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Extracellular vesicles of Janthinobacterium lividum as violacein carriers in melanoma cell treatment.

ABSTRACT: Violacein, a bisindole derivative produced, among others, by bacteria of the genus Janthinobacterium and Chromobacterium, is a compound with proven antimicrobial, anticancer and immunomodulatory properties. The anti-cancer activity of violacein has been tested on many cancer cells, including lung cancer cells, colorectal adenoma cells, acute myeloid leukaemia cells and melanoma cells. Interestingly, in a mouse model, a large difference in the response of cancerous and non-cancerous cells to violacein was observed, further highlighting the therapeutic potential of this compound. In addition, violacein has been observed to reduce the invasive potential of melanoma cells and has a much more potent anticancer effect than temozolomide, a drug used to treat melanoma. Violacein can be isolated from the bacterial cell pellet using solvents, and this metabolite is also secreted into the medium in a form enclosed in extracellular vesicles (EVs), in which the normally insoluble violacein remains suspended in water. The project focuses on the development of an efficient method of violacein application based on the use of EVs. Violacein-containing EVs were isolated from the culture of Janthinobacterium sp. and characterised by their appearance, size and protein composition. The activity of isolated EVs containing violacein was compared with the activity of violacein traditionally isolated from cells using solvents against four skin cell lines (cancerous and non-cancerous)

INSTRUMENT(S): Orbitrap Exploris 480

ORGANISM(S): Janthinobacterium Lividum

TISSUE(S): Cell Culture

SUBMITTER: Ewa Sitkiewicz

LAB HEAD: Małgorzata Milner-Krawczyk

PROVIDER: PXD050374 | Pride | 2024-12-10

REPOSITORIES: Pride

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			Action	DRS
	211184047miln_EVs1.dat	Other
	211184047miln_EVs1.raw	Raw
	211184047miln_EVs1.xml.gz	Xml
	211184048miln_EVs2.dat	Other
	211184048miln_EVs2.raw	Raw

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Acute depletion of the ARID1A subunit of SWI/SNF complexes reveals distinct pathways for EP300 dependent activation and repression of transcription.

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