Alipour Mohsen, Zargar Seyed Jalal, Safarian Shahrokh, Fouladdel Shamileh, Azizi Ebrahim, Jafargholizadeh Naser
Dept. of Cell and Molecular Biology, School of Biology, College of Science, University of Tehran, Tehran, Iran.
Dept. of Pharmacology and Toxicology, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran.
Iran J Cancer Prev. 2013 Spring;6(2):59-64.
The Bcl-2 protein family members have known as essential controllersof mitochondrial pathway of apoptosis. 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.
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.
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.
It seems that CpG island methylation could not play the main role in down-regulation of bax gene in breast and colon cancers.
Bcl-2蛋白家族成员被认为是细胞凋亡线粒体途径的关键调控因子。Bax在某些实体瘤如乳腺癌和结直肠癌中被认为是潜在的肿瘤抑制因子。启动子相关CpG岛的DNA甲基化是肿瘤细胞中基因失活的常见机制。
采用甲基化特异性PCR（MSP）检测结直肠癌和乳腺癌细胞系中bax基因启动子CpG岛的甲基化情况。
在T47D、MCF7（雌激素受体阳性）、MDA-MB-231和MDA-MB-468（雌激素受体阴性）乳腺癌来源的细胞系以及结直肠癌细胞系H29和Caco II中，我们未在bax基因启动子区域检测到任何类型的“CpG岛高甲基化”。
在乳腺癌和结肠癌中，CpG岛甲基化似乎并非bax基因下调的主要机制。
