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Vasoactive Peptides in Tumor Microenvironment

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

Deadline for manuscript submissions: closed (20 July 2022) | Viewed by 2603

Special Issue Editors


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Guest Editor
Department of Pharmaceutical and Pharmacological Sciences, University of Padova, Padova, Italy
Interests: leukemia; skin cancers; adrenomedullin signaling; neuroinflammation; multipotent stem cells; S100B
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Hematology, Department of Biomedicine and Prevention, “Tor Vergata” University of Rome, Roma, Italy
Interests: AML; HSCT; MRD; novel agents; guidelines; ELN; genetics; cytogenetics; MDS; chemotherapy
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Department of Pharmaceutical and Pharmacological Sciences, University of Padova, 35131 Padova, Italy
Interests: tissue engineering; biomaterials; stem cells; breast cancer cells

Special Issue Information

Dear Colleagues,

Numerous peptides participate in the regulation of the cardiovascular system at different levels in the body. Based on structural and functional similarities, they are grouped into two families: 1) vasoconstrictors, such as angiotensin II, vasopressin, endothelins, neuropeptide Y, or urotensin; and 2) vasodilators, such as calcitonin gene-related peptide, adrenomedullin, natriuretic peptides, vasoactive intestinal peptide, or substance P. Vasoactive peptides act as classic hormones, circulating in blood to the targets, or mediate specific effects in a paracrine or autocrine manner. Under pathological conditions, they initiate and maintain maladaptive cellular responses promoting the growth of tumors. Over the last decade, interest in their role in cancer has grown, and strong evidence of their modulatory activity on mitogenesis, apoptosis, angiogenesis, tumor invasion, and development of metastases has been accumulated. Therefore, we invite our colleagues in this field to contribute to this Special Issue by providing research articles or relevant topic reviews on vasoactive peptides and their activities in hematological and not hematological malignancies. We are particularly interested in novel therapeutics, new biomarker studies, genomics, and stem cell research.

Prof. Dr. Rosa Di Liddo
Prof. Dr. Adriano Venditti
Prof. Dr. Maria Teresa Conconi
Guest Editors

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Keywords

  • adrenomedullin
  • endothelin
  • calcitonin gene-related peptide
  • neuropeptide Y
  • vasoactive intestinal peptide
  • angiotensin II
  • leukemia
  • cancer
  • infections
  • inflammation

Published Papers (1 paper)

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Research

12 pages, 1740 KiB  
Article
Vasopressin Receptor Type-2 Mediated Signaling in Renal Cell Carcinoma Stimulates Stromal Fibroblast Activation
by Abeda Jamadar, Nidhi Dwivedi, Sijo Mathew, James P. Calvet, Sufi M. Thomas and Reena Rao
Int. J. Mol. Sci. 2022, 23(14), 7601; https://doi.org/10.3390/ijms23147601 - 9 Jul 2022
Cited by 1 | Viewed by 1772
Abstract
Vasopressin type-2 receptor (V2R) is ectopically expressed and plays a pathogenic role in clear cell renal cell carcinoma (ccRCC) tumor cells. Here we examined how V2R signaling within human ccRCC tumor cells (Caki1 cells) stimulates stromal cancer-associated fibroblasts (CAFs). We found that cell [...] Read more.
Vasopressin type-2 receptor (V2R) is ectopically expressed and plays a pathogenic role in clear cell renal cell carcinoma (ccRCC) tumor cells. Here we examined how V2R signaling within human ccRCC tumor cells (Caki1 cells) stimulates stromal cancer-associated fibroblasts (CAFs). We found that cell culture conditioned media from Caki1 cells increased activation, migration, and proliferation of fibroblasts in vitro, which was inhibited by V2R gene silencing in Caki1 cells. Analysis of the conditioned media and mRNA of the V2R gene silenced and control Caki1 cells showed that V2R regulates the production of CAF-activating factors. Some of these factors were also found to be regulated by YAP in these Caki1 cells. YAP expression colocalized and correlated with V2R expression in ccRCC tumor tissue. V2R gene silencing or V2R antagonist significantly reduced YAP in Caki1 cells. Moreover, the V2R antagonist reduced YAP expression and myofibroblasts in mouse xenograft tumors. These results suggest that V2R plays an important role in secreting pro-fibrotic factors that stimulate fibroblast activation by a YAP-dependent mechanism in ccRCC tumors. Our results demonstrate a novel role for the V2R-YAP axis in the regulation of myofibroblasts in ccRCC and a potential therapeutic target. Full article
(This article belongs to the Special Issue Vasoactive Peptides in Tumor Microenvironment)
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