Overactivation of XBP1 in plasma cells implies worse survival through innate immunity in esophageal squamous cell carcinoma

XBP1型 未折叠蛋白反应 免疫 先天免疫系统 内质网 炎症 生物 癌症研究 免疫学 细胞生物学 免疫系统 RNA剪接 核糖核酸 生物化学 基因
作者
Yin Yin,Yuhao Wang,Xiao Yu,Yang Li,Yahui Zhao,Zhihua Liu
出处
期刊:Cancer Letters [Elsevier]
卷期号:597: 217045-217045 被引量:2
标识
DOI:10.1016/j.canlet.2024.217045
摘要

To maintain protein homeostasis, X-box binding protein 1 (XBP1) undergoes splicing following the activation of the unfolded protein response (UPR) in response to endoplasmic reticulum (ER) stress. Although targeting ER stress represents a promising therapeutic strategy, a comprehensive understanding of XBP1 at the cellular level and the link between XBP1 and the innate nervous system is lacking. Here, TCGA pancancer datasets from 33 cancer types, scRNA pancancer datasets from 454 patients and bulk RNA-seq datasets from 155 paired esophageal squamous cell carcinoma (ESCC) patients were analyzed. To cope with ER stress, plasma cells tend to activate XBP1 after undergoing bacterial infection and inflammatory signaling from the innate immune system. Patients with high XBP1 expression in their plasma cells have a higher tumor grade and worse survival. However, activation of the innate immune system with increased XBP1 expression in plasma cells correlates with an increased lymphocyte ratio, indicative of a more robust immune response. Moreover, XBP1 activation appears to initiate leukocyte migration at the transcriptional level. Our study revealed that the XBP1-induced UPR could mediate the crosstalk between optimal acquired humoral immune responses and innate immunity in ESCC.
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