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1.
Journal of Southern Medical University ; (12): 798-801, 2014.
Article in Chinese | WPRIM | ID: wpr-249356

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the effect of amphotericinB (AmB) on migration and invasion of esophageal carcinoma Eca109 cells exposed to hypoxia and explore the molecular mechanisms.</p><p><b>METHODS</b>Routinely cultured esophageal carcinoma Eca109 cells were treated with 0, 1.25, 2.5, or 5 µg/ml AmB in hypoxic condition (3% O2, 5% CO2, and 92% N2) for 24 h. The cell migration and invasion were assessed by cell scratch test and Transwell chamber assay, respectively. Real-time quantitative PCR and Western blotting were used to detect the mRNA and protein expressions of hypoxia-inducible factor-1α (HIF-1α), matrix metalloproteinase-2 (MMP-2), and E-cadherin in the cells, respectively.</p><p><b>RESULTS</b>Compared with the control cells, the cells treated with different doses of AmB showed attenuated ability of migration and invasion (P<0.05). AmB treatment resulted in significantly lowered mRNA and protein expressions of MMP-2 (P<0.05) and increased expressions of E-cadherin (P<0.05); the protein expression of HIF-1α decreased significantly in cells after AmB treatment (P<0.05) but its mRNA levels showed no significant changes (P>0.05).</p><p><b>CONCLUSION</b>AmB can suppress the migration and invasion of esophageal carcinoma Eca109 cells in hypoxic microenvironment possibly by regulating the expressions of HIF-1α, MMP-2 and E-cadherin.</p>


Subject(s)
Humans , Amphotericin B , Pharmacology , Cadherins , Metabolism , Cell Hypoxia , Cell Line, Tumor , Cell Movement , Down-Regulation , Esophageal Neoplasms , Metabolism , Pathology , Hypoxia-Inducible Factor 1, alpha Subunit , Metabolism , Matrix Metalloproteinase 2 , Metabolism , RNA, Messenger
2.
Journal of Southern Medical University ; (12): 934-938, 2014.
Article in Chinese | WPRIM | ID: wpr-249329

ABSTRACT

<p><b>OBJECTIVE</b>To study the inhibitory effect of CD133 monoclonal antibody labeled with ¹³¹I (¹³¹I-CD133mAb) on Huh-7 human liver cancer cell line overexpressing CD133 antigen in vitro and in mouse models bearing the tumor cell xenograft.</p><p><b>METHODS</b>¹³¹I-CD133mAb was prepared by chloramines-T method and evaluated for its stability. Flow cytometry and immunohistochemistry were used to detect the expression of CD133 in Huh-7 cells and in Huh-7 cell-derived tumors, respectively. Huh-7 cells treated with ¹³¹I-CD133mAb plus cisplatin (DDP), ¹³¹I -CD133mAb, DDP, or no treatment (blank control) were examined for cell proliferation suppression by MTT assay with the IC₅₀ calculated. BALB/c mice bearing subcutaneous Huh-7 cell xenograft in the right forelegs were treated with ¹³¹I -CD133mAb, DDP, or both every two days for two weeks. The tumor size and volume were measured twice a week, and pathological examination of the tumor was carried out after the treatments. The tumor inhibition rate was calculated and tumor cell apoptosis observed with HE staining.</p><p><b>RESULTS</b>The labeling ratio of ¹³¹I-CD133mAb was 90.25% and the radiochemical purity was 97.78%. Huh-7 cells showed obviously higher CD133 expression than HepG2 cells. ¹³¹I-CD133mAb combined with DDP group resulted in a significantly higher tumor inhibition rate than other treatments in the tumor-bearing mice.</p><p><b>CONCLUSION</b>¹³¹I-CD133mAb can inhibit the growth of liver cancer cells with a high CD133 expression both in vivo and in vitro.</p>


Subject(s)
Animals , Humans , Mice , AC133 Antigen , Antibodies, Monoclonal , Pharmacology , Antigens, CD , Allergy and Immunology , Apoptosis , Carcinoma, Hepatocellular , Drug Therapy , Cell Line, Tumor , Cell Proliferation , Cisplatin , Pharmacology , Glycoproteins , Allergy and Immunology , Hep G2 Cells , Liver Neoplasms , Mice, Inbred BALB C , Mice, Nude , Peptides , Allergy and Immunology , Xenograft Model Antitumor Assays
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