Amphotericin B suppresses migration and invasion of esophageal carcinoma Eca109 cells in hypoxic microenvironment by down-regulating hypoxia-inducible factor-1α activity.
- Author:
Qiangqiang KANG
1
;
Min TANG
;
Yanli HOU
;
Liqun DUAN
;
Xingyue CHEN
;
Jin SHU
;
Furong WU
;
Ying WANG
;
Shaolin LI
Author Information
- Publication Type:Journal Article
- MeSH: Amphotericin B; pharmacology; Cadherins; metabolism; Cell Hypoxia; Cell Line, Tumor; drug effects; Cell Movement; drug effects; Down-Regulation; Esophageal Neoplasms; metabolism; pathology; Humans; Hypoxia-Inducible Factor 1, alpha Subunit; metabolism; Matrix Metalloproteinase 2; metabolism; RNA, Messenger
- From: Journal of Southern Medical University 2014;34(6):798-801
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of amphotericinB (AmB) on migration and invasion of esophageal carcinoma Eca109 cells exposed to hypoxia and explore the molecular mechanisms.
METHODSRoutinely 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.
RESULTSCompared 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).
CONCLUSIONAmB 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.