The Role of hMDMX in Cancer Transformation
Author Information
Author(s): K. Lenos, J. de Lange, A. FAS Teunisse, K. Lodder, M. Verlaan-de Vries, E. Wiercinska, M. J. M. van der Burg, K. Szuhai, A. G. Jochemsen
Primary Institution: Leiden University Medical Center
Hypothesis
Does hMDMX function as an oncogene in the transformation of human fibroblasts and embryonic retinoblasts?
Conclusion
hMDMX overexpression contributes to the oncogenic phenotype of transformed human cells by inactivating p53.
Supporting Evidence
- hMDMX overexpression accelerates cell proliferation.
- Transformed cells with high hMDMX levels are resistant to p53 reactivating drugs.
- Both hMDMX overexpression and p53-knockdown lead to similar oncogenic effects.
Takeaway
hMDMX is a protein that can help cancer cells grow by stopping a protective protein called p53 from working properly.
Methodology
In vitro transformation model using RNA interference and gene overexpression in primary human fibroblasts and embryonic retinoblasts.
Limitations
The study primarily focuses on in vitro models, which may not fully replicate in vivo conditions.
Participant Demographics
Primary human fibroblasts and embryonic retinoblasts.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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