Abstract
Laryngeal squamous cell carcinoma (LSCC) is one of the most commonly seen head and neck malignancies. Identifying potent markers and/or targets for early diagnosis and individualized therapies for LSCC remains a considerable challenge. The present study analyzed online data and identified lncRNA KRT16P2 as a significantly upregulated long non-coding RNA (lncRNA) in LSCC. KRT16P2 knockdown in LSCC cells inhibited cancer cell proliferation, invasion, and migration. Similar to KRT16P2, EGFR expression was also significantly upregulated in LSCC. KRT16P2 and EGFR were positively correlated in LSCC tissue samples. EGFR knockdown also dramatically inhibited LSCC cell proliferation and aggressiveness (invasion and migration). Through online data and online tools, miR-1294 was predicted to target KRT16P2 and EGFR 3'UTR simultaneously. KRT16P2 inhibited miR-1294 expression, and miR-1294 inhibited EGFR expression through direct binding. miR-1294 overexpression repressed LSCC cell proliferation and aggressiveness. The effects of KRT16P2 silence on the expression of EGFR, LSCC cell proliferation, invasion, and migration, the protein levels of ki-67, PCNA, and cleaved-Caspase 3, as well as the phosphorylation of AKT, were all significantly reversed by miR-1294 inhibition. In conclusion, we demonstrated a lncRNA KRT16P2/miR-1294/EGFR axis that regulates LSCC cell proliferation, invasion, and migration. The clinical application of this axis needs further in vivo and clinical investigation.