RNAi-mediated silencing of insulin receptor substrate-4 enhances actinomycin D- and tumor necrosis factor-α-induced cell death in hepatocarcinoma cancer cell lines

2009 ◽  
Vol 108 (6) ◽  
pp. 1292-1301 ◽  
Author(s):  
Eva P. Cuevas ◽  
Oscar Escribano ◽  
Jorge Monserrat ◽  
Javier Martínez-Botas ◽  
María G. Sánchez ◽  
...  
Keyword(s):  
Cell Death ◽  
Tumor Necrosis Factor ◽  
Insulin Receptor ◽  
Cell Lines ◽  
Cancer Cell ◽  
Tumor Necrosis ◽  
Actinomycin D ◽  
Insulin Receptor Substrate ◽  
Factor I ◽  
Necrosis Factor

scholarly journals Tumor Necrosis Factor α-induced Phosphorylation of Insulin Receptor Substrate-1 (IRS-1)

1995 ◽  
Vol 270 (40) ◽  
pp. 23780-23784 ◽  
Author(s):  
Hannah Kanety ◽  
Revital Feinstein ◽  
Moshe Z. Papa ◽  
Rina Hemi ◽  
Avraham Karasik
Keyword(s):  
Tumor Necrosis Factor ◽  
Insulin Receptor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Insulin Receptor Substrate ◽  
Insulin Receptor Substrate 1 ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Insulin receptor substrate 1 regulates the cellular differentiation and the matrix metallopeptidase expression of preosteoblastic cells

2010 ◽  
Vol 206 (3) ◽  
pp. 271-277 ◽  
Author(s):  
Yan-Hong Bu ◽  
Yu-Ling He ◽  
Hou-De Zhou ◽  
Wei Liu ◽  
Dan Peng ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Bone Turnover ◽  
Insulin Receptor ◽  
Bone Metabolism ◽  
Intracellular Signaling ◽  
Tumor Necrosis ◽  
Insulin Receptor Substrate ◽  
Insulin Receptor Substrate 1 ◽  
Matrix Metallopeptidase ◽  
Necrosis Factor

Insulin receptor substrate 1 (IRS1) is an essential molecule for the intracellular signaling of IGF1 and insulin, which are potent anabolic regulators of bone metabolism. Osteoblastic IRS1 is essential for maintaining bone turnover; however, the mechanism underlying this regulation remains unclear. To clarify the role of IRS1 in bone metabolism, we employed RNA interference to inhibit IRS1 gene expression and observed the effects of silencing this gene on the proliferation and differentiation of and the expression of matrix metallopeptidase (MMP) and tumor necrosis factor receptor superfamily, member 11b (TNFRSF11B) in MC3T3-E1 cells. Our results showed that IRS1 short hairpin RNAs can effectively suppress the expression of IRS1, and inhibit the phosphorylation of AKT in IRS1 pathway; reduce the expression of MMP2, MMP3, MMP13, and MMP14, decrease the expression of TNFRSF11B and RANKL (also known as tumor necrosis factor (ligand) superfamily, member 11), however increase the RANKL/TNFRSF11B ratio; decrease cell survival, proliferation, and mineralization, and impair the differentiation of MC3T3-E1 cells. The downregulation of IRS1 had no effect on the expression of MMP1. Our findings suggest that IRS1 not only promotes bone formation and mineralization but also might play roles in bone resorption partly via the regulation of MMPs and RANKL/TNFRSF11B ratio, thus regulates the bone turnover.

Halocynthiaxanthin and Peridinin Sensitize Colon Cancer Cell Lines to Tumor Necrosis Factor–Related Apoptosis-Inducing Ligand

2007 ◽  
Vol 5 (6) ◽  
pp. 615-625 ◽  
Author(s):  
Tatsushi Yoshida ◽  
Takashi Maoka ◽  
Swadesh K. Das ◽  
Kazuki Kanazawa ◽  
Mano Horinaka ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Tumor Necrosis Factor ◽  
Cell Lines ◽  
Cancer Cell ◽  
Tumor Necrosis ◽  
Cancer Cell Lines ◽  
Colon Cancer Cell ◽  
Colon Cancer Cell Lines ◽  
Necrosis Factor
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