The goal of the study is to show that phorbol 12-myristate-13-acetate (PMA) stimulated activation of protein kinase C-ç (PKC-ç) in U-251 glioblastoma (GBM) cells resulted in activation of both Akt and the mammalian target of rapamycin (mTOR) signaling pathways and an increase in cell proliferation. The abstract acknowledged that previous studies proved that PMA induced proliferation in glioblastoma cells by PKC-ç. It also states that PKC-ç is involved in cell growth through Akt and motor signaling pathways. The information given introduces how the inhibition of mTOR reduces proliferation and a kinase dead PKC-ç reducing proliferation of expressed GBM cells. The construction of the GBM cells also presents evidence that PKC-ç targets Akt and mTOR signaling. Rapamycin was inhibited in expressed GBM cells with activation of 4E-BP1 and STAT-3 in treated PMA and PKC-ç. The PI-3 kinase inhibitor only activated Akt. The abstract concluded that the study identifies Akt and mTOR as downstream targets of PKC-ç that are involved in GBM cell proliferations.
The introduction of the paper gave sufficient basic information on Glioblastoma multiforme. It was stated that GBM cells have rates of high proliferation within the brain. The astrocyctic tumors express many integrins which promote specific inhibitors and growth factors. When the PKCs are upstream along with other growth factors they aid in the progression of differentiated astrocytic tumors. The materials and methods gave information that best suited the goal of the paper. Methods consisted of cell cultures, retroviral expression, propidium iodide FACS analysis, H-thymidine incorporation, and western blot analysis. The only section not fully understood was the use of the H-thymidine method. The data and graphs set up were helpful to understanding the results. This was observed throughout each figure given. Figure 3, 4, and 5 especially shows the presence and lack of activity of all samples in...
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