Effects of miR-155 Antisense Oligonucleotide on Breast Carcinoma Cell Line MDA-MB-157 and Implanted Tumors

Diverse studies have shown that miR-155 is overexpressed in different tumor types. However, the precise molecular mechanism of the ectopic expression of miR-155 in breast cancer is still poorly understood. To further explore the role of miR-155 in breast tumorigenesis, we here assessed the influence...

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Bibliographic Details
Published inAsian Pacific journal of cancer prevention : APJCP Vol. 14; no. 4; pp. 2361 - 2366
Main Authors Zheng, Shu-Rong, Guo, Gui-Long, Zhai, Qi, Zou, Zhang-Yong, Zhang, Wei
Format Journal Article
LanguageKorean
Published 2013
Subjects
microRNA-155
antisense oligonucleotide
MDA-MB-157 cells
nude mice
Breast neoplasms
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Summary:Diverse studies have shown that miR-155 is overexpressed in different tumor types. However, the precise molecular mechanism of the ectopic expression of miR-155 in breast cancer is still poorly understood. To further explore the role of miR-155 in breast tumorigenesis, we here assessed the influence of miR-155 antisense oligonucleotide (miR-155 ASO) on MDA-MB-157 cell viability and apoptosis in vitro. Furthermore, the effects of inhibitory effects of miR-155 on the growth of xenograft tumors in vivo were determined with performance of immunohistochemistry to detect expression of caspase-3, a pivotal apoptosis regulatory factor, in xenografts. Transfection efficiency detected by laser confocal microscope was higher than 80%. The level of miR-155 expression was significantly decreased (P<0.05) in the cells transfected with miR-155 ASO, compared with that in cells transfected with a negative control. After being transfected with miR-155 ASO, the viability of MDA-MB-157 cells was reduced greatly (P<0.05) and the number of apoptotic cells was increased significantly. Additionally, miR-155 ASO inhibited the growth of transplanted tumor in vivo and significantly increased the expression of caspase-3. Taken together, our study revealed that miR-155 ASO can induce cell apoptosis and inhibit cell proliferation in vitro. Moreover, miR-155 ASO could significantly repress tumor growth in vivo, presumably by inducing apoptosis via caspase-3 up-regulation. These findings provide experimental evidence for using miR-155 as a therapeutic target of breast carcinoma.
Bibliography:KISTI1.1003/JNL.JAKO201321251180888
ISSN:1513-7368
2476-762X