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The effects of miR-181a on proliferation, migration and invasion abilities of esophageal carcinoma cell line TE11 / 肿瘤
Tumor ; (12): 613-618, 2011.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-849168
Responsible library: WPRO
ABSTRACT

Objective:

To investigate the effect of up-regulation of miR-181a expression mediated by constructing miR-181a recombinant eukaryotic expression vector pcDNA3.1(+)-miR-181a on cell proliferation, migration and invasion abilities of esophageal carcinoma cell line TE11.

Methods:

PCR primers were designed and miR-181a precursor sequence was amplified from 95C cell genomic DNA. The product fragments were cloned into pcDNA3.1(+) to construct the recombinant vector pcDNA3.1(+)-miR-181a. The recombinant eukaryotic expression vector pcDNA3.1(+)-miR-181a was transfected into TE11 cells. The expression of miR-181a mRNA was detected by real-time fluorogenic quantitative-PCR (RFQ-PCR). The effects of pcDNA3.1(+)-miR-181a on cell proliferation, migration and invasion abilities of TE11 cells were detected by MTT, wound healing and Boyden chamber methods, respectively.

Results:

The miR-181a recombinant eukaryotic expression vector pcDNA3.1(+)-miR-181a was successfully established. RFQ-PCR revealed that the mature miR-181a was able to effectively express in TE11 cells transfected with recombinant vector pcDNA3.1(+)-miR-181a (P<0.05). The overexpression of miR-181a could significantly increase the proliferation, migration and invasion abilities of TE11 cells.

Conclusion:

Overexpression of miR-181a can increase cell proliferation, migration and invasion abilities of esophageal carcinoma TE11 cells. These results may provide experiment references for further research of the role of miR-181a in cancer development and progression. Copyright© 2011 by Tumor.

Full text: Available Database: WPRIM (Western Pacific) Language: Chinese Journal: Tumor Year: 2011 Document type: Article
Full text: Available Database: WPRIM (Western Pacific) Language: Chinese Journal: Tumor Year: 2011 Document type: Article
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