Abstract | BACKGROUND: miR-30a expression is down-regulated and regulates tumor suppressors in various cancers. AIM: We investigated the mechanisms underlying the biological role of miR-30a in CRC. METHODS:
MicroRNA, mRNA, and protein expression were analyzed by quantitative real-time PCR and Western blot. The migration and invasion abilities of CRC were determined by wound healing assay, and trans-well migration and invasion. A luciferase reporter assay was used to confirm the targets of miR-30a. RESULTS: miR-30a expression was significantly down-regulated in CRC tissues and in CRC tissue with lymph node metastasis compared to CRC tissue without metastasis. Overexpression of miR-30a suppressed migration and invasion through insulin-like growth factor 1 receptor (IGF1R) in CRC cells. miR-30a suppresses IGF1R protein expression and inhibits β- catenin or p-AKT and increases E-cadherin expression. The IGF1R expression level is also up-regulated in CRC tumors and inversely correlated with miR-30a in CRC specimens. CONCLUSIONS: miR-30a functions as a tumor-suppressive miRNA, which may provide a therapeutic strategy for metastasis of CRC.
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Authors | Y C Liu, Y R Park, S L Kim, S T Lee, S W Kim |
Journal | Digestive diseases and sciences
(Dig Dis Sci)
Vol. 62
Issue 11
Pg. 3040-3049
(11 2017)
ISSN: 1573-2568 [Electronic] United States |
PMID | 28932920
(Publication Type: Journal Article)
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Chemical References |
- 3' Untranslated Regions
- Antigens, CD
- CDH1 protein, human
- CTNNB1 protein, human
- Cadherins
- IGF1R protein, human
- MIRN30b microRNA, human
- MicroRNAs
- RNA, Messenger
- Receptors, Somatomedin
- beta Catenin
- Receptor, IGF Type 1
- Proto-Oncogene Proteins c-akt
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Topics |
- 3' Untranslated Regions
- Aged
- Antigens, CD
- Binding Sites
- Cadherins
(metabolism)
- Cell Line, Tumor
- Cell Movement
- Colorectal Neoplasms
(genetics, metabolism, pathology)
- Down-Regulation
- Female
- Gene Expression Regulation, Neoplastic
- HEK293 Cells
- Humans
- Male
- MicroRNAs
(genetics, metabolism)
- Middle Aged
- Neoplasm Metastasis
- Phosphorylation
- Proto-Oncogene Proteins c-akt
(metabolism)
- RNA, Messenger
(genetics, metabolism)
- Receptor, IGF Type 1
- Receptors, Somatomedin
(genetics, metabolism)
- Signal Transduction
- Transfection
- beta Catenin
(metabolism)
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