Apoptosis Induction of Agave lechuguilla Torrey Extract on Human Lung Adenocarcinoma Cells (SK-LU-1)
Autor: | María Eugenia Jaramillo-Flores, Jorge L. Rosas-Trigueros, Eugenia del Carmen Lugo-Cervantes, Luis Alberto Anguiano-Sevilla, Cynthia Ordaz-Pichardo |
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Jazyk: | angličtina |
Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
MAPK/ERK pathway Programmed cell death Necroptosis Catalysis Inorganic Chemistry lcsh:Chemistry 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Physical and Theoretical Chemistry Fragmentation (cell biology) Molecular Biology lcsh:QH301-705.5 Spectroscopy cytotoxic activity mass spectrometry biology Organic Chemistry apoptosis General Medicine molecular docking biology.organism_classification Molecular biology Computer Science Applications 030104 developmental biology chemistry lcsh:Biology (General) lcsh:QD1-999 Apoptosis Cell culture Agave lechuguilla 030220 oncology & carcinogenesis Kaempferol |
Zdroj: | International Journal of Molecular Sciences Volume 19 Issue 12 International Journal of Molecular Sciences, Vol 19, Iss 12, p 3765 (2018) |
ISSN: | 1422-0067 |
DOI: | 10.3390/ijms19123765 |
Popis: | In this study, an ethanol extract of Agave lechuguilla was evaluated against six carcinogenic cell lines (HCT-15, MCF-7, PC-3, U-251, SK-LU-1 and K-562) with an inhibition of 75.7 ± 2.3% against the SK-LU-1 line. Based on the previous result, the extract was hydrolyzed and fractionated, to which the IC50 was determined the cell line was more sensitive to the fractionated extract with an IC50 6.96 ± 0.15 µ g/mL. Characterization by mass spectrometry showed the presence of kaempferol, quercetin and a flavonoid dimer formed by afzelechin-4&beta 8-quercetin, according to the generated fragmentation pattern. The fractionated extract presented cell death by apoptosis with 39.8% at 24 h. Molecular docking was performed with the molecules found to try to describe cell death by apoptosis through death receptors such as FasCD95, TNF-R1, DR4/5 and blocking signaling on the EGFR and K-Ras MAPK/ERK pathway, as well as through the intrinsic pathway activating tBID, which promotes the amplification of the apoptotic signal due to the activation of caspase-3, and consequently caspase-7. In addition to the activation of the IIb complex associated with cell death due to necroptosis. |
Databáze: | OpenAIRE |
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