Violacein negatively modulates the colorectal cancer survival and epithelial-mesenchymal transition.

Autor: de Souza Oliveira PF; Department of Biochemistry and Tissue Biology, University of Campinas, UNICAMP, Campinas, São Paulo, Brazil., Faria AVS; Department of Biochemistry and Tissue Biology, University of Campinas, UNICAMP, Campinas, São Paulo, Brazil., Clerici SP; Department of Biochemistry and Tissue Biology, University of Campinas, UNICAMP, Campinas, São Paulo, Brazil., Akagi EM; Department of Biochemistry and Tissue Biology, University of Campinas, UNICAMP, Campinas, São Paulo, Brazil., Carvalho HF; Department of Biochemistry and Tissue Biology, University of Campinas, UNICAMP, Campinas, São Paulo, Brazil., Justo GZ; Department of Pharmaceutical Sciences and Biochemistry, Federal University of São Paulo (UNIFESP-Diadema), São Paulo, Brazil., Durán N; Laboratory of Urogenital Carcinogenesis and Immunotherapy, Department of Structural and Functional Biology, University of Campinas (UNICAMP), Campinas, São Paulo, Brazil.; Nanomedicine Research Unit (Nanomed), Center for Natural and Human Sciences (CCNH), Federal University of ABC (UFABC), Santo André, Brazil., Ferreira-Halder CV; Department of Biochemistry and Tissue Biology, University of Campinas, UNICAMP, Campinas, São Paulo, Brazil.
Jazyk: angličtina
Zdroj: Journal of cellular biochemistry [J Cell Biochem] 2022 Jul; Vol. 123 (7), pp. 1247-1258. Date of Electronic Publication: 2022 Jun 06.
DOI: 10.1002/jcb.30295
Abstrakt: Violacein is a secondary metabolite produced by several microorganisms including Chromobacterium violaceum, and it is already used in food and cosmetics. However, due to its potent anticancer and low side effects, its molecular action needs to be deeply scrutinized. Therefore, the main objective of this study was to evaluate the violacein's ability to interfere with three cancer hallmarks: growth factors receptor-dependent signaling, proliferation, and epithelial-mesenchymal transition (EMT). Violacein has been associated with the induction of apoptosis in colorectal cancer (CRC) cells. Here, we demonstrate that this molecule is also active in CRC spheroids and inhibits cell migration. Violacein treatment reduced the amount of EGFR and AXL receptors in the HT29 cell line. Accordingly, the inhibition of the AKT, ERK, and PKCδ kinases, which are downstream mediators of the signaling pathways triggered by EGFR and AXL, is detected. Another interesting finding was that even when the cells were stimulated with transforming growth factor-β, the EMT marker (N-cadherin) decreased. Therefore, this study provides further evidence that reinforces the potential of violacein as an antitumor agent, once this biomolecule can "switch off" properties associated with cancer plasticity.
(© 2022 Wiley Periodicals LLC.)
Databáze: MEDLINE
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