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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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Related in: MedlinePlus

Suppression of cell growth by miR-205A, Relative expression of miR-205 in stable clones #17 (miR-205 #17) and #21 (miR-205 #21), as detected by TaqMan real time PCR. MTT assays reveal reduced cell growth for these two stable clones compared to vector control (V) (B) as well as for the transiently transfected MCF-7 cells compared to vector control (C). Values are means of three separate experiments ± SE. **, p < 0.01.
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Figure 2: Suppression of cell growth by miR-205A, Relative expression of miR-205 in stable clones #17 (miR-205 #17) and #21 (miR-205 #21), as detected by TaqMan real time PCR. MTT assays reveal reduced cell growth for these two stable clones compared to vector control (V) (B) as well as for the transiently transfected MCF-7 cells compared to vector control (C). Values are means of three separate experiments ± SE. **, p < 0.01.

Mentions: To test this hypothesis, we performed proliferation assays in MCF-7 cells with miR-205 overexpression. MCF-7 cells were transfected with either miR-205 expression vector or control vector. Two stable clones #17 and #21 were selected out based on the high level of exogenous miR-205 level (Fig. 2A) compared to a pooled vector control (over 20 clones). MTT assays indicated that cell growth for both miR-205 expressing clones was slower than vector control. For example, clones miR-205 #17 and miR-205 #21 grew at 60% and 30% of the vector control, respectively (Fig. 2B), which appears to be negatively correlated with the exogenous miR-205 level (Fig. 2A). We also tested transiently transfected MCF-7 cells. The result was very similar to that of stable clones (Fig. 3C).


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

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

Suppression of cell growth by miR-205A, Relative expression of miR-205 in stable clones #17 (miR-205 #17) and #21 (miR-205 #21), as detected by TaqMan real time PCR. MTT assays reveal reduced cell growth for these two stable clones compared to vector control (V) (B) as well as for the transiently transfected MCF-7 cells compared to vector control (C). Values are means of three separate experiments ± SE. **, p < 0.01.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2664859&req=5

Figure 2: Suppression of cell growth by miR-205A, Relative expression of miR-205 in stable clones #17 (miR-205 #17) and #21 (miR-205 #21), as detected by TaqMan real time PCR. MTT assays reveal reduced cell growth for these two stable clones compared to vector control (V) (B) as well as for the transiently transfected MCF-7 cells compared to vector control (C). Values are means of three separate experiments ± SE. **, p < 0.01.
Mentions: To test this hypothesis, we performed proliferation assays in MCF-7 cells with miR-205 overexpression. MCF-7 cells were transfected with either miR-205 expression vector or control vector. Two stable clones #17 and #21 were selected out based on the high level of exogenous miR-205 level (Fig. 2A) compared to a pooled vector control (over 20 clones). MTT assays indicated that cell growth for both miR-205 expressing clones was slower than vector control. For example, clones miR-205 #17 and miR-205 #21 grew at 60% and 30% of the vector control, respectively (Fig. 2B), which appears to be negatively correlated with the exogenous miR-205 level (Fig. 2A). We also tested transiently transfected MCF-7 cells. The result was very similar to that of stable clones (Fig. 3C).

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