Original Research ARTICLE
Identification of minimal p53 promoter region regulated by MALAT1 in human lung adenocarcinoma cells
- 1Isotope Science Center, The University of Tokyo, Japan
- 2National Institute of Health Sciences (NIHS), Japan
- 3Tokyo University of Science, Japan
- 4Kyushu Institute of Technology, Japan
- 5The University of Tokyo, Japan
The MALAT1 long noncoding RNA is strongly linked to cancer progression. Here we report a MALAT1 function in repressing the promoter of p53 (TP53) tumor suppressor gene. p21 and FAS, well-known p53 targets, were upregulated by MALAT1 knockdown in A549 human lung adenocarcinoma cells. We found that these upregulations were mediated by transcriptional activation of p53 through MALAT1 depletion. In addition, we identified a minimal MALAT1-responsive region in the P1 promoter of p53 gene. Flow cytometry analysis revealed that MALAT1-depleted cells exhibited G1 cell cycle arrest. These results suggest that MALAT1 affects the expression of p53 target genes through repressing p53 promoter activity, leading to influence the cell cycle progression.
Keywords: noncoding RNA, TP53, Transcription, Genetic, Adenocarcinoma, Promoter Regions, Genetic
Received: 03 Aug 2017;
Accepted: 27 Nov 2017.
Edited by:Kinji Ohno, Nagoya University, Japan
Reviewed by:Tohru Yoshihisa, University of Hyogo, Japan
Akio Masuda, Nagoya University Graduate School of Medicine, Japan
Copyright: © 2017 Tano, Onoguchi-Mizutani, Uchiumi, Yada, Suzuki and Akimitsu. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Dr. Nobuyoshi Akimitsu, The University of Tokyo, Isotope Science Center, Bunkyō, Japan, email@example.com