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CIDEA的下调通过调节食管鳞状细胞癌中的JNK-p21/Bad信号通路促进肿瘤生长并导致顺铂耐药。

Down-Regulation of CIDEA Promoted Tumor Growth and Contributed to Cisplatin Resistance by Regulating the JNK-p21/Bad Signaling Pathways in Esophageal Squamous Cell Carcinoma.

作者信息

Gao Ya-Ping, Li Lei, Yan Jie, Hou Xiao-Xia, Jia Yong-Xu, Chang Zhi-Wei, Guan Xin-Yuan, Qin Yan-Ru

机构信息

Department of Clinical Oncology, The First Affiliated Hospital, Zhengzhou University, Zhengzhou, China.

Department of Clinical Oncology, The University of Hong Kong, Hong Kong, China.

出版信息

Front Oncol. 2021 Feb 3;10:627845. doi: 10.3389/fonc.2020.627845. eCollection 2020.

DOI:10.3389/fonc.2020.627845
PMID:33614508
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7888273/
Abstract

Esophageal squamous cell carcinoma (ESCC) is one of the most common malignancies with poor prognosis and lack of effective targeted therapies. In this study, we investigated the tumor suppressive role of the cell death inducing DFF like effector A (CIDEA) in ESCC. Firstly, public datasets and ESCC tissue microarray analysis showed that CIDEA was frequently down-regulated at both the mRNA and protein level. This was significantly associated with low differentiation and TNM stage in ESCC, and indicated poor prognosis for ESCC patients. Bisulfite genomic sequencing (BGS) and methylation-specific PCR (MSP) analysis revealed that the down-regulation of CIDEA was associated with hypermethylation of its promoter, which was also correlated with the poor prognosis in ESCC patients. and functional studies demonstrated that CIDEA decreased cell growth, foci formation, DNA replication, and tumorigenesis in nude mice. Further study revealed that, during starvation or cisplatin induced DNA damage, CIDEA facilitated the G1-phase arrest or caspase-dependent mitochondrial apoptosis through the JNK-p21/Bad pathway. Therefore, CIDEA is a novel tumor suppressor gene that plays an important role in the development and progression of ESCC, and may provide a potential therapeutic target for patients with ESCC.

摘要

食管鳞状细胞癌（ESCC）是最常见的恶性肿瘤之一，预后较差且缺乏有效的靶向治疗方法。在本研究中，我们调查了细胞死亡诱导DFF样效应因子A（CIDEA）在ESCC中的肿瘤抑制作用。首先，公共数据集和ESCC组织芯片分析显示，CIDEA在mRNA和蛋白质水平上均频繁下调。这与ESCC的低分化和TNM分期显著相关，并表明ESCC患者预后不良。亚硫酸氢盐基因组测序（BGS）和甲基化特异性PCR（MSP）分析表明，CIDEA的下调与其启动子的高甲基化有关，这也与ESCC患者的不良预后相关。功能研究表明，CIDEA可降低裸鼠的细胞生长、集落形成、DNA复制和肿瘤发生。进一步研究发现，在饥饿或顺铂诱导的DNA损伤过程中，CIDEA通过JNK-p21/Bad途径促进G1期阻滞或半胱天冬酶依赖性线粒体凋亡。因此，CIDEA是一种新型肿瘤抑制基因，在ESCC的发生发展中起重要作用，可能为ESCC患者提供潜在的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/775e/7888273/ff3331239593/fonc-10-627845-g007.jpg
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