Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học quốc tế cung cấp cho các bạn kiến thức về ngành y đề tài: Cellular stress-induced up-regulation of FMRP promotes cell survival by modulating PI3K-Akt phosphorylation cascades | Jeon et al. Journal of Biomedical Science 2011 18 17 http content 18 1 17 The cost of publication in Journal of Biomedical Science Is borne by the National Science Council Taiwan JOURNAL OF BIOMEDICAL SCIENCE RESEARCH Open Access Cellular stress-induced up-regulation of FMRP promotes cell survival by modulating PI3K-Akt phosphorylation cascades Se Jin Jeon1 Jung Eun Seo1 Sung-Il Yang4 Ji Woong Choi5 David Wells2 Chan Young Shin3 4 Kwang Ho Ko1 Abstract Background Fragile X syndrome FXS the most commonly inherited mental retardation and single gene cause of autistic spectrum disorder occurs when the Fmr1 gene is mutated. The product of Fmr1 fragile X linked mental retardation protein FMRP is widely expressed in HeLa cells however the roles of FMRP within HeLa cells were not elucidated yet. Interacting with a diverse range of mRNAs related to cellular survival regulatory signals understanding the functions of FMRP in cellular context would provide better insights into the role of this interesting protein in FXS. Using HeLa cells treated with etoposide as a model we tried to determine whether FMRP could play a role in cell survival. Methods Apoptotic cell death was induced by etoposide treatment on Hela cells. After we transiently modulated FMRP expression silencing or enhancing by using molecular biotechnological methods such as small hairpin RNA virus-induced knock down and overexpression using transfection with FMRP expression vectors cellular viability was measured using propidium iodide staining TUNEL staining and FACS analysis along with the level of activation of PI3K-Akt pathway by Western blot. Expression level of FMRP and apoptotic regulator BcL-xL was analyzed by Western blot RT-PCR and immunocytochemistry. Results An increased FMRP expression was measured in etoposide-treated HeLa cells which was induced by PI3K-Akt activation. Without FMRP expression cellular defence mechanism via PI3K-Akt-Bcl-xL was weakened and resulted in an .
