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

Marilena Antunes-Ricardo, A. Hernández-Reyes, Ashanti C. Uscanga-Palomeque, Cristina Rodríguez-Padilla, Ana Carolina Martínez-Torres, Janet Alejandra Gutiérrez-Uribe

Research output: Contribution to journalArticle

3 Scopus citations

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.

Original languageEnglish (US)
Article number108734
JournalChemico-Biological Interactions
Volume310
DOIs
StatePublished - Sep 1 2019
Externally publishedYes

Keywords

  • Apoptosis
  • Colon cancer
  • Intrinsic pathway
  • Isorhamnetin glycosides
  • Opuntia ficus-Indica

ASJC Scopus subject areas

  • Toxicology

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