Expression of SATB1 in hepatocellular carcinoma cell lines with different invasive capacities.
- Author:
Guanghui LI
1
;
Dinghua YANG
;
Xianghong LI
;
Kebo ZHONG
;
Xiao LIU
;
Minping BI
;
Yan LIU
;
Xiaoming LIAO
;
Liang LIN
Author Information
- Publication Type:Journal Article
- MeSH: Carcinoma, Hepatocellular; metabolism; pathology; Cell Line, Tumor; Humans; Liver Neoplasms; metabolism; pathology; Matrix Attachment Region Binding Proteins; metabolism; Neoplasm Invasiveness; RNA, Messenger; genetics
- From: Journal of Southern Medical University 2012;32(7):986-994
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the expression of special AT-rich sequence binding protein 1 (SATB1) in hepatocellular carcinoma (HCC) cell lines with different invasive capacities.
METHODSSATB1 expression was detected using real-time fluorescence quantitative PCR, RT-PCR, Western blotting and immunofluorescence in immortalized liver cell line HL-7702, noninvasive HCC cell lines HepG2 and SMMC-7721, MHCC97L cells with low invasiveness, and highly invasive cell lines MHCC97H and HCCLM3.
RESULTSIn comparison with HL-7702 cells, all the 5 HCC cell lines showed overexpression of SATB1 mRNA, which was the highest in the highly invasive HCCLM3 and MHCC97H cells, followed by MHCC97L cell line, and then by SMMC-7721 and HepG2 cell lines (P<0.001). The relative expression quantity of SATB1 protein in HepG2, SMMC-7721, MHCC97L, MHCC97H, and HCCLM3 cell lines was 0.271±0.002, 0.351±0.023, 0.621±0.026, 0.878±0.026, and 1.236±0.006, respectively. SATB1 expression level in HCCLM3 cell line was 4.6-fold higher than that in HepG2 cell line (P<0.001). SATB1 was found to localize in the cytoplasm and cell nuclei of the 5 HCC cell lines, and the highly invasive HCCLM3 and MHCC97H cell lines showed a strong positive staining for SATB1 in immunofluorescence assay.
CONCLUSIONSATB1 expression levels differ distinctly between the HCC cell lines with different invasive capacities and are possibly associated with the metastatic potentials of the cells.