Fig. 7: CANT1 competes with hSET1 at the PI3Kγ promoter in vitro. | Cell Death & Disease

Fig. 7: CANT1 competes with hSET1 at the PI3Kγ promoter in vitro.

From: LncRNA CANT1 suppresses retinoblastoma progression by repellinghistone methyltransferase in PI3Kγ promoter

Fig. 7

a, b ChIP assays demonstrated that CANT1 blocks the recruitment of hSET1 to the PI3Kγ promoter. IgG was used as a negative control. Sites X, Y: ChIP detection sites. Input: total RNA was reverse transcribed before incubation and amplified with primers. M: marker. c, d Real-time qPCR examination of hSET1 changes in the PI3Kγ promoter. All data are presented as the means ± SEM. *P < 0.05: compared with the control and mock. e Model of CANT1 regulation in tumorigenesis. In parent cancer cells, CANT1 lncRNA is inactivated and the hSET1 methyltransferase freely modifies the PI3Kγ promoter, providing histone H3K4 methylation to induce PI3Kγ expression; however, in CANT1-overexpressing cells, CANT1 occupies the PI3Kγ promoter and blocks the hSET1 interaction with the PI3Kγ promoter. Then, free hSET1 fails to methylate the PI3Kγ promoter and silences PI3Kγ expression, thus decreasing PI3K/Akt signaling and inhibiting tumor growth.

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