Abstract
Antagonizing Bcl-2's BH4 domain in cancer.
Highlights
Many cancer cells, including B-cell and lung cancers, display elevated expression of anti-apoptotic Bcl-2 proteins as a survival strategy to cope with oncogenic stress [1]
Editorial since cancers poorly responding to conventional chemotherapy are poor responders to BH3 mimetics, as both responses depend on the “mitochondrial apoptotic priming” status [5]
Correlating with this, in BIRD-2-sensitive diffuse large B-cell lymphoma (DLBCL) cells, BIRD-2 could boost cell death provoked by HA14-1, a Bcl-2 inhibitor that impacts Ca2+ signaling by inhibiting the sarco/endoplasmic reticulum Ca2+ ATPase [6]
Summary
Many cancer cells, including B-cell and lung cancers, display elevated expression of anti-apoptotic Bcl-2 proteins as a survival strategy to cope with oncogenic stress [1]. Editorial since cancers poorly responding to conventional chemotherapy are poor responders to BH3 mimetics, as both responses depend on the “mitochondrial apoptotic priming” status [5]. Distelhorst and co-workers recently showed that prolonged exposure of myeloma cells to BIRD-2 elevated Bim-protein levels via a Ca2+dependent mechanism, thereby increasing their sensitivity to BH3-mimetics and inducing synergistic effects with these drugs [4].
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
