In a new study, researchers revealed that the metastasis-associated gene 1 (MTA1) is “upregulated,” or increased as a result of another variable, in malignant pleural mesothelioma (MPM), and that it can enhance metastasis and lead to poor survival rates.
The research article, “MTA1 promotes metastasis of MPM via suppression of E-cadherin,” was published in the Journal of Experimental & Clinical Cancer Research.
MTA1 is the first discovered gene from the newly identified MTA family, a group of cancer progression-related genes. MTA1 and its correspondent protein have been found to be overexpressed in a series of human cancers, such as hepatocellular and colorectal carcinomas, and non-small cell lung cancers.
The role and potential value of MPA1 as a biomarker have not yet been studied in MPM, a rare and aggressive form of cancer that affects the pleura, the membrane lining of the lungs, mainly attributed to the exposure to asbestos.
Researchers investigated the role of MTA1 in MPM pathogenesis by analyzing MPM and adjacent-to-tumor tissues from 65 patients. The team measured the expression levels of MTA1 and E-cadherin, a protein encoded by the CDH1 tumor suppressor gene and whose loss of expression results in enhanced cellular motility, being associated with cancer metastasis and progression. The effects of the knockdown of MTA1 in MPM cell lines were also evaluated, as well as the migration and invasion patterns of MPM cells.
The results showed that MTA1 expression in the MPM tissues was higher than in the adjacent tissues, while E-cadherin was found to have the opposite expression pattern. Furthermore, MTA1 knockdown was correlated with an increase in E-cadherin expression.
The findings led the researchers to theorize that decreased expression of MTA1 could enhance E-cadherin expression in MPM cells. And, researchers observed that tissue samples from patients with higher levels of MTA1 expression had a significantly shorter overall survival compared with patients with lower expression levels of MTA1. The team therefore suggested that MTA1 overexpression could potentially be a marker for poor prognosis.
“MTA1 expression is upregulated in MPM and shown a negative correlation with E-cadherin expression. MTA1 could enhance the invasion and migration of MPM cells via suppressing the expression of E-cadherin. MTA1 overexpression is associated with pathology, metastasis and survival rate of MPM patients,” the team concluded in its study. “MTA1 is a novel biomarker and indicative of a poor prognosis in MPM patients.”
Further studies are required to better understand the role of MTA1 in tumorigenesis and metastasis development.
