Isorhamnetin glycoside isolated from Opuntia ficus-indica (L.) MilI induces apoptosis in human colon cancer cells through mitochondrial damage. (1st September 2019)

• Record Type: Journal Article
• Authors: Antunes-Ricardo, Marilena; Hernández-Reyes, Annia; Uscanga-Palomeque, Ashanti C.; Rodríguez-Padilla, Cristina; Martínez-Torres, Ana Carolina; Gutiérrez-Uribe, Janet Alejandra
• Is Part Of: Chemico-biological interactions. Volume 310(2019)
• Publication Date: 2019-09-01
• Subjects: Apoptosis -- Colon cancer -- Intrinsic pathway -- Isorhamnetin glycosides -- Opuntia ficus-Indica; Biochemistry -- Periodicals; Toxicological chemistry -- Periodicals; Biochemistry -- Periodicals; Biologie moléculaire -- Périodiques; Biochimie -- Périodiques; Toxicologie biochimique -- Périodiques; 572
• DOI: 10.1016/j.cbi.2019.108734
• Languages: English
• ISSNs: 0009-2797

Abstract

Abstract: This work aimed to evaluate the mechanisms involved in the apoptosis induction of isorhamnetin-3- O -glucosyl-pentoside (IGP) in metastatic human colon cancer cells (HT-29). To achieve this, we assessed phosphatidylserine (PS) exposure, cell membrane disruption, chromatin condensation, cell cycle alterations, mitochondrial damage, ROS production, and caspase-dependence on cell death. Our results showed that IGP induced cell death on HT-29 cells through PS exposure (48%) and membrane permeabilization (30%) as well as nuclear condensation (54%) compared with control cells. Moreover, IGP treatment induced cell cycle arrest in G2/M phase. Bax/Bcl-2 ratio increased and the loss of mitochondrial membrane potential (63%) was observed in IGP-treated cells. Finally, as apoptosis is a caspase-dependent cell death mechanism, we used a pancaspase-inhibitor (Q-VD-OPh) to demonstrate that the cell death induced by IGP was caspase-dependent. Overall these results indicated that IGP induced apoptosis through caspase-dependent mitochondrial damage in HT-29 colon cancer cells. Highlights: Isorhamnetin glycoside IGP treatment induces cell cycle arrest in G2/M phase. Isorhamnetin glycoside IGP induced apoptosis by the modulation of the Bax/Bcl-2 expression. IGP induced apoptosis through mitochondrial damage and the increase of ROS levels.