3-Deoxy-d-myo-inositol 1-Phosphate, 1-Phosphonate, and Ether Lipid Analogues as Inhibitors of Phosphatidylinositol-3-kinase Signaling and Cancer Cell Growth

1998 ◽  
Vol 41 (18) ◽  
pp. 3303-3306 ◽  
Author(s):  
Lixin Qiao ◽  
Fajun Nan ◽  
Mark Kunkel ◽  
Alfred Gallegos ◽  
Garth Powis ◽  
...  
Keyword(s):  
Cell Growth ◽  
Cancer Cell ◽  
Ether Lipid ◽  
Kinase Signaling ◽  
Phosphatidylinositol 3 Kinase ◽  
Cancer Cell Growth ◽  
Inositol 1 ◽  
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.

3-(Hydroxymethyl)-Bearing Phosphatidylinositol Ether Lipid Analogues and Carbonate Surrogates Block PI3-K, Akt, and Cancer Cell Growth

2000 ◽  
Vol 43 (16) ◽  
pp. 3045-3051 ◽  
Author(s):  
Youhong Hu ◽  
Lixin Qiao ◽  
Shaomeng Wang ◽  
Suo-bao Rong ◽  
Emmanuelle J. Meuillet ◽  
...  
Keyword(s):  
Cell Growth ◽  
Cancer Cell ◽  
Ether Lipid ◽  
Cancer Cell Growth

794: Valproic Acid Inhibits Prostate Cancer Cell Growth in Vitro and in Vivo

2006 ◽  
Vol 175 (4S) ◽  
pp. 257-257
Author(s):  
Jennifer Sung ◽  
Qinghua Xia ◽  
Wasim Chowdhury ◽  
Shabana Shabbeer ◽  
Michael Carducci ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Valproic Acid ◽  
Cell Growth ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Cancer Cell Growth

Screening for naturally occurring oxyprenylated secondary metabolites as cancer cell growth inhibitory agents

Planta Medica ◽  
2012 ◽  
Vol 78 (11) ◽  
Author(s):  
F Epifano ◽  
S Genovese ◽  
P Lullo ◽  
S Fiorito ◽  
G Trivisonno ◽  
...  
Keyword(s):  
Cell Growth ◽  
Secondary Metabolites ◽  
Cancer Cell ◽  
Cancer Cell Growth ◽  
Naturally Occurring ◽  
Growth Inhibitory ◽  
Inhibitory Agents
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