RFPL3 and CBP synergistically upregulate hTERT activity and promote lung cancer growth.

摘要: hTERT is the key component of telomerase and its overactivation contributes to maintaining telomere length cell immortalization. Previously, we identified RFPL3 as a new transcription activator in lung cancers. However, exact mechanism mediating activation associated signal regulatory network remain unclear. In this study, found that colocalized interacted directly with CBP nucleus cancer cells. Immunohistochemical analysis tissue microarrays cancers revealed simultaneous overexpression both predicted relatively poor prognosis. Furthermore, confirmed their synergistic stimulation on expression tumor growth. The binding promoter was reduced markedly when knocked down by specific siRNA or suppressed inhibitor cells stable RFPL3. When one two proteins upregulated downregulated, whereas another remains unchanged, activity were activated repressed accordingly. meantime, growth also promoted attenuated coordinated upregulate through CBP-induced acetylation protein co-anchoring at region. Collectively, our results reveal regulation suggest RFPL3/CBP/hTERT signaling pathway may be targets for treatment.