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Survival Pathways Involved in Resistance to Apoptosis in Cancer 2.0

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: closed (31 August 2021) | Viewed by 2429

Special Issue Editor

Special Issue Information

Dear Colleagues,

This Special Issue, “Survival Pathways Involved in Resistance to Apoptosis in Cancer”, will cover a selection of recent research topics and current review articles related to the intracellular signaling of resistance to apoptosis in cancer. Up-to-date review articles, commentaries, and experimental papers are all welcome.

Programmed cell death or apoptosis is a natural mechanism by which organisms control the number of cells. It plays an important role in embryonic development and in maintaining cell homeostasis. Deregulation of apoptosis machinery induces resistance to apoptosis. This resistance is characterized by inhibition of cell death triggering or delay in cell death unfolding in response to an apoptotic stimulus. Apoptosis resistance plays an important role in tumor development. Uncontrolled cell proliferation combined with resistance to apoptosis is both necessary and sufficient for tumor progression to a malignant phenotype. Although there are several mechanisms by which cells escape apoptosis, the majority of these lead to an inability for the cell to trigger the intrinsic pathway of apoptosis (called the mitochondrial pathway). Despite numerous studies of the survival pathways in the apoptosis resistance mechanism, the signaling pathways involved have not yet been fully elucidated, and there are disparities regarding their role in this mechanism.

Prof. Dr. Bertrand Liagre
Guest Editor

Manuscript Submission Information

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Keywords

  • cancer
  • apoptosis
  • survival pathways
  • new treatment
  • clinical trials

Published Papers (1 paper)

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Research

15 pages, 2124 KiB  
Article
CD40 Cross-Linking Induces Migration of Renal Tumor Cell through Nuclear Factor of Activated T Cells (NFAT) Activation
by Paola Pontrelli, Margherita Gigante, Federica Spadaccino, Giuseppe Stefano Netti, Marilisa Saldarelli, Luigi Balducci, Maddalena Gigante, Michele Battaglia, Walter J. Storkus, Giuseppe Castellano, Giovanni Stallone, Loreto Gesualdo and Elena Ranieri
Int. J. Mol. Sci. 2021, 22(16), 8871; https://doi.org/10.3390/ijms22168871 - 18 Aug 2021
Cited by 4 | Viewed by 1984
Abstract
CD40 crosslinking plays an important role in regulating cell migration, adhesion and proliferation in renal cell carcinoma (RCC). CD40/CD40L interaction on RCC cells activates different intracellular pathways but the molecular mechanisms leading to cell scattering are not yet clearly defined. Aim of our [...] Read more.
CD40 crosslinking plays an important role in regulating cell migration, adhesion and proliferation in renal cell carcinoma (RCC). CD40/CD40L interaction on RCC cells activates different intracellular pathways but the molecular mechanisms leading to cell scattering are not yet clearly defined. Aim of our study was to investigate the main intracellular pathways activated by CD40 ligation and their specific involvement in RCC cell migration. CD40 ligation increased the phosphorylation of extracellular signal-regulated kinase (ERK), c-Jun NH (2)-terminal kinase (JNK) and p38 MAPK. Furthermore, CD40 crosslinking activated different transcriptional factors on RCC cell lines: AP-1, NFkB and some members of the Nuclear Factor of Activated T cells (NFAT) family. Interestingly, the specific inhibition of NFAT factors by cyclosporine A, completely blocked RCC cell motility induced by CD40 ligation. In tumor tissue, we observed a higher expression of NFAT factors and in particular an increased activation and nuclear migration of NFATc4 on RCC tumor tissues belonging to patients that developed metastases when compared to those who did not. Moreover, CD40-CD40L interaction induced a cytoskeleton reorganization and increased the expression of integrin β1 on RCC cell lines, and this effect was reversed by cyclosporine A and NFAT inhibition. These data suggest that CD40 ligation induces the activation of different intracellular signaling pathways, in particular the NFATs factors, that could represent a potential therapeutic target in the setting of patients with metastatic RCC. Full article
(This article belongs to the Special Issue Survival Pathways Involved in Resistance to Apoptosis in Cancer 2.0)
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