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. 2018 Dec 4;19(2):771–782. doi: 10.3892/mmr.2018.9721

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Copyright: © Wang et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 2. — Underlying regulatory mechanisms of CCAT1 in human cancer. (A) C-Myc is able to directly bind to E-box element in CCAT1 promoter regions to activate CCAT1 transcription. (B) CCAT1, which may be activated by H3K27-acetylation, is able to serve as a scaffold for PRC2 and SUV39H1, and modulate the histone methylation of promoter of SPRY4, thereby epigenetically silencing tumour suppressor gene SPRY4. (C) CCAT1 additionally functions as competing endogenous RNA by sponging microRNA to free its target mRNA for protein production. (D) CCAT1 may activate the ERK/MAPK signalling pathway. CCAT1, colon cancer-associated transcript 1; ERK/MAPK, extracellular signal-regulated kinase/mitogen-activated protein kinase; lncRNA, long non-coding RNA; PRC2, polycomb repressive complex 2; SPRY4, sprouty RTK signalling antagonist 4; SUV39H1, suppressor of variegation 3–9 homolog 1.