Journal
ONCOTARGET
Volume 7, Issue 35, Pages 57254-57267Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.11138
Keywords
ARID1A; cancer; miR-31; stem cell; suppressor
Categories
Funding
- Ministry of Science and Technology [MOST102-2628-B-010-011-MY3, MOST103-2314-B-010-020-MY3]
- Ministry of Health and Welfare for Excellence for Cancer Research [MOHW105-TDU-B-211-134-003]
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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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