囊性纤维化跨膜传导调节器
表观遗传学
癌症研究
小RNA
DNA甲基化
肺癌
生物
癌症
甲基转移酶
甲基化
下调和上调
囊性纤维化
基因表达
医学
遗传学
基因
内科学
作者
Wenyan Huang,Kin Lam Fok,Xiao Jiang,Hsiao Chang Chan
标识
DOI:10.1096/fasebj.28.1_supplement.1048.9
摘要
Cystic fibrosis transmembrane conductance regulator (CFTR), a member of the ATP‐binding cassette (ABC) transporter family, is expressed in a wide variety of epithelial tissues. Recently, it has been found that CFTR is downregulated in various human cancers, which functionally suppress cancer malignancy. Previous studies have indicated that there are at least two promising epigenetic mechanisms for regulation of CFTR expression, including promoter methylation and microRNAs targeting CFTR. However, the exact interaction between CFTR and epigenetic modulation in human cancers is poorly understood. In the present study, we found that the promoter of CFTR was methylated and could be reversed by DNA methyltransferase (DNMT) inhibitor 5‐aza‐2’‐deoxycydine (5‐aza) in lung cancer cell lines. Meanwhile, CFTR expression was also upregulated by two microRNA inhibitors including mir‐145 and mir‐494 inhibitors in A549 cell line and could be suppressed by mir‐384 mimic in Calu3 cell line. In addition, we demonstrated that both DNMTs and candidate CFTR regulating microRNAs levels were altered by hypoxia in lung cancer cell lines. These results may shed new light into our understanding of CFTR regulation during cancer development.
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