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Suppression of cell growth and invasion by miR-205 in breast cancer.

Wu H, Zhu S, Mo YY - Cell Res. (2009)

Bottom Line: In this study, we report that miR-205 is significantly underexpressed in breast tumor compared to the matched normal breast tissue.Of interest, ectopic expression of miR-205 significantly inhibits cell proliferation and anchorage independent growth, as well as cell invasion.Furthermore, miR-205 was shown to suppress lung metastasis in an animal model.

View Article: PubMed Central - PubMed

Affiliation: Department of Medical Microbiology, Immunology and Cell Biology, Southern Illinois University School of Medicine, 825 N. Rutledge, PO Box 19626, Springfield, IL 62794, USA.

ABSTRACT
MicroRNAs (miRNAs) are endogenous, small, non-coding RNAs, which are capable of silencing gene expression at the post-transcriptional level. In this study, we report that miR-205 is significantly underexpressed in breast tumor compared to the matched normal breast tissue. Similarly, breast cancer cell lines, including MCF-7 and MDA-MB-231, express a lower level miR-205 than the non-malignant MCF-10A cells. Of interest, ectopic expression of miR-205 significantly inhibits cell proliferation and anchorage independent growth, as well as cell invasion. Furthermore, miR-205 was shown to suppress lung metastasis in an animal model. Finally, western blot combined with the luciferase reporter assays demonstrate that ErbB3 and vascular endothelial growth factor A (VEGF-A) are direct targets for miR-205, and this miR-205-mediated suppression is likely through the direct interaction with the putative miR-205 binding site in the 3'-untranslated region (3'-UTR) of ErbB3 and VEGF-A. Together, these results suggest that miR-205 is a tumor suppressor in breast cancer.

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Suppression of the endogenous ErbB3 and VEGF-A by miR-205A and B, Western blot revealing reduced level of ErbB3 in miR-205 transfected MCF-7 cells and reduced VEGF-A level in miR-205 MDA-MB-231 cells. C. Detection of ErbB3 in MCF-7 cells by immunofluorescence staining. Note that the ErbB3 signal was very weak in the miR-205 transfected cells in right panel.
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Figure 6: Suppression of the endogenous ErbB3 and VEGF-A by miR-205A and B, Western blot revealing reduced level of ErbB3 in miR-205 transfected MCF-7 cells and reduced VEGF-A level in miR-205 MDA-MB-231 cells. C. Detection of ErbB3 in MCF-7 cells by immunofluorescence staining. Note that the ErbB3 signal was very weak in the miR-205 transfected cells in right panel.

Mentions: To determine whether miR-205 suppresses the endogenous ErbB3, we performed Western blot for transiently transfected MCF-7 cells. As shown in Fig. 6A, miR-205 suppressed significantly the ErbB3 level in MCF-7 cells, compared to vector control. Moreover, we detected even more dramatic reduction of VEGF-A in miR-205 MDA-MB-231 cells compared to vector control (Fig. 6B). To better determine this suppression of ErbB3 at the cellular level, we performed immunofluorescence staining for transiently transfected MCF-7 cells. Since miR-205 expression vector was tagged with GFP, the green cells represented miR-205 expressing cells. As shown in Fig. 6C, ectopic expression of miR-205 clearly suppressed ErbB3 expression (arrows in right panel). In contrast, the vector control had no effect on its expression. Thus, these results further confirmed that miR-205 can negatively regulate the expression of ErbB3.


Suppression of cell growth and invasion by miR-205 in breast cancer.

Wu H, Zhu S, Mo YY - Cell Res. (2009)

Suppression of the endogenous ErbB3 and VEGF-A by miR-205A and B, Western blot revealing reduced level of ErbB3 in miR-205 transfected MCF-7 cells and reduced VEGF-A level in miR-205 MDA-MB-231 cells. C. Detection of ErbB3 in MCF-7 cells by immunofluorescence staining. Note that the ErbB3 signal was very weak in the miR-205 transfected cells in right panel.
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC2664859&req=5

Figure 6: Suppression of the endogenous ErbB3 and VEGF-A by miR-205A and B, Western blot revealing reduced level of ErbB3 in miR-205 transfected MCF-7 cells and reduced VEGF-A level in miR-205 MDA-MB-231 cells. C. Detection of ErbB3 in MCF-7 cells by immunofluorescence staining. Note that the ErbB3 signal was very weak in the miR-205 transfected cells in right panel.
Mentions: To determine whether miR-205 suppresses the endogenous ErbB3, we performed Western blot for transiently transfected MCF-7 cells. As shown in Fig. 6A, miR-205 suppressed significantly the ErbB3 level in MCF-7 cells, compared to vector control. Moreover, we detected even more dramatic reduction of VEGF-A in miR-205 MDA-MB-231 cells compared to vector control (Fig. 6B). To better determine this suppression of ErbB3 at the cellular level, we performed immunofluorescence staining for transiently transfected MCF-7 cells. Since miR-205 expression vector was tagged with GFP, the green cells represented miR-205 expressing cells. As shown in Fig. 6C, ectopic expression of miR-205 clearly suppressed ErbB3 expression (arrows in right panel). In contrast, the vector control had no effect on its expression. Thus, these results further confirmed that miR-205 can negatively regulate the expression of ErbB3.

Bottom Line: In this study, we report that miR-205 is significantly underexpressed in breast tumor compared to the matched normal breast tissue.Of interest, ectopic expression of miR-205 significantly inhibits cell proliferation and anchorage independent growth, as well as cell invasion.Furthermore, miR-205 was shown to suppress lung metastasis in an animal model.

View Article: PubMed Central - PubMed

Affiliation: Department of Medical Microbiology, Immunology and Cell Biology, Southern Illinois University School of Medicine, 825 N. Rutledge, PO Box 19626, Springfield, IL 62794, USA.

ABSTRACT
MicroRNAs (miRNAs) are endogenous, small, non-coding RNAs, which are capable of silencing gene expression at the post-transcriptional level. In this study, we report that miR-205 is significantly underexpressed in breast tumor compared to the matched normal breast tissue. Similarly, breast cancer cell lines, including MCF-7 and MDA-MB-231, express a lower level miR-205 than the non-malignant MCF-10A cells. Of interest, ectopic expression of miR-205 significantly inhibits cell proliferation and anchorage independent growth, as well as cell invasion. Furthermore, miR-205 was shown to suppress lung metastasis in an animal model. Finally, western blot combined with the luciferase reporter assays demonstrate that ErbB3 and vascular endothelial growth factor A (VEGF-A) are direct targets for miR-205, and this miR-205-mediated suppression is likely through the direct interaction with the putative miR-205 binding site in the 3'-untranslated region (3'-UTR) of ErbB3 and VEGF-A. Together, these results suggest that miR-205 is a tumor suppressor in breast cancer.

Show MeSH
Related in: MedlinePlus