Lactate dehydrogenase A is implicated in the pathogenesis of B‐cell lymphoma through regulation of the FER signaling pathway

乳酸脱氢酶A 拉吉细胞 发病机制 乳酸脱氢酶 淋巴瘤 基因敲除 B细胞淋巴瘤 活力测定 细胞 糖酵解 细胞生长 细胞培养 癌症研究 生物 生物化学 免疫学 遗传学
作者
Xiumei Feng,Jing Ren,Xunqi Zhang,Dexiao Kong,Linlin Yin,Qian Zhou,Shunye Wang,Ai Li,Yanan Guo,Sheng Wang,Xiaoli Feng,Xiaoyun Wang,Jianhua Niu,Yang Jiang,Chengyun Zheng
出处
期刊:Biofactors [Wiley]
标识
DOI:10.1002/biof.2053
摘要

Abstract Lactate dehydrogenase A (LDHA) is highly expressed in various tumors. However, the role of LDHA in the pathogenesis of B‐cell lymphoma remains unclear. Analysis of data from The Cancer Genome Atlas (TCGA) and Genotype‐Tissue Expression (GTEx) databases revealed an elevated LDHA expression in diffuse large B‐cell lymphoma (DLBC) tissues compared with normal tissues. Similarly, our results demonstrated a significant increase in LDHA expression in tumor tissues from the patients with B‐cell lymphoma compared with those with lymphadenitis. To further elucidate potential roles of LDHA in B‐cell lymphoma pathogenesis, we silenced LDHA in the Raji cells (a B‐cell lymphoma cell line) using shRNA techniques. Silencing LDHA led to reduced mitochondrial membrane integrity, adenosine triphosphate (ATP) production, glycolytic activity, cell viability and invasion. Notably, LDHA knockdown substantially suppressed in vivo growth of Raji cells and extended survival in mice bearing lymphoma (Raji cells). Moreover, proteomic analysis identified feline sarcoma‐related protein (FER) as a differential protein positively associated with LDHA expression. Treatment with E260, a FER inhibitor, significantly reduced the metabolism, proliferation and invasion of Raji cells. In summary, our findings highlight that LDHA plays multiple roles in B‐cell lymphoma pathogenesis via FER pathways, establishing LDHA/FER may as a potential therapeutic target.
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