DLX6 promotes cell proliferation and survival in oral squamous cell carcinoma

被引:10
|
作者
Liang, Jun [1 ]
Liu, Jingang [2 ]
Deng, Zhaoming [1 ]
Liu, Zhigang [3 ]
Liang, Lizhong [1 ]
机构
[1] Sun Yat Sen Univ, Affiliated Hosp 5, Dept Oral & Maxillofacial Surg, 52 Meihua East Rd, Zhuhai 519000, Peoples R China
[2] Zhuhai Peoples Hosp, Dept Stomatol, Zhuhai, Peoples R China
[3] Sun Yat Sen Univ, Affiliated Hosp 5, Canc Ctr, Dept Head & Neck Oncol,Phase Clin Trial Ward 1, 52 Meihua East Rd, Zhuhai 519000, Peoples R China
关键词
apoptosis; distal‐ less homeobox 6; oral squamous cell carcinoma; proliferation; SIGNALING PATHWAY; DOWN-REGULATION; GENES; EXPRESSION; HEAD;
D O I
10.1111/odi.13728
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
Objective Distal-less homeobox 6 (DLX6) has been reported to play important roles in the development of craniofacial structures, inner ear, limb, and brain. We found in our previous investigation that DLX6 was significantly highly expressed in oral cancer tissues in The Cancer Genome Atlas database. This study aimed to explore its roles and regulation mechanism in oral squamous cell carcinoma. Materials and methods We analyzed the expression of DLX6 and its association with overall survival in OSCC by real-time quantitative PCR. Besides, clone formation, proliferation, and apoptosis were detected after knocking down DLX6 and microarray analysis was performed to explore the possible regulatory mechanism. Results DLX6 was overexpressed in oral cancer tissues and was associated with advance tumor stage and poor prognosis. In vitro studies have shown that DLX6 promotes proliferation and inhibits cell apoptosis in oral cancer cells. Microarray analysis along with Western blotting results indicated that DLX6 significantly associated with malignant tumors and may regulate OSCC cells proliferation through EGFR-CCND1 axis. Conclusion DLX6 promotes cell proliferation and suppresses cell apoptosis in oral cancer cells. EGFR-CCND1 pathway might be the potential mechanism participating in the regulating axis.
引用
收藏
页码:87 / 96
页数:10
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