Insulin-like growth factor-1 induces the phosphorylation of PRAS40 via the PI3K/Akt signaling pathway in PC12 cells

Wang, Haitao; Qishan, Zhang; Zhang, Lang; Little, Peter J.; Xie, Xiao-chun; Meng, Qingwei; Ren, Yannan; Zhou, Ling; Gao, Guoquan; Quirion, Rémi; Zheng, Wenhua

doi:10.1016/j.neulet.2012.03.068

Cited by 20 publications

(17 citation statements)

References 21 publications

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“…We then examined whether supplementation of differentiation medium with IGF-1 would affect the extent or the kinetics of Brn-4 expression. Hippocampal NSCs were transferred to differentiation medium containing IGF-1 (100 ng/ml) as described by others [16] , [17] , [18] for 3, 6 or 24 h. Control hippocampal NSCs were cultured only with differentiation medium for 24 h. As shown in Fig. 4C, and D , supplementation with IGF-1 brought a rapid increase in levels of Brn-4 mRNA determined by RT-PCR, with a marked upregulation at 3 h versus differentiation medium alone (compare Fig.…”

Section: Resultsmentioning

confidence: 99%

“…NSCs were transferred to differentiation medium containing the following supplements: (1) no addition, (2) IGF-1 (100 ng/ml), (3) IGF-1 (100 ng/ml) plus PD98059 (50 µM), (4) IGF-1 (100 ng/ml) plus LY294002 (50 µM) (5) DMSO (1%), and (6) DMSO (1%)+IGF-1 (100 ng/ml). In all cases treatment with either inhibitor (PD98059 and LY294002) or vehicle (DMSO) was commenced 40 min [17] , [18] before addition, where appropriate, of IFG-1. After 6 h of IGF-1 treatment, total protein and RNA were extracted and examined for Brn-4 expression using RT-PCR and western blotting.…”

Section: Resultsmentioning

confidence: 99%

“…Depending on cell type and context, IGF-1 is known to promote neuronal survival, maturation [41] , [42] , [43] , [44] , [45] , and cell-cycle progression [46] by activating the PI3K/Akt and/or Ras/MAPK pathways. Using previously established protocols [16] , [17] , [18] , we investigated whether inhibition of either the PI3K or MAPK pathways would interfere with IGF-1-induced upregulation of Brn-4. We clarified that cells treated with the PI3K inhibitor LY294002 failed to upregulate Brn-4 in response to IGF-1, whereas Brn-4 upregulation was unaffected by treatment with the MAPK inhibitor PD98059.…”

Section: Discussionmentioning

confidence: 99%

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IGF-1 Promotes Brn-4 Expression and Neuronal Differentiation of Neural Stem Cells via the PI3K/Akt Pathway

Zhang

Cheng

et al. 2014

PLoS ONE

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Our previous studies indicated that transcription factor Brn-4 is upregulated in the surgically denervated hippocampus in vivo, promoting neuronal differentiation of hippocampal neural stem cells (NSCs) in vitro. The molecules mediating Brn-4 upregulation in the denervated hippocampus remain unknown. In this study we examined the levels of insulin-like growth factor-1 (IGF-1) in hippocampus following denervation. Surgical denervation led to a significant increase in IGF-1 expression in vivo. We also report that IGF-1 treatment on NSCs in vitro led to a marked acceleration of Brn-4 expression and cell differentiation down neuronal pathways. The promotion effects were blocked by PI3K-specific inhibitor (LY294002), but not MAPK inhibitor (PD98059); levels of phospho-Akt were increased by IGF-1 treatment. In addition, inhibition of IGF-1 receptor (AG1024) and mTOR (rapamycin) both attenuated the increased expression of Brn-4 induced by IGF-1. Together, the results demonstrated that upregulation of IGF-1 induced by hippocampal denervation injury leads to activation of the PI3K/Akt signaling pathway, which in turn gives rise to upregulation of the Brn-4 and subsequent stem cell differentiation down neuronal pathways.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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IGF-1 Promotes Brn-4 Expression and Neuronal Differentiation of Neural Stem Cells via the PI3K/Akt Pathway

