Unraveling an Aggressive Cancer: The Role of Epigenetics in Pancreas Cancer

A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: closed (31 January 2022) | Viewed by 7121

Special Issue Editors


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Guest Editor
Department of Biological and Biomedical Sciences, Yale School of Medicine, New Haven, CT 06511, USA
Interests: biomarker; early detection; epigenetics; colorectal cancer; pancreas cancer

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Guest Editor
Division of Research, Department of Surgery, Medical College of Wisconsin, Milwaukee, WI 53226, USA
Interests: epigenetics; transcription; differential gene expression; gene expression and chromatin biology; pancreatic diseases; methylation; histone modification; epigenomics; gene transcription; ChIP-sequencing; promoter analysis; chromatin remodeling; cancer epigenetics; chromatin biology; histone proteins

Special Issue Information

Dear Colleagues,

Pancreas cancer is one of the most lethal malignancies and will become the 2nd leading cause of cancer death by 2030. Epigenetic mechanisms are essential for normal development and tissue-specific expression patterns. Cancer formation is synonymous with widespread changes in the epigenomic landscape with cellular reprogramming. The role of epigenetic mechanisms, such as histone changes, chromatin modifications, noncoding RNAs and DNA methylation, are only recently being identified in pancreas cancer. Understanding of these epigenetic changes and manipulation of the epigenome has the potential to alter the course of this dismal cancer. In this series, we will have experts from various domains, ranging from the clinical arena to mechanistic epigenetics to translational biology, to address emerging themes in understanding the epigenome of pancreas cancer and discuss rapidly transpiring insights into use of the epigenome for the diagnosis and potential treatment of pancreas cancer.

Prof. Dr. Nita K. Ahuja
Dr. Gwen Lomberk
Guest Editors

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Published Papers (2 papers)

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16 pages, 2285 KiB  
Article
Promoter Hypermethylation Promotes the Binding of Transcription Factor NFATc1, Triggering Oncogenic Gene Activation in Pancreatic Cancer
by Yenan Wu, Lea Kröller, Beiping Miao, Henning Boekhoff, Andrea S. Bauer, Markus W. Büchler, Thilo Hackert, Nathalia A. Giese, Jussi Taipale and Jörg D. Hoheisel
Cancers 2021, 13(18), 4569; https://doi.org/10.3390/cancers13184569 - 11 Sep 2021
Cited by 7 | Viewed by 2499
Abstract
Studies have indicated that some genes involved in carcinogenesis are highly methylated in their promoter regions but nevertheless strongly transcribed. It has been proposed that transcription factors could bind specifically to methylated promoters and trigger transcription. We looked at this rather comprehensively for [...] Read more.
Studies have indicated that some genes involved in carcinogenesis are highly methylated in their promoter regions but nevertheless strongly transcribed. It has been proposed that transcription factors could bind specifically to methylated promoters and trigger transcription. We looked at this rather comprehensively for pancreatic ductal adenocarcinoma (PDAC) and studied some cases in more detail. Some 2% of regulated genes in PDAC exhibited higher transcription coupled to promoter hypermethylation in comparison to healthy tissue. Screening 661 transcription factors, several were found to bind specifically to methylated promoters, in particular molecules of the NFAT family. One of them—NFATc1—was substantially more strongly expressed in PDAC than control tissue and exhibited a strong oncogenic role. Functional studies combined with computational analyses allowed determining affected genes. A prominent one was gene ALDH1A3, which accelerates PDAC metastasis and correlates with a bad prognosis. Further studies confirmed the direct up-regulation of ALDH1A3 transcription by NFATc1 promoter binding in a methylation-dependent process, providing insights into the oncogenic role of transcription activation in PDAC that is promoted by DNA methylation. Full article
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20 pages, 2061 KiB  
Review
Ca2+ Signaling and Its Potential Targeting in Pancreatic Ductal Carcinoma
by Louay Bettaieb, Maxime Brulé, Axel Chomy, Mel Diedro, Malory Fruit, Eloise Happernegg, Leila Heni, Anaïs Horochowska, Mahya Housseini, Kekely Klouyovo, Agathe Laratte, Alice Leroy, Paul Lewandowski, Joséphine Louvieaux, Amélie Moitié, Rémi Tellier, Sofia Titah, Dimitri Vanauberg, Flavie Woesteland, Natalia Prevarskaya and V’yacheslav Lehen’kyiadd Show full author list remove Hide full author list
Cancers 2021, 13(12), 3085; https://doi.org/10.3390/cancers13123085 - 21 Jun 2021
Cited by 11 | Viewed by 4039
Abstract
Pancreatic cancer (PC) is a major cause of cancer-associated mortality in Western countries (and estimated to be the second cause of cancer deaths by 2030). The main form of PC is pancreatic adenocarcinoma, which is the fourth most common cause of cancer-related death, [...] Read more.
Pancreatic cancer (PC) is a major cause of cancer-associated mortality in Western countries (and estimated to be the second cause of cancer deaths by 2030). The main form of PC is pancreatic adenocarcinoma, which is the fourth most common cause of cancer-related death, and this situation has remained virtually unchanged for several decades. Pancreatic ductal adenocarcinoma (PDAC) is inherently linked to the unique physiology and microenvironment of the exocrine pancreas, such as pH, mechanical stress, and hypoxia. Of them, calcium (Ca2+) signals, being pivotal molecular devices in sensing and integrating signals from the microenvironment, are emerging to be particularly relevant in cancer. Mutations or aberrant expression of key proteins that control Ca2+ levels can cause deregulation of Ca2+-dependent effectors that control signaling pathways determining the cells’ behavior in a way that promotes pathophysiological cancer hallmarks, such as enhanced proliferation, survival and invasion. So far, it is essentially unknown how the cancer-associated Ca2+ signaling is regulated within the characteristic landscape of PDAC. This work provides a complete overview of the Ca2+ signaling and its main players in PDAC. Special consideration is given to the Ca2+ signaling as a potential target in PDAC treatment and its role in drug resistance. Full article
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