Abstract:
:Aberrant splicing is frequently found in cancer, yet the biological consequences of such alterations are mostly undefined. Here we report that the Hippo-YAP signalling, a key pathway that regulates cell proliferation and organ size, is under control of a splicing switch. We show that TEAD4, the transcription factor that mediates Hippo-YAP signalling, undergoes alternative splicing facilitated by the tumour suppressor RBM4, producing a truncated isoform, TEAD4-S, which lacks an N-terminal DNA-binding domain, but maintains YAP interaction domain. TEAD4-S is located in both the 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 tumour growth in xenograft mouse models. Furthermore, TEAD4-S is reduced in human cancers, and patients with elevated TEAD4-S levels have improved survival. Altogether, these data reveal a splicing switch that serves to fine tune the Hippo-YAP pathway.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Qi Y,Yu J,Han W,Fan X,Qian H,Wei H,Tsai YH,Zhao J,Zhang W,Liu Q,Meng S,Wang Y,Wang Zdoi
10.1038/ncomms11840subject
Has Abstractpub_date
2016-06-13 00:00:00pages
ncomms11840issn
2041-1723pii
ncomms11840journal_volume
7pub_type
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