Oncotarget

Research Papers:

miR-31 targets ARID1A and enhances the oncogenicity and stemness of head and neck squamous cell carcinoma

Wen-Cheng Lu, Chung-Ji Liu, Hsi-Feng Tu, Yu-Tung Chung, Cheng-Chieh Yang, Shou-Yen Kao, Kuo-Wei Chang _ and Shu-Chun Lin

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Oncotarget. 2016; 7:57254-57267. https://doi.org/10.18632/oncotarget.11138

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Abstract

Wen-Cheng Lu1, Chung-Ji Liu2,3, Hsi-Feng Tu2, Yu-Tung Chung1, Cheng-Chieh Yang1,2,4, Shou-Yen Kao2,4, Kuo-Wei Chang1,2,4, Shu-Chun Lin1,2,4

1Institute of Oral Biology, National Yang-Ming University, Taipei, Taiwan

2Department of Dentistry, National Yang-Ming University, Taipei, Taiwan

3Department of Dentistry, MacKay Memorial Hospital, Taipei, Taiwan

4Department of Stomatology, Taipei Veterans General Hospital, Taipei, Taiwan

Correspondence to:

Kuo-Wei Chang, email: ckcw@ym.edu.tw

Shu-Chun Lin, email: sclin@ym.edu.tw

Keywords: ARID1A, cancer, miR-31, stem cell, suppressor

Received: April 13, 2016     Accepted: July 27, 2016     Published: August 9, 2016

ABSTRACT

miR-31 is oncogenic for head and neck squamous cell carcinoma (HNSCC). Proteins containing the AT-rich interacting domain (ARID) modulate the accessibility of chromatin to the transcription machinery needed for gene expression. In this study, we showed that miR-31 was able to target ARID1A in HNSCC. HNSCC tumors had an inverse miR-31 and ARID1A expression. miR-31 associated oncogenicities were rescued by ARID1A expression in HNSCC cells. Furthermore, ARID1A repressed the stemness properties and transcriptional activity of Nanog/OCT4/Sox2/EpCAM via the protein’s affinity for AT-rich sites within promoters. HNSCC patients with tumors having high level of miR-31 expression and high levels of Nanog/OCT4/Sox2/EpCAM expression, together with low level of ARID1A expression, were found to have the worst survival. This study provides novel mechanistic clues demonstrating that miR-31 inhibits ARID1A and that this enriches the oncogenicity and stemness of HNSCC.


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