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| Status |
Public on Apr 30, 2024 |
| Title |
Loss of tumor-derived SMAD4 enhances primary tumor growth but not metastasis following BMP4 signalling |
| Organism |
Homo sapiens |
| Experiment type |
Expression profiling by high throughput sequencing
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| Summary |
We have reported previously that in preclinical models, BMP4 is a potent inhibitor of breast cancer metastasis and that high BMP4 protein levels predict favourable patient outcome. Here, we investigated the requirement for functional SMAD4 in mediating the anti-metastatic response of BMP4, given reports of promotion of metastasis by BMP4 in cancers where SMAD4 is frequently deleted. BMP4-induced inhibition of metastasis does not require functional SMAD4 in tumor cells. However, tumor cell intrinsic signalling using a constitutively active BMP receptor does require functional SMAD4 to suppress metastasis, thus implicating BMP4 mediated paracrine signalling as a contributor to the inhibition of metastasis.
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| Overall design |
Comparison of the transcriptomic profiles of cancer cells retrieved from primary tumours with modified expression of BMP4 and/or SMAD4.
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| Web link |
https://doi.org/10.1186/s12964-024-01559-0
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| |
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| Contributor(s) |
Chi L, Anderson RL, Haslem A |
| Citation(s) |
38689334 |
| |
| Submission date |
Mar 28, 2022 |
| Last update date |
May 03, 2024 |
| Contact name |
Lap Hing Chi |
| Organization name |
Olivia Newton-John Cancer Research Institute
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| Department |
Translational Breast Cancer Program
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| Lab |
Metastasis Research Lab
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| Street address |
145 Studley Road
|
| City |
Heidelberg |
| State/province |
Victoria |
| ZIP/Postal code |
3084 |
| Country |
Australia |
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| Platforms (1) |
| GPL18573 |
Illumina NextSeq 500 (Homo sapiens) |
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| Samples (16)
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| Relations |
| BioProject |
PRJNA820866 |
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