Expression of SATB1 in hepatocellular carcinoma cell lines with different invasive capacities / 南方医科大学学报
Journal of Southern Medical University
;
(12): 986-994, 2012.
Article
in Chinese
| WPRIM
| ID: wpr-268949
ABSTRACT
<p><b>OBJECTIVE</b>To study the expression of special AT-rich sequence binding protein 1 (SATB1) in hepatocellular carcinoma (HCC) cell lines with different invasive capacities.</p><p><b>METHODS</b>SATB1 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.</p><p><b>RESULTS</b>In 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.</p><p><b>CONCLUSION</b>SATB1 expression levels differ distinctly between the HCC cell lines with different invasive capacities and are possibly associated with the metastatic potentials of the cells.</p>
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Pathology
/
RNA, Messenger
/
Carcinoma, Hepatocellular
/
Matrix Attachment Region Binding Proteins
/
Cell Line, Tumor
/
Genetics
/
Liver Neoplasms
/
Metabolism
/
Neoplasm Invasiveness
Limits:
Humans
Language:
Chinese
Journal:
Journal of Southern Medical University
Year:
2012
Type:
Article
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