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. 2022 Jan 31;12:678025. doi: 10.3389/fonc.2022.678025

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Copyright © 2022 Qiu, Wu, Shi, Liu, Li, Wu and Lin

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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ASF1B targets p-AKT, AKT, and FOXP3, and rescue assays confirm that FOXP3 is an important downstream effector of ASF1B. Western blot analyses (A) and relative protein level test (B) indicated that ASF1B silencing decreased p-AKT, AKT, and FOXP3 protein levels, *p < 0.05. (C) RT-qPCR confirmed the overexpression of FOXP3 in FOXP3 overexpressing plasmid-transfected group, *p < 0.05. (D) Cell proliferation was detected by CCK-8 assays for three separate treatments, *p < 0.05. (D) The effect of FOXP3 overexpression on in ASF1B-silenced KTC-1 cell proliferation was determined by CCK-8 assay, *p < 0.05. (F, G) Cell migration activity was performed by wound healing assay in ASF1B-silenced KTC-1 cells after transfection with FOXP3-overexpressing plasmid or empty plasmid, *p < 0.05.