MicroRNA-214 suppresses growth, migration and invasion through a novel target, high mobility group AT-hook 1, in human cervical and colorectal cancer cells

被引:54
|
作者
Chandrasekaran, Karthik Subramanian [1 ]
Sathyanarayanan, Anusha [1 ]
Karunagaran, Devarajan [1 ]
机构
[1] Indian Inst Technol Madras, Bhupat & Jyoti Mehta Sch Biosci, Dept Biotechnol, Madras 600036, Tamil Nadu, India
关键词
microRNA-214; tumour suppressor; HMGA1; human cervical cancer; human colorectal cancer; proliferation; migration; invasion; TRANSCRIPTION FACTOR; HMGA1; EXPRESSION; DOWN-REGULATION; BREAST-CANCER; BETA-CATENIN; MIR-214; PROTEINS; SURVIVAL; PROLIFERATION; PROGRESSION;
D O I
10.1038/bjc.2016.234
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Background: MicroRNA-214 (miR-214) has been shown to act as a tumour suppressor in human cervical and colorectal cancer cells. The aim of this study was to experimentally validate high mobility group AT-hook 1 as a novel target for miR-214-mediated suppression of growth and motility. Methods: HMGA1 and miR-214 expression levels were estimated in cervical and colorectal clinical specimens using qPCR. HMGA1 30 untranslated region luciferase assays were performed to validate HMGA1 as a target of miR-214. Effect of altering the expression of miR-214 or HMGA1 on proliferation, migration and invasion of human cervical and colorectal cancer cells was investigated. Results: miR-214 expression was poor while that of HMGA1 was high in cervical and colorectal cancer tissues. miR-214-reexpression or HMGA1 downregulation inhibited proliferation, migration and invasion of cancer cells while miR-214 inhibition had opposite effects. miR-214 was demonstrated to bind to the wild-type 30 untranslated region of HMGA1 but not with its mutant. Conclusions: Low expression of miR-214 concurrent with elevated levels of HMGA1 may contribute to cervical and colorectal cancer progression. miR-214-mediated regulation of HMGA1 is a novel mechanism for its tumour-suppressive actions in human cervical and colorectal cancer cells and opens up avenues for novel therapeutic strategies for these two cancers.
引用
收藏
页码:741 / 751
页数:11
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