A splicing switch of TEAD4 regulates Hippo-YAP signaling pathway to inhibit tumor proliferation
Ontology highlight
ABSTRACT: Splicing dysregulations extensively occur in cancers, yet the biological consequences of such alterations are mostly undefined. Here we report that the Hippo-YAP signaling, a key pathway that regulates cell proliferation and organ size, is under control of a new splicing switch. We show that TEAD4, the transcription factor that mediates Hippo-YAP signaling, undergoes alternative splicing facilitated by the tumor suppressor RBM4, producing a truncated isoform, TEAD4-S, which lacks N-terminal DNA-binding domain but maintains YAP-interaction domain. TEAD4-S is located in both nucleus and cytoplasm, acting as a dominant negative isoform to YAP activity. Consistently, TEAD4-S is reduced in cancer cells, and its re-expression suppresses cancer cell proliferation and migration, inhibiting tumor g
ORGANISM(S): Homo sapiens
SUBMITTER: Zefeng Wang
PROVIDER: E-GEOD-80372 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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