PAX5 and circ1857 affected DLBCL progression and B‐cell proliferation through regulating GINS1

Author:

Wang Ting1,Chen Zhenfa1,Li Cui1,Zhang Wei1,Huang Wenbin2,Xue Jun3,Wang Jundong4,Li Shufeng1ORCID

Affiliation:

1. Key Laboratory of Developmental Genes and Human Disease in Ministry of Education, Jiangsu Provincial Key Laboratory of Critical Care Medicine, Department of Biochemistry and Molecular Biology Medical School of Southeast University Nanjing China

2. Department of Pathology, Nanjing First Hospital Nanjing Medical University Nanjing China

3. Department of Hematology, Nanjing First Hospital Nanjing Medical University Nanjing China

4. Department of Ultrasound, Nanjing First Hospital Nanjing Medical University Nanjing China

Abstract

AbstractPAX5, a member of the paired box gene family of transcription factors, is a B‐cell‐specific activator protein that plays important roles during B lymphopoiesis. Two putative PAX5 binding sites in the human GINS1 promoter region were identified. EMSA, ChIP and luciferase assay showed that PAX5 functions as a positive transcription factor for GINS1 expression. Furthermore, coordinated expression of PAX5 and GINS1 was observed in mice B cells under physiological conditions and LPS stimulation situations. A similar pattern was also observed in human DLBCL cell lines under differentiation‐inducing conditions. In addition, both PAX5 and GINS1 were highly expressed and significantly correlated in DLBCL specimens and cell lines. These findings suggested that dysregulation of PAX5 played an extremely important role in controlling the universal phenomenon of tumor progression through increased expression of GINS1 in DLBCL. In addition, circ1857 that was generated using back splicing of PAX5 pre‐mRNA could further stabilize GINS1 mRNA, modulate GINS1 expression and promote lymphoma progression. To the best of our knowledge, this report is the first to demonstrate the role of GINS1 in DLBCL progression, and the mechanism of GINS1 upregulation using both circ1857 and PAX5 in DLBCL was revealed. Our results suggested that GINS1 may be a possible therapeutic target for DLBCL.

Publisher

Wiley

Subject

Cancer Research,Oncology,General Medicine

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