Artemisia vulgaris Induces Tumor-Selective Ferroptosis and Necroptosis via Lysosomal Ca2+ Signaling.

Autor:	Zamarioli, Lucas dos Santos, Santos, Michele Rosana Maia, Erustes, Adolfo Garcia, Meccatti, Vanessa Marques, Pereira, Thaís Cristine, Smaili, Soraya S., Marcucci, Maria Cristina, Oliveira, Carlos Rocha, Pereira, Gustavo J. S., Bincoletto, Claudia
Předmět:	CANCER chemotherapy ORGANIC compound analysis CHINESE medicine LYSOSOMES IN vitro studies LIQUID chromatography-mass spectrometry RESEARCH funding BREAST tumors WORMWOOD CALCIUM-binding proteins APOPTOSIS NECROSIS CHRONIC myeloid leukemia CELLULAR signal transduction PHYTOCHEMICALS DESCRIPTIVE statistics FIBROBLASTS PLANT extracts CELL lines CELL death ORGANIC compounds CELL survival DATA analysis software
Zdroj:	Chinese Journal of Integrative Medicine; Jun2024, Vol. 30 Issue 6, p525-533, 9p
Abstrakt:	Objective: To evaluate the chemical composition and effects of Artemisia vulgaris (AV) hydroalcoholic extract (HEAV) on breast cancer cells (MCF-7 and SKBR-3), chronic myeloid leukemia (K562) and NIH/3T3 fibroblasts. Methods: Phytochemical analysis of HEAV was done by high-performance liquid chromatography-mass (HPLC) spectrometry. Viability and cell death studies were performed using trypan blue and Annexin/FITC-7AAD, respectively. Ferrostatin-1 (Fer-1) and necrostatin-1 (Nec-1) were used to assess the mode of HEAV-induced cell death and acetoxymethylester (BAPTA-AM) was used to verify the involvement of cytosolic calcium in this event. Cytosolic calcium measurements were made using Fura-2-AM. Results: HEAV decreased the viability of MCF-7, SKBR-3 and K562 cells (P<0.05). The viability of HEAV-treated K562 cells was reduced compared to HEAV-exposed fibroblasts (P<0.05). Treatment of K562 cells with HEAV induced cell death primarily by late apoptosis and necrosis in assays using annexin V-FITC/7-AAD (P<0.05). The use of Nec-1 and Fer-1 increased the viability of K562 cells treated with HEAV relative to cells exposed to HEAV alone (P<0.01). HEAV-induced Ca2+ release mainly from lysosomes in K562 cells (P<0.01). Furthermore, BAPTA-AM, an intracellular Ca2+ chelator, decreased the number of non-viable cells treated with HEAV (P<0.05). Conclusions: HEAV is cytotoxic and activates several modalities of cell death, which are partially dependent on lysosomal release of Ca2+. These effects may be related to artemisinin and caffeoylquinic acids, the main compounds identified in HEAV. [ABSTRACT FROM AUTHOR]
Databáze:	Complementary Index
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