Amphotericin B suppresses migration and invasion of esophageal carcinoma Eca109 cells in hypoxic microenvironment by down-regulating hypoxia-inducible factor-1α activity / 南方医科大学学报
Journal of Southern Medical University
;
(12): 798-801, 2014.
Artículo
en Chino
| 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>
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Patología
/
Farmacología
/
ARN Mensajero
/
Neoplasias Esofágicas
/
Cadherinas
/
Hipoxia de la Célula
/
Regulación hacia Abajo
/
Movimiento Celular
/
Anfotericina B
/
Metaloproteinasa 2 de la Matriz
Límite:
Humanos
Idioma:
Chino
Revista:
Journal of Southern Medical University
Año:
2014
Tipo del documento:
Artículo
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