Inhibition of phosphatidylinositol 3-kinase (PI3K) enzyme and human skin carcinoma cell growth by Combretum apiculatum Sond.

2021 ◽  
Vol 140 ◽  
pp. 95-102
Author(s):  
Jacqueline Maphutha ◽  
Danielle Twilley ◽  
Namrita Lall
Keyword(s):  
Cell Growth ◽  
Human Skin ◽  
Carcinoma Cell ◽  
Skin Carcinoma ◽  
Phosphatidylinositol 3 Kinase ◽  
Combretum Apiculatum ◽  
Phosphatidylinositol 3

scholarly journals Insulin Generates Free Radicals by an NAD(P)H, Phosphatidylinositol 3'-Kinase-Dependent Mechanism in Human Skin Fibroblasts Ex Vivo

Diabetes ◽  
2004 ◽  
Vol 53 (5) ◽  
pp. 1344-1351 ◽  
Author(s):  
G. Ceolotto ◽  
M. Bevilacqua ◽  
I. Papparella ◽  
E. Baritono ◽  
L. Franco ◽  
...  
Keyword(s):  
Free Radicals ◽  
Human Skin ◽  
Ex Vivo ◽  
Skin Fibroblasts ◽  
Human Skin Fibroblasts ◽  
Phosphatidylinositol 3 Kinase ◽  
Dependent Mechanism ◽  
Phosphatidylinositol 3

scholarly journals Cancer Cell-Derived Clusterin Modulates the Phosphatidylinositol 3′-Kinase-Akt Pathway through Attenuation of Insulin-Like Growth Factor 1 during Serum Deprivation

2008 ◽  
Vol 28 (13) ◽  
pp. 4285-4299 ◽  
Author(s):  
Hakryul Jo ◽  
Yonghui Jia ◽  
Kulandayan K. Subramanian ◽  
Hidenori Hattori ◽  
Hongbo R. Luo
Keyword(s):  
Growth Factor ◽  
Cell Growth ◽  
Cancer Cell ◽  
Regulatory System ◽  
Serum Deprivation ◽  
Akt Pathway ◽  
Growth Factor Signaling ◽  
Insulin Like Growth Factor ◽  
Phosphatidylinositol 3 Kinase ◽  
Phosphatidylinositol 3

ABSTRACT Cancer cells in their respective microenvironments must endure various growth-constraining stresses. Under these conditions, the cancer cell-derived factors are thought to modulate the signaling pathways between cell growth and dormancy. Here, we describe a cancer cell-derived regulatory system that modulates the phosphatidylinositol 3′-kinase (PI3K)-Akt pathway under serum deprivation stress. Through the use of biochemical purification, we reveal that cancer cell-secreted insulin-like growth factor 1 (IGF-1) and clusterin, an extracellular stress protein, constitute this regulatory system. We show that secreted clusterin associates with IGF-1 and inhibits its binding to the IGF-1 receptor and hence negatively regulates the PI3K-Akt pathway during serum deprivation. This inhibitory function of clusterin appears to prefer IGF-1, as it fails to exert any effects on epidermal growth factor signaling. We demonstrate furthermore that the constitutive activation of oncogenic signaling downstream of IGF-1 confers insensitivity to the inhibitory effects of clusterin. Thus, the interplay between cancer cell-derived clusterin and IGF-1 may dictate the outcome of cell growth and dormancy during tumorigenic progression.

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