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overexpressed in pNEN tissues and was positively correlated with H19 expression to promote cancer progression. Moreover, higher VGF expression was markedly related to poor differentiation and advanced stage. RNA sequence analysis revealed that H19 activates PI3K/Akt/CREB
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University of the Chinese Academy of Sciences, Beijing, China
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knockdown efficiencies were verified by qPCR assay. CT represents cell transfection with control lentivirus; 1A, 2A and 3A represent cells transfected with three kinds of H19 shRNA lentiviruses. (C, D and E) Proliferation of H19-knockdown and control QGP-1
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phosphatidylinositol-3-kinase (PI3K)/Akt signaling pathway. Moreover, inhibition of COX2 and PGE2 attenuates EGF-induced cancer cell invasion. These results demonstrate that COX2 and PGE2 are involved in EGF-induced human ovarian cancer cell invasion. Materials and
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with mTOR inhibitors, direct Akt inhibition with perifosine appears to have a more broad inhibitory effect on the PI(3)K–Akt–mTOR pathway without compensatory activation of PI(3)K and ERK1/2 signaling. On the other hand, perifosine induced CREB and JNK
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). The serine/threonine protein kinase PKB/Akt has emerged as a crucial regulator of growth, proliferation, differentiation and apoptosis, and is a major downstream effector of PI3K. Three isoforms of Akt (Akt1, Akt2, Akt3) have been cloned that are in
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is a key feature of breast cancer cells transformed by oncogenic PI3K–AKT signaling ( Zhang et al . 2011 , Fig. 1 ). It is also becoming clear that aberrant FOXO activity promotes a number of characteristic features of hormone-independent breast
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. For instance, activation of the PI3K/Akt pathway results in an active export of FOXOs into the cytoplasm. By contrast, in response to stress, FOXOs are activated by the members of the c-Jun-N-terminal kinase (JNK) leading to nuclear FOXO accumulation
Department of Gynecology, Department of Gynecologic Oncology, Systems Biology, Experimental Therapeutics, Department of Obstetrics and Gynecology, Obstetrics and Gynecology Hospital of Fudan University, 419 Fang Xie Road, Shanghai 200011, People's Republic of China
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Department of Gynecology, Department of Gynecologic Oncology, Systems Biology, Experimental Therapeutics, Department of Obstetrics and Gynecology, Obstetrics and Gynecology Hospital of Fudan University, 419 Fang Xie Road, Shanghai 200011, People's Republic of China
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Department of Gynecology, Department of Gynecologic Oncology, Systems Biology, Experimental Therapeutics, Department of Obstetrics and Gynecology, Obstetrics and Gynecology Hospital of Fudan University, 419 Fang Xie Road, Shanghai 200011, People's Republic of China
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(A) SKOV-3 cells and (B) ES-2 cells with different kinetics but did not affect pCREB and pIκB expression. The molecules pAKT, AKT, pJUN, cJUN, pCREB, CREB, pIκB, and IκB were detected by western blot. (C and D) The PI3K/AKT inhibitor LY294002 (LY) and
Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, Nebraska, USA
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Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, Nebraska, USA
Section of Urology, Department of Surgery, College of Medicine, University of Nebraska Medical Center, Omaha, Nebraska, USA
Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, Nebraska, USA
College of Pharmacy, Kaohsiung Medical University, Kaohsiung, Taiwan
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benign cell lines, and induction of miR-331-3p in cancer cells suppresses tumor phenotype through inhibition of PI3K/AKT signaling ( Epis et al. 2009 ). Interestingly, human antigen R (HuR) is an RNA-binding protein with elevated levels in PCa, which
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Foundation for Advanced Biomedical Research, Veneto Institute of Molecular Medicine (VIMM), Padova, Italy
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Department of Molecular Medicine, University of Pavia, Pavia, Italy
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) and PI3K-PKB/Akt ( Widenmaier et al. 2009 , Prabakaran et al. 2010 , Yabe & Seino 2011 ) or by reducing caspase 3 activity as well as the expression of the pro-apoptotic bax gene through a Foxo1 indirect effect (revised in Seino et al. 2010