Specific death of ALT cells through TSPYL5 depletion

Abstract

Some tumors acquire replicative immortality by activating an ALTernative telomerase-independent telomere maintenance mechanism. ALT offers interesting therapeutic perspectives but lacks any known specific targets. We discovered a crucial role for TSPYL5 (Testis-Specific Y-encoded-Like Protein 5) in keeping ALT cell viability by protecting POT1 (Protection Of Telomeres 1) from proteasomal degradation.