4.7 Article

FAM83A promotes proliferation and metastasis via Wnt/β-catenin signaling in head neck squamous cell carcinoma

期刊

JOURNAL OF TRANSLATIONAL MEDICINE
卷 19, 期 1, 页码 -

出版社

BMC
DOI: 10.1186/s12967-021-03089-6

关键词

FAM83A; Head Neck Squamous Cell Carcinoma; Wnt/beta-catenin Signaling; Proliferation; Metastasis

资金

  1. Nature Science Foundation of Jiangsu Province [BK20180669]
  2. Health Committee of Jiangsu Province [M2020003]

向作者/读者索取更多资源

This study identifies FAM83A as an oncogene of HNSCC with overexpression significantly associated with tumor size, lymph node status, and clinical tumor stages. FAM83A promotes HNSCC cell growth and metastasis by inducing EMT through activation of the Wnt/beta-catenin signaling pathway. Knockdown of FAM83A suppresses tumor growth and distant metastasis in xenograft animal models of HNSCC.
This research aimed to investigate the expression and function of FAM83A in the proliferation and metastasis in head and neck squamous cell carcinoma (HNSCC). FAM83A mRNA and protein expressions in HNSCC were detected in primary HNSCC samples and cell lines. The associations between FAM83A expression and clinicopathologic variables were evaluated through tissue microarrays. Besides, FAM83A knockdown and overexpression cell lines were constructed to assess cell growth and metastasis in vitro and the relationship between FAM83A and epithelial-mesenchymal transition (EMT). Furthermore, two models of xenograft tumors in nude mice were used to assess the tumorigenicity and metastasis ability of FAM83A in vivo. In the present study, overexpression of FAM83A in HNSCC samples was significantly associated with tumor size, lymph node status and clinical tumor stages. Mechanically, FAM83A could promote HNSCC cell growth and metastasis by inducing EMT via activating Wnt/beta-catenin signaling pathway. Rescue experiment demonstrated the inhibition of beta-catenin could counteract the function of FAM83A. Also, the FAM83A knockdown could suppress tumor growth and distant metastasis in the xenograft animal models of HNSCC. In conclusion, this study identifies FAM83A as an oncogene of HNSCC. This study provides new insights into the molecular pathways that contribute to EMT in HNSCC. We revealed a previously unknown FAM83A-Wnt-beta-catenin signaling axis involved in the EMT of HNSCC. There may be a potential bi-directional signaling loop between FAM83A and Wnt/beta-catenin signaling pathway in HNSCC.

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