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Special Issue "Cyclooxygenase and Cancer: Fundamental Molecular Investigations"

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: 31 May 2020.

Special Issue Editor

Prof. Mauro Coluccia
E-Mail Website
Guest Editor
Department of Pharmacy-Drug Sciences, University of Bari “Aldo Moro”, Via E. Orabona 4, I-70125 Bari, Italy
Interests: anticancer drugs; targeted anticancer therapeutics; cellular response to anticancer treatment; inflammation and inflammation mediators

Special Issue Information

Dear Colleagues,

Today, we have a very rich, perhaps overwhelming, scientific literature on cyclooxygenases and cancer. In particular, the prognostic relevance of cyclooxygenase expression, the pathophysiological mechanisms connecting cyclooxygenase products and the various features of tumor phenotype, and finally the possibility of using cyclooxygenase inhibitors in chemoprevention and therapy have been largely investigated in the last few decades.

Each of the abovementioned topics could be the subject of a collection of papers on cyclooxygenase and cancer. However, in this IJMS Special Issue, we would like to collect scientific papers mainly focusing on fundamental molecular investigations about cyclooxygenases, the relevant lipid signaling molecules, and cancer pathophysiology. Original articles and reviews concerning biochemical, molecular and cellular biology, and molecular medicine aspects are welcome. In addition to the publication of experimental research specific results as well as of high-level review articles, the founding ambition of this IJMS special issue is to render a concretely useful service to the oncological research community interested in cyclooxygenase and cancer relationship. To this end, all authors of experimental papers are warmly invited to provide a state-of-the-art and careful description of the topic under investigation as far as the scientific content and technology/methodology issues are concerned. Moreover, it is recommended that the discussion/conclusion section, generally devoted to the “strong points”, future directions and/or clinical impact of the findings, includes also the potential limitations of the study.

From all contributions as a whole, we hope that people already working on specific topics are successfully updated on issues not directly linked to their research activity, and that possible concerns of people approaching this fascinating and complex cyclooxygenase and cancer relationship might be at least partly reduced.

Prof. Mauro Coluccia
Guest Editor

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

  • cyclooxygenase
  • cyclooxygenase inhibitor
  • prostaglandin
  • eicosanoid
  • lipid signaling molecules
  • cancer biology
  • cancer pathophysiology

Published Papers (1 paper)

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Research

Open AccessArticle
Multifocal Signal Modulation Therapy by Celecoxib: A Strategy for Managing Castration-Resistant Prostate Cancer
Int. J. Mol. Sci. 2019, 20(23), 6091; https://doi.org/10.3390/ijms20236091 - 03 Dec 2019
Abstract
Background: Prostate cancer (PCa) is a significant health concern throughout the world. Standard therapy for advanced disease consists of anti-androgens, however, almost all prostate tumors become castration resistant (CRPC). Progression from androgen-sensitive PCa to CRPC is promoted by inflammatory signaling through cyclooxygenase-2 (COX-2) [...] Read more.
Background: Prostate cancer (PCa) is a significant health concern throughout the world. Standard therapy for advanced disease consists of anti-androgens, however, almost all prostate tumors become castration resistant (CRPC). Progression from androgen-sensitive PCa to CRPC is promoted by inflammatory signaling through cyclooxygenase-2 (COX-2) expression and ErbB family receptors/AKT activation, compensating androgen receptor inactivity. Methods: Making use of CRPC cell lines, we investigated the effects of the anti-inflammatory drug celecoxib. Biochemical data obtained using immunoblotting, enzyme-linked immunosorbent assay (ELISA), invasion, and xenografts were further integrated by bioinformatic analyses. Results: Celecoxib reduced cell growth and induced apoptosis through AKT blockade, cleavage of poly (ADP-ribose) polymerase-1 (PARP-1), and proteasomal degradation of the anti-apoptotic protein Mcl-1. Epidermal growth factor receptor (EGFR), ErbB2, and ErbB3 degradation, and heterogeneous nuclear ribonucleoprotein K (hnRNP K) downregulation, further amplified the inhibition of androgen signaling. Celecoxib reduced the invasive phenotype of CRPC cells by modulating NF-κB activity and reduced tumor growth in mice xenografts when administered in association with the anti-EGFR receptor antibody cetuximab. Bioinformatic analyses on human prostate cancer datasets support the relevance of these pathways in PCa progression. Conclusions: Signaling nodes at the intersection of pathways implicated in PCa progression are simultaneously modulated by celecoxib treatment. In combination therapies with cetuximab, celecoxib could represent a novel therapeutic strategy to curb signal transduction during CRPC progression. Full article
(This article belongs to the Special Issue Cyclooxygenase and Cancer: Fundamental Molecular Investigations)
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Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Title: Endoplasmic reticulum stress contributed to indomethacin-induced glioma apoptosis

Authors: Cheng-Yi Chang, Jian-Ri Li, Chih-Cheng Wu, Jiaan-Der Wang, Su-Lan Liao, Wen-Ying Chen, Wen-Yi Wang, Chun-Jung Chen
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