miR-31 targets ARID1A and enhances the oncogenicity and stemness of head and neck squamous cell carcinoma
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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
Kuo-Wei Chang, email: email@example.com
Shu-Chun Lin, email: firstname.lastname@example.org
Keywords: ARID1A, cancer, miR-31, stem cell, suppressor
Received: April 13, 2016 Accepted: July 27, 2016 Published: August 9, 2016
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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