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Molecular Insights into Epigenetics in Cancer

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 20 January 2025 | Viewed by 1879

Special Issue Editor


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Guest Editor
Department of Pharmaceutical Sciences, Università del Piemonte Orientale “Amedeo Avogadro”, 28100 Novara, Italy
Interests: cancer; mesothelioma; signal transduction; epigenetics; drug resistance; epigenetic drugs

Special Issue Information

Dear Colleagues,

In general, cancer development results from the alteration of genetic and epigenetic mechanisms. Epigenetic aberrations, including DNA methylation, histone modifications, chromatin remodelling and non-coding RNAs, affect several aspects of tumour development and drug resistance. Elucidation of this complex crosstalk network may offer new insights into the molecular interactions involved in carcinogenesis. Focusing on translational medicine, new scenarios can drive to move toward personalised therapies and to develop novel and more effective diagnostic, prognostic and therapy strategies. This Special Issue will discuss the implications of epigenetic alterations in tumour biology, diagnosis and therapy.

As the Guest Editor of this Special Issue, “Molecular Insights into Epigenetics in Cancer”, in IJMS, I expect submissions from many researchers working on epigenetic modifications in cancer with a particular focus on molecular insights and therapeutic challenges. Manuscripts regarding the involvement of epigenetics in different aspects of carcinogenesis, biomarkers based on DNA methylation gene patterns, epigenetic strategies to offer alternative therapeutic targets, the role of epigenetic modifiers in chemo- and immuno-therapy resistances are also very welcome. The formats for submissions include original research reports, reviews, perspectives/opinions and methodology articles.

Dr. Giulia Pinton
Guest Editor

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Published Papers (1 paper)

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Research

17 pages, 2967 KiB  
Article
Alteration of Cadherin 3 Expression and DNA Methylation in Association with Aggressive Renal Cell Carcinoma
by Pouriya Faraj Tabrizi, Inga Peters, Inga Schimansky, Natalia Dubrowinskaja, Christel Reese, Hossein Tezval, Markus Antonius Kuczyk and Jürgen Serth
Int. J. Mol. Sci. 2023, 24(22), 16476; https://doi.org/10.3390/ijms242216476 - 18 Nov 2023
Cited by 2 | Viewed by 1393
Abstract
Cadherins (calcium-dependent adhesion proteins) are important in cellular adhesion and may play a role in the development and progression of renal cell carcinoma (RCC). This study investigated changes in cadherin 3 (CDH3; P-cadherin) mRNA expression, DNA methylation, and protein expression in [...] Read more.
Cadherins (calcium-dependent adhesion proteins) are important in cellular adhesion and may play a role in the development and progression of renal cell carcinoma (RCC). This study investigated changes in cadherin 3 (CDH3; P-cadherin) mRNA expression, DNA methylation, and protein expression in RCC and compared the results with the histopathological and clinical characteristics of patients. The possible contribution of CDH3 to tumor cell invasiveness was tested in a functional assay using siRNA-based suppression of CDH3 expression and subsequent real-time impedance analysis using a Matrigel invasion model. Our analyses revealed a tumor-specific loss of CDH3 mRNA expression, CDH3 DNA hypermethylation, and loss of distal tubular and collecting duct CDH3 protein expression in RCC. A relatively higher methylation level in tumors was associated with a loss of cell differentiation and higher clinical stage. siRNA-induced suppression of CDH3 expression modulated the invasion characteristics of tumor cells in the impedance-based real-time cellular analysis. Our results indicate that loss of CDH3 expression is common in RCC and may contribute to the pathogenesis of a subset of RCC. Further studies to reveal the mechanisms of loss of expression and its effects on the invasive behavior of renal tumor cells are required. Full article
(This article belongs to the Special Issue Molecular Insights into Epigenetics in Cancer)
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