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Antiproliferative and apoptosis inducing activity of Markhamia tomentosa leaf extract on HeLa cells
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Cancer Science & Therapy

ISSN: 1948-5956

Open Access

Antiproliferative and apoptosis inducing activity of Markhamia tomentosa leaf extract on HeLa cells


International Conference on Cancer Biology & Drug Delivery

September 18-19, 2017 | Philadelphia, USA

Ibrahim M Bolanle

University of Lagos, Nigeria

Posters & Accepted Abstracts: J Cancer Sci Ther

Abstract :

Markhamia tomentosa (Benth) K. Schum ex. Engl. (Bignoniaceae), a tree widely dispersed in west tropical Africa, is used traditionally to treat various diseases as it possesses antimicrobial, antioxidant, analgesic, anti-inflammatory and anticancer activities. This study evaluates the cytotoxic effect and underlying mechanisms of the ethanolic leaf extract of Markhamia tomentosa on HeLa and MCF-7 cancer cell lines and Vero non-cancerous cell line. Brine shrimp lethality test was used for preliminary screening. Cytotoxicity was determined using the MTT assay and IC50 was calculated. Effect of Markhamia tomentosa on the cell cycle was monitored by flow cytometry and the apoptosis-induction capability confirmed by exposure of phosphatidylserine to the outer leaflet of the plasma membrane. Loss of mitochondrial membrane potential was analyzed by flow cytometry using JC-1. Markhamia tomentosa leaf extract was toxic to brine shrimps with LD50 of 31.62 mg/ml. Cell viability and growth of HeLa cells was inhibited by the extract with an IC50 of 189.1�±1.76 mg/ml at 24 h post treatment. However, no cytotoxic effect was observed in MCF-7 and Vero cell lines. The extract induced cell cycle arrest in HeLa cells in the G0/G1 phase resulting in cell death after 24 h exposure. Induction of apoptosis in HeLa cells was substantiated by Annexin V-FITC/PI double staining showing phosphatidylserine translocation and depolarization of the mitochondrial membrane potential by flow cytometry of JC-1 stained cells. In conclusion, the ethanolic leaf extract of Markhamia tomentosa induces G0/G1 cell cycle arrest in HeLa cells followed by induction of the intrinsic pathway of apoptosis.

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