SIX4 promotes metastasis via activation of the PI3K-AKT pathway in colorectal cancer

被引:31
|
作者
Li, Guodong [1 ]
Hu, Fuqing [1 ]
Luo, Xuelai [1 ]
Hu, Junbo [1 ]
Feng, Yongdong [1 ]
机构
[1] Huazhong Univ Sci & Technol, Canc Res Inst, Tongji Hosp, Wuhan, Hubei, Peoples R China
来源
PEERJ | 2017年 / 5卷
关键词
Colorectal cancer; SIX4; PI3K-AKT pathway; TCGA; GEO; MESENCHYMAL TRANSITION; EXPRESSION; OVEREXPRESSION; PHOSPHATASE; HOMOLOG; PTEN;
D O I
10.7717/peerj.3394
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Background: Several studies report aberrant expression of sine oculis homeobox (SIX) homolog family members during cancer development and progression. SIX4 participates in organ development, such as myogenesis and neurogenesis. However, the expression and clinical implication of SIX4 in colorectal cancer (CRC) remains unclear. Methods: The SIX4 expression levels in colorectal patients were assessed in nine different human cancer arrays and compared using patient survival data. SIX4 expression was silenced in two cell culture lines for invasion and wound healing assessment. Finally, bioinformatics assessments ascertained the pathways impacted by SIX4. Results: SIX4 was upregulated in The Cancer Genome Atlas CRC cohort and other gene expression omnibus (GEO) cohorts. In addition, SIX4 expression significantly correlated with lymph node metastasis and advanced Tumor Node Metastasis (TNM) stages. Moreover, SIX4 overexpression was related to unfavorable prognosis in CRC patients. Silencing SIX4 inhibited CRC cell metastasis by surpressing AKT phosphorylation. Discussion: SIX4 is upregulated in CRC and can be used as a prognosis biomarker.
引用
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页数:17
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