Author/Authors :
Alipour، Mohsen نويسنده , , Zargar، Seyed Jalal نويسنده Dept. of Cell and Molecular Biology, School of Biology, College of Science, University of Tehran, Tehran, Iran , , Safarian، Shahrokh نويسنده , , Fouladdel، Shamileh نويسنده Dept. of Pharmacology and Toxicology, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran , , Azizi، Ebrahim نويسنده , , Jafargholizadeh، Naser نويسنده Dept. of Cell and Molecular Biology, School of Biology, College of Science, University of Tehran, Tehran, Iran ,
Abstract :
Abstract
Background: The Bcl-2 protein family members have known as essential controllers of mitochondrial pathway of apoptosis. Bax is a proapoptotic member of Bcl-2 protein family, which is well known to play crucial roles for apoptosis control. bax has been implicated as potential tumor suppressor in certain solid tumors such as breast and colorectal carcinoma. DNA methylation of promoter associated CpG islands has known as a common mechanism for gene inactivation in tumor cells.
Methods: The Methylation Specific PCR (MSP) has used to find the methylation profile of the bax gene promoter CpG islands in colorectal and breast cancer cell lines.
Results: We have not detected any kind of "CpG islands hypermethylation" in promoter region of the bax gene in T47D, MCF7 (as ER positive), MDA-MB-231 and MDA-MB-468 (as ER negative) breast carcinoma-derived cell lines and colorectal cancer cell lines H29 and Caco II.
Conclusion: It seems that CpG island methylation could not play the main role in down-regulation of bax gene in breast and colon cancers.
