癌变·畸变·突变2012,Vol.24Issue(5):325-329,5.DOI:10.3969/j.issn.1004-616x.2012.05.001
RNA干扰HIF-1α对低氧状态下食管鳞癌Eca109细胞放射敏感性的影响
Effect of HIF-1α by RNAi on radiosensitivity in esophageal squamous carcinoma cell line Eca109 under hypoxia
摘要
Abstract
OBJECTIVE: To investigate the expression of HIF-1 α and EGFR in esophageal squamous carcinoma cell line Ecal09 under hypoxia, in order to explore the effect of HIF-1α on radiosensitivity and its possible molecular mechanism. METHODS: CoCl2 was used to mimic hypoxic tumor microenvironment. mRNA levels of HIF-1 a and EGFR under hypoxia were detected by reverse transcription-polymerase chain reaction(RT-PCR), and protein levels were measured by immunohistoehemistry. The effect silenced of HIF-1 a gene on EGFR expression was assayed by Western blot. Radiosensitivity was evaluated via detection of apoptosis after radiation by flow cytometer (FCM), and then the effect of silencing HIF-1 a on radiosensitivity was measured. RESULTS: Under hypoxia, HIF-1 α mRNA had no significant change (P>0.05), while its protein increased obviously. EGFR mRNA was up-regulated (P<0.05), and its protein also increased accordingly. The siRNA targeting HIF-1α gene down-regulated HIF-1 a in Ecal09 cells efficiently under hypoxia, and EGFR protein levels were down-regulated as well (P<0.05). The radiosensitivity in esophageal carcinoma cell line Eeal09 was lower under hypoxia than that in normoxia. The siRNA targeting HIF-1 α could partially reverse radioresistance. CONCLUSION: Hypoxia could increase HIF-1 a protein expression in esophageal squamous carcinoma Ecal09 cell. Resistance to radiation enhanced in Ecal09 cells maybe correlated with HIF-1 α up-regulating the expression of EGFR mRNA and protein levels. Radiosensitivity could be augmented if HIF-1 α was effectively suppressed.关键词
低氧诱导因子-1α/食管肿瘤/放射敏感性/RNA干扰/凋亡Key words
hypoxiainducible factor- 1 α / esophagealcarcinoma/ radiosensitivity/ RNA interference/ apoptosis分类
医药卫生引用本文复制引用
景绍武,王雅棣,郑明民,孙国贵,刘青,程云杰,杨从容,李成林..RNA干扰HIF-1α对低氧状态下食管鳞癌Eca109细胞放射敏感性的影响[J].癌变·畸变·突变,2012,24(5):325-329,5.基金项目
高等学校博士学科点专项科研基金(20091323110011) (20091323110011)