ELOVL6 promotes the progression of head and neck squamous cell carcinoma via activating WNT/β‐catenin pathway

头颈部鳞状细胞癌 生物 Wnt信号通路 癌症研究 基因敲除 细胞生长 流式细胞术 癌症 信号转导 细胞凋亡 分子生物学 头颈部癌 细胞生物学 遗传学 生物化学
作者
Ruoya Wang,Xianzhi Liu,Xiyao Li,Ming Qian,Xi Yang,Qi‐Chuan Jiang,Yijie Wang,Hao Liu,Jianguo Chen,Xuefeng Wang,Liang Gong
出处
期刊:Molecular Carcinogenesis [Wiley]
卷期号:63 (6): 1079-1091 被引量:2
标识
DOI:10.1002/mc.23710
摘要

Abstract This study was to explore the role of ELOVL6 in the development of head and neck squamous cell carcinoma (HNSCC). Considering its previously identified oncogenic role in hepatocellular carcinoma. ELOVL6 gene expression, clinicopathological analysis, enrichment analysis, and immune infiltration analysis were based on the data from Gene Expression Omnibus and The Cancer Genome Atlas, with additional bioinformatics analyses performed. Human HNSCC tissue microarray and cell lines were used. The expression of ELOVL6 in HNSCC was detected by quantitative polymerase chain reaction, immunohistochemistry assay, and western blot analysis. The proliferation ability of HNSCC cells, invasion, and apoptosis were evaluated using cell counting kit‐8 method, Transwell assay, and flow cytometry, respectively. Based on the data derived from the cancer databases and our HNSCC cell and tissue studies, we found that ELOVL6 was overexpressed in HNSCC. Moreover, ELOVL6 expression level had a positive correlation with clinicopathology of HNSCC. Gene set enrichment analysis showed that ELOVL6 affected the occurrence of HNSCC through WNT signaling pathway. Functional experiments demonstrated that ELOVL6 knockdown inhibited the proliferation and invasion of HNSCC cells while promoting apoptosis. Additionally, compound 3f, an agonist of WNT/β‐catenin signaling pathway, enhances the effect of ELOVL6 on the progression of HNSCC cells. ELOVL6 is upregulated in HNSCC and promotes the development of HNSCC cells by inducing WNT/β‐catenin signaling pathway. ELOVL6 stands a potential target for the treatment of HNSCC and a prognosis indicator of human HNSCC.
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