英文论文写作浅谈解决方案.pptVIP

主题 Akt, the serine-threonine protein kinase, mediates many of the downstream effects of PI3K and consequently plays an important role in human malignancy. Akt phosphorylates a variety of substrates involved in the regulation of oncogenesis. Akt promotes glioma cell survive by activating the activity of mTOR, TSC2, and S6. Akt also contributes to glioma cells invasion by increasing expression of MMPs (18, 19). Akt can be activated by a number of growth factors and their receptors, especially and EGFR, and negatively regulated by PTEN (20-22). Overexpression or mutation of EGFR may also potentially activate AkT in glioblastoma. Loss of PTEN in glioma is highly correlated with activation of AkT. Therefore, Akt activation frequently occurs in the majority of malignant gliomas. Our Western blot analysis revealed that overexpression of miR-221/222 led to an obvious activation of phosphorylated-Akt was in U251 cells. To confirm these data, we determined Akt activation after overexpression miR-221/222 in C6 cells and similar results were abtained. Thus, our study indicated that Akt pathway contributed to miR-221/222 regulation in gliomagenesis. 讨论（第二段） 主题 p27kip1, successfully identified as a direct target of miR-221/222, has a major contribution to the control of cancer cell proliferation and invasion. In the human androgen-independent prostate cancer PC3 cell line, exogenous expression of p27kip1 inhibits the proliferation of PC3 cells through induction of G1 arrest and apoptosis, and this process correlates with inhibition of EGFR/PI3K/Akt signaling pathway (23). In the human breast cancer cell line MDA-MB-231, up-regulation of p27kip1 remarkably inhibits the invasion of the breast cancer cells, in part due to the reduced expression of MMP-9 (24). In contrast, Akt regulates cell proliferation in breast cancer cells by preventing p27kip1-mediated growth arrest (25). EGFR can enhance cell proliferation in part by down-regulation of p27kip1 through activation of PI3K/Akt p