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. 2021 Jun 9;11:657965. doi: 10.3389/fonc.2021.657965

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Copyright © 2021 Farooqi, Nayyab, Martinelli, Berardi, Katifelis, Gazouli and Cho

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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(A) PLACT1 mediated inhibition of IκBα by epigenetic inactivation. PLACT1 also enhanced loading of hnRNPA1 to the promoter region of IκBα. E2F1 induced activation of PLACT1. (B) HOTTIP formed a complex with adaptor protein WDR5 and MLL1 (H3K4 methyltransferase) to trans-activate oncogenic proteins by increasing the levels of trimethylated lysine-4 at histone-3 (H3K4) at their promoters. (C) SLC7A11-AS1 blocked β-TRCP-induced ubiquitination and degradation of NRF2. (D) SOX2OT destabilized FUS protein by binding directly to FUS. FUS transcriptionally repressed CCND1. (E) DUSP1 (Dual-specificity phosphatase-1) mediated dephosphorylation of SAPK resulted in inhibition of the pathway. LINC01111 sponged away DUSP1 from miR-3924 and promoted expression of DUSP1. DUSP1 dephosphorylated SAPK and prevented its nuclear accumulation. (F) RREB1-stimulated expression of AGAP2-AS1. AGAP2-AS1 interacted with EZH2 and repressed expression of ANGPTL4 and ANKRD1.