CAPG facilitates diffuse large B-cell lymphoma cell progression through PI3K/AKT signaling pathway

癌症研究 生物 PI3K/AKT/mTOR通路 蛋白激酶B 弥漫性大B细胞淋巴瘤 CEBPA公司 淋巴瘤 细胞生长 流式细胞术 信号转导 细胞生物学 免疫学 突变 基因 遗传学 生物化学
作者
Ganggang Wang,Hu Liu,Lin An,Shuling Hou,Qiaohua Zhang
出处
期刊:Human Immunology [Elsevier BV]
卷期号:83 (12): 832-842 被引量:5
标识
DOI:10.1016/j.humimm.2022.10.001
摘要

Diffuse large B-cell lymphoma (DLBCL) is a genetically heterogeneous tumor. Currently, macrophage-capping protein (CAPG) has been discovered to play a crucial part as a regulator in various cancers. However, it still remains unclear regarding its regulatory mechanism in DLBCL. Therefore, this study focused on revealing the mechanism underlying CAPG in DLBCL.The bioinformatics analysis was conducted to predict the expression of CAPG in DLBCL and its downstream target genes. qRT-PCR was utilized to detect mRNA expression levels of CAPG and CEBPA. Western blot was performed to examine the expression levels of related proteins. Then we employed flow cytometry for the analysis of cell cycle and apoptosis. We also used MTT assay to measure cell survival and IHC assay to detect CAPG expression in DLBLC tissues. Then, ChIP was used to determine the binding of CEBPA and CAPG. For in vivo experiments, xenograft models were employed to investigate the effect of CAPG on DLBCL.High-level of CAPG expression was found in DLBCL cells and tissues. CAPG could strengthen the proliferative and invasive abilities of DLBCL cells, inhibit cell apoptosis, and activate PI3K/AKT signaling pathway. CAPG overexpression accelerated malignant progression of DLBCL cells. In addition, CAPG expression was regulated by CEBPA.CAPG enhances the proliferation and invasion of DLBCL cells by promoting PI3K/AKT signaling pathway, which is expected to be a promising target for DLBCL.

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