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Department of Genetics, Faculty of Advanced Science and Technology, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran. , f8forouzesh@gmail.com
Abstract:   (367 Views)
Background: Colorectal cancer is one of the most common cancers and among the most common causes of cancer death worldwide. Dexamethasone is a glucocorticoid medication which has anti-proliferative and anti-inflammatory properties that induce apoptosis and growth inhibition in human myeloma cell lines in vitro. The aim of the current study was to determine the effects of dexamethasone against human colorectal cancer HT-29 cell lines, relying on the expression of genes which are involved in extrinsic (Fas and Fasl) and intrinsic pathway of apoptosis (Bax and Bcl2).

Materials and methods: An experimental study was conducted.  HT-29 cell line was cultured and then treated with various concentrations of dexamethasone (from 0.1 to 1000 µM) for 24h, 48h, and 72h incubation. The cytotoxicity was measured using MTT assay and IC50 was determined. Then, RNA was extracted from treated and untreated cells and cDNA was synthesized. Gene expression was investigated using qReal-Time PCR method. Data analysis was performed using the livak method.
Results:  Dexamethasone at 1000µM significantly inhibited the growth of treated HT-29 cells after 24h, 48h, and 72h incubation and IC50 was 1000μM after 48h. After treating cells at IC50 concentration, the mRNA expression of Fas and FasL did not change significantly in comparison with untreated cells (p <0.05), while Bax and Bcl-2 mRNA expression increased and decreased respectively in comparison with untreated cells (p <0.05). Dexamethasone was effective against human colorectal cancer HT-29 cell line in a dose -dependent manner and induced the intrinsic genes of apoptosis.

Conclusion:  Dexamethasone can inhibit the growth of human colon cancer HT-29 cell lines and induces apoptosis through the intrinsic pathway of apoptosis, while it has no effect on the extrinsic pathway of apoptosis.
Type of Study: Original | Subject: Genetic
Received: 2019/04/12 | Accepted: 2019/07/14

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