their biological functions in ovarian cancer, highlights recent insights into the interplay between different modifications (crosstalk), and evaluates ongoing therapeutic strategies that aim to reverse epigenetic dysregulation. By elucidating the complex epigenetic landscape, this review supports the development of next-generation diagnostic, prognostic, and therapeutic approaches in ovarian cancer.

Epigenetic alteration in cervical cancer induced by human papillomavirus

The critical role of a subset of Human Papillomavirus in cervical cancer has been widely acknowledged and studied. Despite progress in our understanding of the viral molecular mechanisms of pathogenesis, knowledge of how infection with HPV oncogenic variants progresses from latent infection to incurable cancer has not been completely elucidated. In this paper we reviewed the relationship between HPV infection and epigenetic mechanisms such as histone acetylation and deacetylation, DNA methylation and non-coding RNAs associated with this infection and the carcinogenic process.

Epigenetic regulation in ovarian cancer

Ovarian cancer is one of the diseases that have the highest mortality rate for women, especially women over 50 years old. In the future, incidence and mortality rates are predicted to extend in countries with low HDI. Instability in the structure and function of genetic factors has long been known as a cause of cancer, including ovarian cancer. Besides understanding gene mutations, epigenetic alterations have emerged as another aspect leading to the pathogenesis of ovarian neoplasm. The development and progression of this fatal disease have been found to be associated with abnormalities of epigenetic regulation. DNA methylation, histone modification, and non-coding RNAs-based gene silencing are processes of interest in developing ovarian carcinoma and are also new targets for cancer detection or treatment.

Exploring TLR signaling pathways as promising targets in cervical cancer: The road less traveled

Cervical cancer is the leading cause of cancer-related deaths for women globally. Despite notable advancements in prevention and treatment, the identification of novel therapeutic targets remains crucial for cervical cancer. Toll-like receptors (TLRs) play an essential role in innate immunity as pattern-recognition receptors. There are several types of pathogen-associated molecular patterns (PAMPs), including those present in cervical cancer cells, which have the ability to activate toll-like receptors (TLRs). Recent studies have revealed dysregulated toll-like receptor (TLR) signaling pathways in cervical cancer, leading to the production of inflammatory cytokines and chemokines that can facilitate tumor growth and metastasis. Consequently, TLRs hold significant promise as potential targets for innovative therapeutic agents against cervical cancer. This book chapter explores the role of TLR signaling pathways in cervical cancer, highlighting their potential for targeted therapy while addressing challenges such as tumor heterogeneity and off-target effects. Despite these obstacles, targeting TLR signaling pathways presents a promising approach for the development of novel and effective treatments for cervical cancer.

Omentum: Friend or foe in ovarian cancer immunotherapy?

Ovarian cancer often spreads out of the ovary before a patient is diagnosed and is the deadliest gynecological malignancy. The aggressiveness of ovarian cancer is determined by the progression in the form of peritoneal carcinomatosis, a stage with a poor prognosis and an untreatable condition in most patients. One of the first tumor nests or the origin of metastasis in the peritoneal cavity is the omentum. The omentum contains immune aggregates, called milky spots, embedded in adipose tissue, which support tumor growth by various mechanisms, including immunosuppressive immune cells and metabolic functions. In this sense, the abundance of blood vessels, omental resident macrophages, and chemokines, among other factors, are known to promote invasiveness, proliferation and resistance to cancer therapies. As a result, surgical practice employed in advanced-stage ovarian cancer almost constantly includes omentectomy. Paradoxically, the omentum is considered the "abdominal policeman" that contributes to peritoneal immunity by capturing antigens and pathogens from the peritoneal cavity and promoting effective immune responses against microbes. Why immunosurveillance against the metastatic tumor does not take place in the omentum? Could omental immune responses be activated with immunotherapeutic interventions? The omentum has largely been ignored in cancer immunology and immunotherapy, and the potential translational implications of this in ovarian cancer are still unclear. Here, we focus on the dual role of the omentum in ovarian cancer: its role in antitumor immune responses versus its activities fostering cancer progression.