Is par6 an essential mediator of apoptotic response to transforming growth factor beta in NMuMG immortalized mammary cells?
Par6 and TGFbeta receptor I activation are both necessary for TGFbeta-induced apoptosis in NMuMG cells. Importantly, Par6 overexpression enhances the sensitivity of NMuMG to TGFbeta-induced apoptosis, notably upon prolonged exposure to this growth factor, when NMuMG parental cells are usually apoptosis-resistant. Thus, endogenous Par6 level might be important in determining whether TGFbeta will function as either a pro-apoptotic or pro-survival factor in breast cancer, and potentially aid in predicting patient's prognosis and therapy response.
While the results of this preliminary study confirm previous findings of differential outcomes for children with different levels of preoperative residual hearing, they suggest that children with severe to profound hearing impairments should be considered for cochlear implantation.