Twist1 promotes gastric cancer cell proliferation through up-regulation of FoxM1

Twist-related protein 1 (Twist1), also known as class A basic helix-loop-helix protein 38 (bHLHa38), has been implicated in cell lineage determination and differentiation. Previous studies demonstrate that Twist1 expression is up-regulated in gastric cancer with poor clinical outcomes. Besides, Twis...

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Bibliographic Details
Published in:PloS one 2013-10, Vol.8 (10), p.e77625-e77625
Main Authors: Qian, Jianxin, Luo, Yizhou, Gu, Xiaoqiang, Zhan, Wang, Wang, Xi
Format: Article
Language:English
Subjects:
Apoptosis
Breast cancer
Cancer
Cell adhesion & migration
Cell cycle
Cell Cycle - genetics
Cell growth
Cell Line, Tumor
Cell lineage
Cell Proliferation
Event-related potentials
Forkhead Box Protein M1
Forkhead Transcription Factors - genetics
Forkhead Transcription Factors - metabolism
Gastric cancer
Gene Expression Regulation, Neoplastic - genetics
Helix-loop-helix proteins
Helix-loop-helix proteins (basic)
Humans
Immunoglobulins
Lung cancer
Metastasis
Nuclear Proteins - genetics
Nuclear Proteins - metabolism
Oncology
Promoter Regions, Genetic - genetics
Stomach cancer
Stomach Neoplasms - genetics
Transcription
Transcription factors
Transcription, Genetic - genetics
Transcriptional Activation - genetics
Twist-Related Protein 1 - genetics
Twist-Related Protein 1 - metabolism
Up-regulation
Up-Regulation - genetics
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Summary:Twist-related protein 1 (Twist1), also known as class A basic helix-loop-helix protein 38 (bHLHa38), has been implicated in cell lineage determination and differentiation. Previous studies demonstrate that Twist1 expression is up-regulated in gastric cancer with poor clinical outcomes. Besides, Twist1 is suggested to be involved in progression of human gastric cancer. However, its biological functions remain largely unexplored. In the present study, we show that Twist 1 overexpression leads to a significant up-regulation of FoxM1, which plays a key role in cell cycle progression in gastric cancer cells. In contrast, knockdown of Twist 1 reduces FoxM1 expression, suggesting that FoxM1 might be a direct transcriptional target of Twist 1. At the molecular level, we further reveal that Twist 1 could bind to the promoter region of FoxM1, and subsequently recruit p300 to induce FoxM1 mRNA transcription. Therefore, our results uncover a previous unknown Twist 1/FoxM1 regulatory pathway, which may help to understand the mechanisms of gastric cancer proliferation.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0077625