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Special Issue "Advances in Pancreatic Cancer Research: Underlying Mechanisms and Therapeutic Targets"

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

Deadline for manuscript submissions: 28 February 2021.

Special Issue Editors

Prof. Dr. Srikumar Chellappan
Website
Guest Editor
H. Lee Moffitt Cancer Center and Research Institute, 12902 Magnolia Dr., Mail Code SRB3 Tampa, FL 33612, USA
Interests: molecular mechanisms that regulate cell proliferation; tumor progression; angiogenesis and metastasis; the role of nicotine in promoting growth and metastasis of tumors; cancer stem cells; mechanisms of drug resistance; novel drug targets
Special Issues and Collections in MDPI journals
Dr. Jaya Padmanabhan
Website
Guest Editor
1. Department of Molecular Medicine, University of South Florida, 12901 Bruce B. Downs Blvd, Tampa, FL 33612, USA
2. Department of Tumor Biology, Moffitt Cancer Center and Research Institute, 12902 Magnolia Drive, Tampa, FL 33612, USA
Interests: molecular mechanisms associated with neurodegeneration and pancreatic cancer; brain cancers, including glioblastoma; Alzheimer’s disease; CDKs in cancer and neurodegeneration; proteases in cancer; calcium signaling and pancreatic cancer; cell cycle regulation; signal transduction; epithelial–mesenchymal transition
Special Issues and Collections in MDPI journals

Special Issue Information

Dear Colleagues:

This Special Issue is a continuation of our 2018 Special Issue “Cell and Molecular Biology of Pancreatic Disorders”.

Pancreatic cancer is one of the deadliest cancers, with a 5 year survival rate of about 6%. Recent studies have elucidated the molecular mechanisms underlying the genesis and progression of this disease, which has enabled the development of novel therapeutics; while this is promising, however, it has not translated into prolonged survival rates due to the complex nature of the disease. Further, due to a lack of reliable early detection methods, the cancer is detected only at a late stage, when it is aggressive and highly invasive. Additionally, the highly fibrotic tumor microenvironment—which is enriched with growth factors and cytokines—significantly supports the growth and metastasis of the tumor and hinders the therapeutic efficacy. This thematic Special Issue is expected to cover the molecular and cellular mechanisms associated with pancreatic ductal adenocarcinomas, as well as the recent therapeutic strategies being developed to target specific signaling pathways. Other relevant aspects, such as the contribution of microenvironmental factors, cancer stem cells, behavior correlates such as smoking, and role of environmental pollutants in genesis and progression as well as response to therapy, will be covered in this issue. We expect that this Special Issue will provide the latest information on the mechanisms driving PDACs and will be of interest to scientists and clinicians working in this area.

Prof. Dr. Srikumar Chellappan
Dr. Jaya Padmanabhan
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Signaling pathways in PDCACs
  • Novel therapeutic targets for PDACs
  • Pancreatic neuroendocrine tumors
  • Pancreatic intraepithelial neoplasia
  • Intraductal papillary mucinous neoplasms
  • Pancreatic cancer stem cells
  • Pancreatic stromal cells
  • Pancreatic microenvironment
  • Genetic changes
  • Transcription and translation
  • Cell metabolism
  • Intracellular and intercellular signaling
  • Genomics/proteomics/lipidomics
  • Inflammation
  • Metastasis

Published Papers (1 paper)

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Research

Open AccessArticle
Peptidylarginine Deiminase Inhibitor Application, Using Cl-Amidine, PAD2, PAD3 and PAD4 Isozyme-Specific Inhibitors in Pancreatic Cancer Cells, Reveals Roles for PAD2 and PAD3 in Cancer Invasion and Modulation of Extracellular Vesicle Signatures
Int. J. Mol. Sci. 2021, 22(3), 1396; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22031396 - 30 Jan 2021
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive malignancies with limited survival rate. Roles for peptidylarginine deiminases (PADs) have been studied in relation to a range of cancers with roles in epigenetic regulation (including histone modification and microRNA regulation), cancer invasion, [...] Read more.
Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive malignancies with limited survival rate. Roles for peptidylarginine deiminases (PADs) have been studied in relation to a range of cancers with roles in epigenetic regulation (including histone modification and microRNA regulation), cancer invasion, and extracellular vesicle (EV) release. Hitherto though, knowledge on PADs in PDAC is limited. In the current study, two PDAC cell lines (Panc-1 and MiaPaCa-2) were treated with pan-PAD inhibitor Cl-amidine as well as PAD2, PAD3, and PAD4 isozyme-specific inhibitors. Effects were assessed on changes in EV signatures, including EV microRNA cargo (miR-21, miR-126, and miR-221), on changes in cellular protein expression relevant for pancreatic cancer progression and invasion (moesin), for mitochondrial housekeeping (prohibitin, PHB), and gene regulation (deiminated histone H3, citH3). The two pancreatic cancer cell lines were found to predominantly express PAD2 and PAD3, which were furthermore expressed at higher levels in Panc-1, compared with MiaPaCa-2 cells. PAD2 isozyme-specific inhibitor had the strongest effects on reducing Panc-1 cell invasion capability, which was accompanied by an increase in moesin expression, which in pancreatic cancer is found to be reduced and associated with pancreatic cancer aggressiveness. Some reduction, but not significant, was also found on PHB levels while effects on histone H3 deimination were variable. EV signatures were modulated in response to PAD inhibitor treatment, with the strongest effects observed for PAD2 inhibitor, followed by PAD3 inhibitor, showing significant reduction in pro-oncogenic EV microRNA cargo (miR-21, miR-221) and increase in anti-oncogenic microRNA cargo (miR-126). While PAD2 inhibitor, followed by PAD3 inhibitor, had most effects on reducing cancer cell invasion, elevating moesin expression, and modulating EV signatures, PAD4 inhibitor had negligible effects and pan-PAD inhibitor Cl-amidine was also less effective. Compared with MiaPaCa-2 cells, stronger modulatory effects for the PAD inhibitors were observed in Panc-1 cells, which importantly also showed strong response to PAD3 inhibitor, correlating with previous observations that Panc-1 cells display neuronal/stem-like properties. Our findings report novel PAD isozyme regulatory roles in PDAC, highlighting roles for PAD isozyme-specific treatment, depending on cancer type and cancer subtypes, including in PDAC. Full article
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