[HTML][HTML] Effects of miR-155 antisense oligonucleotide on breast carcinoma cell line MDA-MB-157 and implanted tumors

SR Zheng, GL Guo, Q Zhai, ZY Zou… - Asian Pacific Journal of …, 2013 - koreascience.kr
SR Zheng, GL Guo, Q Zhai, ZY Zou, W Zhang
Asian Pacific Journal of Cancer Prevention, 2013koreascience.kr
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 …
Abstract
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.
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