Knockdown of CBP or inhibition of its HAT activity inhibits lung cancer cell growth and induces apoptosis.
Knockdown of CBP or inhibition of its HAT activity inactivates MAPK signaling pathway.
CBP interacts with and acetylates CPSF4 to promote hTERT expression and tumor growth in lung cancer cells.
Overexpression of both CBP and CPSF4 predicted poor prognosis of the patients with lung adenocarcinomas.