These results suggest that miR-141 functions as a tumor suppressor in HNSCC and that it suppresses tumor growth and metastasis by suppressing EGFR signaling.
In addition, SNHG15 presented a downside tendency on regulating miR-141, and the miR-141 inhibitor dramatically changeover the impacts of SNHG15 depression on tumor growth and metastasis.
The effects of miR-141 mimics were investigated with respect to angiogenesis by vascular endothelial growth factor (VEGF), epithelial-mesenchymal transition (EMT) by E-cadherin, metastasis by Igfbp-4 and Tinagl1 enzyme-linked immunosorbent assays, invasion by an invasion chamber, and apoptosis by Annexin V.
Moreover, the expression levels of miR-182, miR-183, miR-141, and miR-21 were demonstrated to be associated with a gradual increase in fold change expression with depth of tumor invasion (all P < .05), lymph node invasion (all P < .001), and maximal increase with distant metastasis (all P < .001).