Zhang

Cheng

et al. 2014

PLoS ONE

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“…Overexpression of IGF-1R may be a useful predictor of lymph node metastasis, recurrence and post-surgical outcomes in patients with NSCLC (16). Under normal conditions, the binding of IGFs to IGF-1R leads to activation of downstream signaling pathways, such as the phosphatidylinositol 3′-kinase/AKT-kinase (PI3K/AKT) signaling pathway, and increasing proliferation and survival (17). …”

Section: Introductionmentioning

confidence: 99%

Celecoxib inhibits insulin-like growth factor 1 induced growth and invasion in non-small cell lung cancer

Liu

Bao

et al. 2013

Oncology Letters

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Despite a large number of studies indicating that celecoxib plays an important role in the prevention and treatment of tumors, the detailed molecular mechanisms are not well understood. The aim of the present study was to investigate the effect of celecoxib on insulin-like growth factor 1 (IGF-1)-induced growth and invasion in non-small cell lung cancer (NSCLC). For these experiments, IGF-1-induced cell growth and invasion were analyzed in A549 cells in the presence and absence of celecoxib. The effects of celecoxib on the expression of phosphorylated type-1 IGF receptor (IGF-1R) and phosphorylated AKT (p-AKT) were examined using western blot analysis. The influence of celecoxib on IGF-binding protein-3 (IGFBP-3) expression was analyzed using ELISA. Celecoxib inhibited IGF-1-stimulated growth and invasion in a dose-dependent manner. Celecoxib also reduced the expression of IGF-1R, IGFBP-3 and phosphorylation of AKT. The results suggest that modulating the IGF axis may be a new mechanism for the anticancer effect of celecoxib on NSCLC.

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“…Upregulating FoxO3a expression inhibits the proliferation of breast cancer cells (24,25). Previous studies have demonstrated that IGF-1 is able to activate the phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway in UM cells, and the activated PI3K/Akt pathway has been demonstrated to promote the phosphorylation of FoxO3a (26). FoxO3a phosphorylation induces its translocation into the cytoplasm from the nucleus and inhibits its function.…”

Section: Discussionmentioning

confidence: 99%

Forkhead box protein O3 suppresses uveal melanoma development by increasing the expression of Bcl‑2‑like protein 11 and cyclin‑dependent kinase inhibitor 1B

et al. 2017

Self Cite

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Forkhead box protein O3 (FoxO3a) is a forkhead box family transcription factor which serves an important role in a number of biological functions, including tumor growth. A previous study indicated that FoxO3a serves a role in insulin like growth factor‑induced growth, migration and invasion of uveal melanoma (UM) cells; however, whether FoxO3a is associated with the development and formation of UM remains unknown. In the present study, the role of FoxO3a in UM development and formation was investigated by modulating the expression of FoxO3a in a human UM cell line. The results of the present study demonstrated that FoxO3a overexpression in UM cells inhibited cell proliferation and promoted cellular apoptosis, leading to an accumulation of cells at the G1 cell cycle phase. Western blot analysis demonstrated that FoxO3a overexpression increased the transcription and protein expression of Bcl‑2‑like protein 11 and cyclin‑dependent kinase inhibitor 1B, and inhibited cyclin D1 transcription and expression. The opposite effects were observed when FoxO3a was knocked down in UM cells. The results of the present study indicated that FoxO3a may exhibit a negative role in UM development and formation, which is consistent with its role as a tumor suppressor.

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Insulin-like growth factor-1 induces the phosphorylation of PRAS40 via the PI3K/Akt signaling pathway in PC12 cells

Cited by 20 publications

References 21 publications

IGF-1 Promotes Brn-4 Expression and Neuronal Differentiation of Neural Stem Cells via the PI3K/Akt Pathway

IGF-1 Promotes Brn-4 Expression and Neuronal Differentiation of Neural Stem Cells via the PI3K/Akt Pathway

Celecoxib inhibits insulin-like growth factor 1 induced growth and invasion in non-small cell lung cancer

Forkhead box protein O3 suppresses uveal melanoma development by increasing the expression of Bcl‑2‑like protein 11 and cyclin‑dependent kinase inhibitor 1B

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