Translational regulation of x-linked inhibitor of apoptosis protein by interleukin-6: a novel mechanism of tumor cell survival.

摘要: Interleukin-6 (IL-6) is a pleiotropic cytokine with diverse biological effects. IL-6 has been implicated in autocrine signaling pathways promoting tumor progression and chemoresistance some human tumors. However, the mechanisms by which modulates these responses are unknown. Aberrant apoptosis as fundamental mechanism of chemotherapeutic resistance. Thus, we investigated whether alters expression regulatory proteins drug We provide evidence that rapidly phosphorylates translation initiation factor eukaryotic factor-4E triggers antiapoptotic cholangiocarcinoma cells. Reduction cellular RNA interference decreases IL-6-induced effects on cytotoxic drug-induced caspase activation apoptosis. Furthermore, increases endogenous X-linked inhibitor protein at an internal ribosome entry site. Our findings translationally regulates reveal novel mediates cell survival may be targeted therapeutically to decrease chemoresistance.