Silencing of long noncoding RNA MALAT1 by miR-101 and miR-217inhibits proliferation, migration and invasion of esophageal squamous cell carcinoma cells [Molecular Bases of Disease]

December 23rd, 2014 by Wang, X., Li, M., Wang, Z., Han, S., Tang, X., Ge, Y., Zhou, L., Zhou, C., Yuan, Q., Yang, M.

MALAT1, a highly conserved long noncoding RNA, is deregulated in several types of cancers. However, its role in esophageal squamous cell carcinoma (ESCC) and its posttranscriptional regulation remain poorly understood. In this study, we provide first evidences that a posttranscriptional regulation mechanism of MALAT1 by miR-101 and miR-217 exists in ESCC cells. This posttranscriptional silencing of MALAT1 could significantly suppress the proliferation of ESCC cells through the arrest of G2/M cell cycle, which may be due to MALAT1-mediated upregulation of P21 and P27 expression and the inhibition of B-MYB expression. Moreover, we also found the abilities of migration and invasion of ESCC cells were inhibited after overexpression of miR-101, miR-217 or MALAT1 siRNA. This might be attributed to the deregulation of down-stream genes of MALAT1, such as MIA2, HNF4G, ROBO1, CCT4 and CTHRC1. A significant negative correlation exists between miR-101 or miR-217 and MALAT1 in 42 pairs of ESCC tissue samples and adjacent normal tissues. Mice exnograft data also support the tumor suppressor role of both miRNAs in ESCC.
  • Posted in Journal of Biological Chemistry, Publications
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