RP11‑156L14.1 regulates SSR1 expression by competitively binding to miR‑548ao‑3p in hypopharyngeal squamous cell carcinoma.

Abstract

Emerging studies have demonstrated that long non-coding RNAs (lncRNAs) play essential roles in tumorigenesis. However, the role and function of lncRNAs in hypopharyngeal squamous cell carcinoma (HSCC) have not been completely elucidated. The present study explored the function of a novel lncRNA, RP11-156L14.1, in HSCC. RP11-156L14.1 was revealed to be highly expressed in HSCC tissues and cell lines. Knockdown of RP11-156L14.1 inhibited proliferation, migration, and invasion in HSCC cells. Furthermore, RP11-156L14.1 regulated epithelial-mesenchymal transition (EMT) by controlling EMT-related protein expression. Mechanistically, RP11-156L14.1 exerted its function as a competing endogenous RNA (ceRNA) and directly interacted with miR-548ao-3p. The present study also demonstrated that miR-548ao-3p regulated signal sequence receptor subunit 1 (SSR1) expression by targeting SSR1 3′-UTR. Moreover, the xenograft HSCC tumor model revealed that knockdown of RP11-156L14.1 markedly suppressed HSCC tumor growth in vivo. In summary, these findings indicated that the lncRNA RP11-156L14.1 functions as an oncogene in HSCC by competing with miR-548ao-3p in regulating SSR1 expression. The RP11-156L14.1/miR-548ao-3p/SSR1 axis could be utilized as a potential novel biomarker and therapeutic target for HSCC.