Open AccessShort communication: Canarium odontophyllum Miq. (dabai) stem bark arrested HCT 116 cell line at G0/G1 checkpoint
Author(s) -
Dayang Fredalina Basri,
Ngieng Sheng Ee,
Nor Fadilah Rajab,
Dharrshine Yoganathan,
Raha Ahmad Raus
Publication year - 2021
Publication title -
asia-pacific journal of molecular biology and biotechnology/asia pacific journal of molecular biology and biotechnology
Language(s) - English
Resource type - Journals
eISSN - 2521-9839
pISSN - 0128-7451
DOI - 10.35118/apjmbb.2021.029.3.05
Subject(s) - cell cycle checkpoint , apoptosis , propidium iodide , traditional medicine , cell cycle , ic50 , chemistry , acetone , botany , biology , medicine , in vitro , biochemistry , programmed cell death
Canarium odontophyllum Miq. is an exotic plant which is native in Borneo and belong to the Burseraceae family. It contains phytochemicals such as saponin, terpenoid, flavonoid and phenolic compound with potential anticancer property. It has been found that the extract of this plant negatively affected colorectal cancer cells by stimulating apoptosis. To elucidate the apoptosis mechanism induced by the plant extract, this study evaluated the effect of C. odontophyllum stem bark acetone extract on cell cycle distribution of HCT 116 cell line using propidium iodide assay. For this purpose, IC50 of the acetone extract of C. odontophyllum was first determined by treating HCT 116 cells with the extract for 24, 48 and 72 hours. It was found that the acetone extract of C. odontophyllum inhibited proliferation of HCT 116 at IC50 value of 55.09 ± 18.29 µg/mL for 24 hours treatment, 37.81 ± 5.09 µg/mL for 48 hours treatment, and 114.9 ± 16.08 µg/mL following 72 hours treatment. Using IC50 value of 48 hours treatment, it was observed that C. odontophyllum acetone extract arrested the HCT 116 cells at G0/G1 checkpoint. Based on this result, it can be concluded that one of the apoptosis mechanisms induced by C. odontophyllum is by arresting cell cycle of HCT 116 cells at G0/G1 checkpoint. This finding warrants further investigation on how C. odontophyllum causes the cell cycle arrest and its potential to become anticancer agent.