SIX4 的上调表明食管鳞癌的临床预后不良，并促进肿瘤生长和细胞转移。
Upregulation of SIX4 indicates poor clinical outcome and promotes tumor growth and cell metastasis in esophageal squamous cell carcinoma.
机构信息
Department of Gastroenterology, Rizhao Hospital of TCM, Rizhao, China.
Outpatient Department, Qingdao Eighth People's Hospital, Qingdao, China.
出版信息
Thorac Cancer. 2021 Mar;12(6):752-759. doi: 10.1111/1759-7714.13832. Epub 2021 Jan 22.
BACKGROUND
The role of sine oculis homeobox 4 (SIX4) has been found in some malignant tumors. However, there have been few studies on the function of SIX4 in esophageal squamous cell carcinoma (ESCC). This study aimed to explore the regulatory mechanism of SIX4 in ESCC.
METHODS
RT-qPCR and Western blot analysis were used to measure mRNA and protein expression. The function of SIX4 was investigated using CCK-8, colony formation, flow cytometry, wound healing and transwell assays. A mouse xenograft tumor assay was designed to perform in vivo experiments.
RESULTS
SIX4 was upregulated in ESCC and indicated poor clinical outcomes in ESCC patients. Functionally, knockdown of SIX4 inhibited cell proliferation and induced apoptosis in ESCC. In addition, the silencing of SIX4 inhibited cell migration, invasion and EMT in ESCC. More importantly, upregulation of SIX4 could activate the PI3K/AKT pathway in ESCC cells and promote tumor growth in vivo.
CONCLUSIONS
Upregulation of SIX4 indicates poor clinical outcomes in ESCC patients and promotes tumor growth and cell metastasis in ESCC.
背景
sine oculis 同源盒 4（SIX4）的作用已在一些恶性肿瘤中发现。然而，关于 SIX4 在食管鳞状细胞癌（ESCC）中的功能研究甚少。本研究旨在探讨 SIX4 在 ESCC 中的调控机制。
方法
使用 RT-qPCR 和 Western blot 分析测量 mRNA 和蛋白表达。通过 CCK-8、集落形成、流式细胞术、划痕愈合和 Transwell 测定来研究 SIX4 的功能。设计了小鼠异种移植肿瘤实验来进行体内实验。
结果
SIX4 在 ESCC 中上调，并预示 ESCC 患者的临床结局不良。功能上，SIX4 的敲低抑制 ESCC 中的细胞增殖并诱导细胞凋亡。此外，SIX4 的沉默抑制 ESCC 中的细胞迁移、侵袭和 EMT。更重要的是，SIX4 的上调可激活 ESCC 细胞中的 PI3K/AKT 通路，并促进体内肿瘤生长。
结论
SIX4 的上调预示 ESCC 患者的临床结局不良，并促进 ESCC 中的肿瘤生长和细胞转移。
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