Herbal formulation C168 attenuates proliferation and induces apoptosis in HCT 116 human colorectal carcinoma cells

Role of oxidative stress and DNA damage

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2 Citations (Scopus)

Abstract

The use of herbal formulations has gained scientific interest, particularly in cancer treatment. In this study, the herbal formulation of interest, denoted as C168, is a mixture of eight genera of plants. This study aims to investigate the antiproliferative effect of C168 methanol extract (CME) on various cancer cells and its underlying mechanism of action on the most responsive cell line, namely, HCT 116 cells. CME exerted antiproliferative activities on HCT 116 colorectal carcinoma cells and HepG2 hepatocellular carcinoma cells but not on CCD-841-CoN normal colon epithelial cells, Jurkat E6.1 lymphoblastic leukemic cells, and V79-4 Chinese hamster lung fibroblasts. Further investigation on HCT 116 cells showed that CME induced G2/M cell-cycle arrest and apoptosis. Treatment of CME induced oxidative stress in HCT 116 cells by increasing the superoxide anion level and decreasing the intracellular glutathione. CME also increased tail moment value and H2AX phosphorylation in HCT 116 cells, suggesting DNA damage as an early signal of CME induced apoptosis. Loss of mitochondrial membrane potential in CME-treated cells also indicated the involvement of mitochondria in CME induced apoptosis. This study indicated the selectivity of CME toward colon cancer cells with the involvement of oxidative damage as its possible mechanism of action.

Original languageEnglish
Article number2091085
JournalEvidence-based Complementary and Alternative Medicine
Volume2016
DOIs
Publication statusPublished - 2016

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DNA Damage
Methanol
Colorectal Neoplasms
Oxidative Stress
Apoptosis
HCT116 Cells
G2 Phase Cell Cycle Checkpoints
Mitochondrial Membrane Potential
Hep G2 Cells
Cricetulus
Cell Extracts
Superoxides
Colonic Neoplasms
Glutathione
Tail
Hepatocellular Carcinoma
Neoplasms
Mitochondria
Colon
Fibroblasts

ASJC Scopus subject areas

  • Complementary and alternative medicine

Cite this

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title = "Herbal formulation C168 attenuates proliferation and induces apoptosis in HCT 116 human colorectal carcinoma cells: Role of oxidative stress and DNA damage",
abstract = "The use of herbal formulations has gained scientific interest, particularly in cancer treatment. In this study, the herbal formulation of interest, denoted as C168, is a mixture of eight genera of plants. This study aims to investigate the antiproliferative effect of C168 methanol extract (CME) on various cancer cells and its underlying mechanism of action on the most responsive cell line, namely, HCT 116 cells. CME exerted antiproliferative activities on HCT 116 colorectal carcinoma cells and HepG2 hepatocellular carcinoma cells but not on CCD-841-CoN normal colon epithelial cells, Jurkat E6.1 lymphoblastic leukemic cells, and V79-4 Chinese hamster lung fibroblasts. Further investigation on HCT 116 cells showed that CME induced G2/M cell-cycle arrest and apoptosis. Treatment of CME induced oxidative stress in HCT 116 cells by increasing the superoxide anion level and decreasing the intracellular glutathione. CME also increased tail moment value and H2AX phosphorylation in HCT 116 cells, suggesting DNA damage as an early signal of CME induced apoptosis. Loss of mitochondrial membrane potential in CME-treated cells also indicated the involvement of mitochondria in CME induced apoptosis. This study indicated the selectivity of CME toward colon cancer cells with the involvement of oxidative damage as its possible mechanism of action.",
author = "Leong, {Lek Mun} and {Kok Meng}, Chan and Asmah Hamid and Jalifah Latip and Rajab, {Nor Fadilah}",
year = "2016",
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AU - Leong, Lek Mun

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AU - Rajab, Nor Fadilah

PY - 2016

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