Hepatocellular carcinoma: thyroid hormone promotes tumorigenicity through inducing cancer stem-like cell self-renewal

被引:12
|
作者
Wang, Tao [1 ]
Xia, Lei [2 ]
Ma, Sicong [1 ]
Qi, Xingxing [1 ]
Li, Qigen [2 ]
Xia, Yun [2 ]
Tang, Xiaoyin [1 ]
Cui, Dan [1 ]
Wang, Zhi [1 ]
Chi, Jiachang [1 ]
Li, Ping [1 ]
Feng, Yu-Xiong [1 ]
Xia, Qiang [2 ]
Zhai, Bo [1 ]
机构
[1] Shanghai Jiao Tong Univ, Sch Med, Renji Hosp, Dept Intervent Oncol, Shanghai 200127, Peoples R China
[2] Shanghai Jiao Tong Univ, Sch Med, Renji Hosp, Dept Hepat Surg, Shanghai 200127, Peoples R China
来源
SCIENTIFIC REPORTS | 2016年 / 6卷
基金
中国国家自然科学基金;
关键词
NF-KAPPA-B; BREAST-CANCER; MECHANISMS; RECEPTORS; BMI1;
D O I
10.1038/srep25183
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
Cancer stem-like cells (CSCs) play a key role in maintaining the aggressiveness of hepatocellular carcinoma (HCC), but the cell-biological regulation of CSCs is unclear. In the study, we report that thyroid hormone (TH) promotes cell self-renewal in HCC cells. TH also increases the percentage of CD90 + HCC cells and promotes drug resistance of HCC cells. By analyzing primary human HCC samples, we found that TR alpha transcript level is significantly elevated in primary liver cancer and portal vein metastatic tumor, compared to that of adjacent normal liver tissue. Knocking down TR alpha not only inhibits HCC self-renewal in vitro but also suppresses HCC tumor growth in vivo. Interestingly, treatment of TH leads to activation of NF-kappa B, which is required for the function of TH on inducing HCC cell self-renewal. We also found TR alpha and p65 cooperatively drive the expression of BMI1 by co-binding to the promoter region of BMI1 gene. In summary, our study uncovers a novel function of TH signaling in regulating the CSCs of HCC, and these findings might be useful for developing novel therapies by targeting TH function in HCC cells.
引用
收藏
页数:9
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