Sentence examples for mouse prostate epithelial from inspiring English sources
These results suggest that PTEN is required for TRAIL-induced apoptosis in mouse prostate epithelial cells.
In addition, members of the TGFβ superfamily (TGFβ, bone morphogenic proteins and activins) have roles in mouse prostate epithelial morphogenesis [18], [19], [20].
More importantly, we demonstrate that loss of PTEN confers TRAIL resistance in both mouse prostate epithelial and human breast T47D cells.
We thank Dr. Yong Chen for providing PTEN knockdout mouse prostate epithelial cells and Dr. Mengjer Lee for providing adenoviruses expressing PTEN.
PTEN-knockout mouse prostate epithelial cells (PTEN−/− and PTEN+/−) and normal cells (PTEN+/+) were obtained from Dr. Young Chen (Wake Forest University) and maintained in DMEM with 10% FBS, as described previously [16].
We also show that the underlying mechanism may be due to loss of functional PTEN because PTEN knockout mouse prostate epithelial cells are resistant to TRAIL while cells with intact PTEN are sensitive to TRAIL.
We show that the onset of MYC protein overexpression coincides precisely with the morphological transformation of mouse prostate luminal epithelial cells into PIN cells an appearance that is highly similar to human high grade PIN.
The results showed restoration of PPAR γ2 rescues and drives mouse prostate benign epithelial cell differentiation associated with AR activation.
Recent evidence has shown that in early, postnatal, mouse prostate development, epithelial homeostasis is maintained by basal multipotent stem cells that differentiate into basal, luminal, and neuroendocrine cells, as well as by unipotent basal and luminal progenitors [24].
The treatment was found to have minimal or no effects on normal prostatic epithelial cells in the mouse prostate and on benign prostate epithelial cells (e.g. BPH-1) arrested in a growth-quiescent state, which is the state most normal epithelial cells are in in vivo (20, 21).
Furthermore, Niu et al. found in the TRAMP mouse model studies that the mice with AR knockdown in prostate epithelial cells had increased metastatic PCa with earlier deaths.
