Seyed Mohammad Amin Kormi - Cancer Genetics Research Unit, Reza Radiation Oncology Center, Mashhad, Iran
Gholamreza Motalleb - University Of Zabol
Mohammad Amin Kerachian - Department Of Medical Genetics, Faculty Of Medicine, Mashhad University Of Medical Sciences (MUMS), Mashhad, Iran
Shima Ardehkhani - University Of Applied Science And Technology, Tehran, Iran

Colorectal cancer is the third most commonly diagnosed cancer and the third leading cause ofcancer death in both men and women in the US. It has low survival, poor prognosis and the highestincidence rate in all of the world. So, investigating its underlying mechanisms is essential for earlydetection and treatment. Several genetic and epigenetics alterations are involved in carcinogenesisof colorectal cancer. Among them, promoter hyper-methylation is an important epigeneticmechanism of gene silencing. Otherwise, down regulation of tropomyosin isoforms, a family ofcytoskeleton proteins, has been shown important in colorectal cancer. So, the role of promoterhyper-methylation in tropomyosin suppression was investigated in several studies in colorectalcancer. In this review, we are focusing on the crucial role of epigenetic changes in tropomysin incolorectal cancer. Methylase enzyme inhibition significantly increases TM1 expression.Additionally, TPM1 and TPM2 mRNA are unregulated upon inhibition of methylation. Bisulfitesequencing showed considerable cytosine methylation in metastatic cell lines that correlated with areduced expression of TPM1 and TPM2. Nearly all of the studies suggest that epigeneticsuppression of TPM1 and TPM2 may change TGF beta tumor suppressor function and cause tometastatic properties of tumor cells. Furthermore, promoter hyper-methylation of TPM1 and TPM2genes seems to play an important role in tropomyosin down regulation in ESCC.