Aim
This study set out to determine the effect of methylation on MALAT1 gene in primary colorectal lesions and tumors to gain further knowledge about the diagnostic and prognostic value of MALAT. Background: Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is one of the long non-coding RNAs that plays an important role in invasion, cell proliferation, and metastasis of various cancers. However, there is insufficient information on the association between MALAT1 and the methylation process as well as its role in the development of colorectal cancer.
Background
Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is one of the long non-coding RNAs that plays an important role in invasion, cell proliferation, and metastasis of various cancers. However, there is insufficient information on the association between MALAT1 and the methylation process as well as its role in the development of colorectal cancer.
Conclusion
This study dealt with determining the effect of methylation on MALAT1 gene in primary colorectal lesions and tumors to gain further knowledge about the diagnostic and prognostic value of MALAT.
Methods
Methylation pattern of MALAT1 promoter was determined by Methylation-Specific Polymerase Chain Reaction (MSP) in 86 colorectal primary lesions, tumors, and normal specimens. MALAT1 methylation pattern was compared in tumor and polyp tissue. In order to obtain more accurate
Results
The results indicated that the MALAT1 promoter methylation pattern in the tumor tissue, primary lesion tissue, and normal was not significantly different (p=0.430). Comparison of the MALAT1 promoter methylation pattern between polyp types and tumor tissue groups was not significant either (p=0.437). Surprisingly, the methylation frequency of MALAT1 methylation was significantly higher in colon lesions than in their rectum lesion (p = 0.035). In addition, no significant hypermethylation of MALAT1 was observed between the other patients' clinicopathological data in both polyp 46/66 and tumor tissues 20/66.