Actin-like 6A enhances the proliferative and invasive capacities of laryngeal squamous cell carcinoma by potentiating th
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Actin-like 6A enhances the proliferative and invasive capacities of laryngeal squamous cell carcinoma by potentiating the activation of YAP signaling Yabin Dang 1 & Ligang Zhang 1 & Xiaoyan Wang 2 Received: 4 September 2020 / Accepted: 11 October 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
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 upregulation 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. Keywords Actin-like 6A . Laryngeal squamous cell carcinoma . YAP
Introduction Laryngeal squamous cell carcinoma (LSCC), the primary pathological type of malignant larynx tumor, is an aggressive malignancy with high rates of incidence and mortality (Genden et al. 2007; Bray et al. 2018). Although cancer treatment options have improved throughout recent decades, the prognosis of LSCC patients remains poor, especially for those diagnosed at advanced stages and those prone recurrence and metastasis (Marur and Forastiere 2016; Steuer et al. 2017). Various genetic features of LSCC have been described, however the precise molecular mechanisms that facilitate LSCC oncogenesis remain largely unknown (Makitie and Monni 2009). Therefore, it is important to uncover key genes that * Xiaoyan Wang [email protected] 1
Department of Otolaryngology, Xianyang Hospital of Yan’an University, Xianyang City 712000, Shaanxi Province, China
2
Department of Otolaryngology, Xianyang Central Hospital, 78 Renmin East Road, Xianyang City 712000, Shaanxi Province, China
play pivotal roles in the pathogenesis of LSCC in order to identify promising molecular targets for LSCC treatment. Actin-like 6A (ACTL6A) is a core component of the SWItch/Sucrose NonFermentable complex that plays a vital role in LSCC development and disease onset (Wu 2012; Son and Crabtree 2014; Panwalkar et al. 2020). ACTL6A mod
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