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The Cyclooxygenase-2 Inhibitor Celecoxib Induces Apoptosis by Blocking Akt Activation in Human Prostate Cancer Cells Independently of Bcl-2*
TLDR
The data demonstrate that inhibition of Akt activation may play a crucial role in the induction of apoptosis by celecoxib, supported by studies showing that overexpression of constitutively active Akt protects PC-3 cells from Celecoxib-induced apoptosis.
The Tumor Suppressor Par-4 Activates an Extrinsic Pathway for Apoptosis
TLDR
Interestingly, extracellular Par-4 induced apoptosis by binding to the stress response protein, glucose-regulated protein-78 (GRP78), expressed at the surface of cancer cells, and activates an extrinsic pathway involving cell surface GRP78 receptor for induction of apoptosis.
Identification of a Unique Core Domain of Par-4 Sufficient for Selective Apoptosis Induction in Cancer Cells
TLDR
A unique death-inducing domain selective for apoptosis induction in cancer cells (SAC domain) is identified which holds promise for identifying key differences between cancer and normal cells and for molecular therapy of cancer.
Expression and function of the leucine zipper protein Par-4 in apoptosis
TLDR
Findings suggest that the leucine zipper domain is required for the Par-4 protein to function in apoptosis.
Binding and phosphorylation of par-4 by akt is essential for cancer cell survival.
TLDR
Par-4 is essential for PTEN-inducible apoptosis, and inactivation of Par-4 by Akt promotes cancer cell survival, suggesting that inhibition of the PI3K-Akt pathway leads to Par- 4-dependent apoptosis.
A novel repressor, par-4, modulates transcription and growth suppression functions of the Wilms' tumor suppressor WT1
TLDR
A novel repressor that modulates transcription as well as growth suppression functions of WT1 is identified, and par-4, but not a mutant unable to interact with WT1, rescued growth suppression caused by WT1.
Par-4 drives trafficking and activation of Fas and Fasl to induce prostate cancer cell apoptosis and tumor regression.
TLDR
Findings identify a mechanism of apoptosis by Par-4 and suggest that Par- 4 may have therapeutic potential and identify the Fas pathway activation alone nor inhibition of NF-kappaB activity with IkappaB-super repressor was sufficient to induce apoptosis of prostate cancer cells.
Phosphorylation of Par-4 by Protein Kinase A Is Critical for Apoptosis
TLDR
Evidence is presented that the proapoptotic protein Par-4 utilizes one such common tumorigenic trait to become selectively activated and induce apoptosis in cancer cells, and observations suggest that selective apoptosis of cancer cells by the SAC domain of Par- 4 involves phosphorylation of T155 by PKA.
Suppression of PTEN expression by NF-kappa B prevents apoptosis.
TLDR
It is reported here that the tumor suppressor PTEN, which functions as a negative regulator of phosphatidylinositol (PI)-3 kinase/Akt-mediated cell survival pathway, is down regulated by p65 but not by p50, indicating a negative regulatory loop involving PTEN and NF-kappa B.
Commonality of the gene programs induced by effectors of apoptosis in androgen-dependent and -independent prostate cells.
TLDR
Together, par-1, -3, -4, and -5 represent an apoptosis response gene program common to both androgen-dependent and -independent prostate cells, and are predicted to be important components of diverse effector-driven apoptotic pathways.
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