Actin-like 6A enhances the proliferative and invasive capacities of laryngeal squamous cell carcinoma by potentiating the activation of YAP signaling.

Abstract

Overexpression of Actin-like 6A (ACTL6A) has been observed in a wide spectrum of tumors and exerts an outstanding oncogenic function throughout cancer progression. However, the detailed relevance of ACTL6A for laryngeal squamous cell carcinoma (LSCC) is not fully understood. In this work, we aimed to elucidate the precise role of ACTL6A in LSCC. Here, we show that ACTL6A expression was significantly upregulated in LSCC versus normal tissues. In vitro functional assays demonstrated that silencing of ACTL6A significantly diminished the capacity of LSCC cells to proliferate and invade, whilst up-regulation of ACTL6A drove proliferation and invasion in LSCC cells. Further investigation revealed that knockdown of ACTL6A repressed the activation of Yes-associated protein (YAP)-mediated signaling in LSCC cells, while reactivation of YAP markedly reversed ACTL6A-silencing-mediated inhibition of proliferation and invasion in LSCC cells. Moreover, suppression of YAP markedly diminished ACTL6A-overexpression-induced promotion of tumor formation in LSCC. In addition, ACTL6A silencing diminished the tumorigenicity of LSCC cells in vivo. To summarize, our work indicates that ACTL6A may enhance LSCC progression via potentiating the activation of YAP signaling. Thus, ACTL6A may be an attractive anticancer target for the treatment of LSCC.