Z Zhao1, J Ma2, K Wu3, L Chen1, J Yu1, W Hu1, K Zhang4. 1. Pancreato-Biliary Surgery Department, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510080, Guangdong, People's Republic of China. 2. Thoracic Surgery Department, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510080, Guangdong, People's Republic of China. 3. Colorectal Surgery Department, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510080, Guangdong, People's Republic of China. 4. Pancreato-Biliary Surgery Department, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510080, Guangdong, People's Republic of China. drzhangks@163.com.
Abstract
BACKGROUND: Intrahepatic cholangiocarcinoma (ICC) is the second most common primary malignant tumor of the liver with a poor prognosis. Upregulation of special AT-rich sequence-binding protein 1 (SATB1) promotes tumor progression. However, little is known about the role of SATB1 in ICC tumorigenesis. METHODS: We firstly investigated the expression of SATB1 in 88 cases of ICC by immunohistochemistry (IHC), QRT-PCR, and western blot. Meanwhile, we constructed stably knockdown (shRNA) of SATB1 in ICC cell lines to evaluate the effects of SATB1 on the ability of cell proliferation and invasion by MTT and transwell invasion assay. RESULTS: Our result showed that SATB1 was overexpressed in ICC tissues samples. Knockdown of SATB1 could inhibit ICC cell proliferation, and suppress ICC cell invasion of ICC cell lines. In addition, the depletion of SATB1 expression suppressed the MYC levels in vitro. CONCLUSIONS: Our results highlight the significance of SATB1 in ICC and suggest that SATB1 could be a promising therapy target and a potential biomarker for prognosis in ICC patients.
BACKGROUND:Intrahepatic cholangiocarcinoma (ICC) is the second most common primary malignant tumor of the liver with a poor prognosis. Upregulation of special AT-rich sequence-binding protein 1 (SATB1) promotes tumor progression. However, little is known about the role of SATB1 in ICC tumorigenesis. METHODS: We firstly investigated the expression of SATB1 in 88 cases of ICC by immunohistochemistry (IHC), QRT-PCR, and western blot. Meanwhile, we constructed stably knockdown (shRNA) of SATB1 in ICC cell lines to evaluate the effects of SATB1 on the ability of cell proliferation and invasion by MTT and transwell invasion assay. RESULTS: Our result showed that SATB1 was overexpressed in ICC tissues samples. Knockdown of SATB1 could inhibit ICC cell proliferation, and suppress ICC cell invasion of ICC cell lines. In addition, the depletion of SATB1 expression suppressed the MYC levels in vitro. CONCLUSIONS: Our results highlight the significance of SATB1 in ICC and suggest that SATB1 could be a promising therapy target and a potential biomarker for prognosis in ICC patients.