期刊
JOURNAL OF CELLULAR BIOCHEMISTRY
卷 123, 期 7, 页码 1247-1258出版社
WILEY
DOI: 10.1002/jcb.30295
关键词
cancer hallmarks; colorectal cancer; epithelial-mesenchymal transition; violacein
资金
- Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior [88882.329748/2019-01, 88887.373112/2019-00, 88887.657592/2021-00]
- Fundacao de Amparo a Pesquisa do Estado de Sao Paulo [2015/20412-7, 2017/16625-0, 2018/03593-6, 2017/08119-8, 2020/04409-4, 2014/50938-8]
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico [465699/2014-6, 303900/2017-2]
This study evaluates the ability of violacein to interfere with cancer hallmarks and demonstrates its inhibitory effects on cell migration and signaling pathways in colorectal cancer cells and spheroids. These findings further reinforce the potential of violacein as an antitumor agent.
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 PKC delta 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-beta, 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.
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