Anindya Goswami

TL;DR: 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.

TL;DR: 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.

TL;DR: 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.

TL;DR: It is found that Par-4 participates in mediating apoptosis by PTEN, the tumor suppressor responsible for blocking PI3K/Akt signaling, and may provide a useful focus for the development of cancer-selective therapeutics.

TL;DR: The in vitro result strongly suggests that sub-toxic doses of 3-azidoWA enhanced the secretion of extracellular Par-4 that abolished secretory MMP-2 expression and activity and implied that 3-AZidoWA attenuated internal phospho-ERK and phospho -Akt expression in a dose dependent manner might play a key role in inhibition of mouse angiogenesis by 3-razidoWA.