Journal
JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY
Volume 138, Issue 6, Pages 1073-1079Publisher
SPRINGER
DOI: 10.1007/s00432-012-1213-3
Keywords
GDF3; TGF-beta superfamily; Breast cancer; Apoptosis; Taxol
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Funding
- National 863 project of China [2006AA020501]
- National Key Sci-Tech Special Project of China [2008ZX10002-020]
- Shanghai Municipal Science and Technology Commission [03dz14086]
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The aim of this study is to investigate whether GDF3 is related to the progression of human breast cancer and the effects of GDF3 on breast cancer cells. The expression of GDF3 in 24 breast cancer specimens paired with corresponding neighboring nontumorous tissue was studied by Western blot. Breast cancer cells were treated with different concentrations of recombinant human GDF3 protein. Using lentivirus containing sh-RNA, we knocked down the expression of GDF3. Soft agar assay was performed to explore the effects of GDF3 on colony formation. Different anti-tumor drugs dealt with MCF-7 cells stably expressing GDF3. We found that GDF3 expression level was significantly down-regulated in breast cancer tissues compared to the surrounding nontumorous tissues. GDF3 proteins could inhibit the proliferation of MCF-7 and T47D cells. We also found that the knockdown of GDF3 resulted in the promotion of colony formation and enhanced the ability of anchorage-independent cell growth in soft agar. Furthermore, overexpression of GDF3 could promote the apoptosis induced by Taxol. Our data indicated that GDF3 expression is significantly decreased in human breast cancer tissues, and reconstitution of GDF3 in breast cancer may be a potential therapeutic approach to inhibit aggressive growth of breast cancer.
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