Issue
Copyright (c) 2023 Yang Wang, Yinsha Miao, Wen Zhou, Yu Bi, Yanhong Ji, Yunfeng Ma
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
The undersigned hereby assign all rights, included but not limited to copyright, for this manuscript to CMB Association upon its submission for consideration to publication on Cellular and Molecular Biology. The rights assigned include, but are not limited to, the sole and exclusive rights to license, sell, subsequently assign, derive, distribute, display and reproduce this manuscript, in whole or in part, in any format, electronic or otherwise, including those in existence at the time this agreement was signed. The authors hereby warrant that they have not granted or assigned, and shall not grant or assign, the aforementioned rights to any other person, firm, organization, or other entity. All rights are automatically restored to authors if this manuscript is not accepted for publication.Activation-induced cytidine deaminase displays an alternative co-factor for modulating PIM1 expression in diffuse large B cell lymphoma cell lines
Corresponding Author(s) : Yunfeng Ma
Cellular and Molecular Biology,
Vol. 69 No. 3: Issue 3
Abstract
Diffuse large B cell lymphoma (DLBCL) is a B cell neoplasm characterized by high PIM1 expression, which is responsible for poor prognosis. Activation-induced cytidine deaminase (AID) is closely linked to PIM1 hypermutation in DLBCL. Here, we found that the DNA methyltransferase 1 (DNMT1) level decreased with AID depletion in the DLBCL cell line SU-DHL-4, and increased significantly when AID was highly expressed. The double ablation of AID and DNMT1 contributed to increased PIM1 expression, which initiated faster DLBCL cell proliferation, whereas ten-eleven translocation family member 2 (TET2) decreased with AID deficiency and increased with AID overexpression in DLBCL cell line OCI-LY7. The double depletion of AID and TET2 was associated with decreased PIM1 levels and showed slower cell division. We suggest an alternative role of AID as a co-factor of DNA methylation cooperated with DNMT1, or of DNA demethylation associated with TET2 in modulating PIM1 expression. Our findings demonstrate that AID interacts with either DNMT1 or TET2 to form a complex to bind with a PIM1 promoter and thus is responsible for the modulation of PIM1 expression. These results provide insights into an alternative role of AID to DLBCL-associated genes.
Keywords
Download Citation
Endnote/Zotero/Mendeley (RIS)BibTeX
