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SCARA5通过抑制上皮-间质转化来抑制胃癌进展。

SCARA5 inhibits gastric cancer progression via epithelial-mesenchymal transition suppression.

作者信息

Zhang Hangyu, Liu Changgang, Wang Xinbo, Wang Yongfang, Zheng Jie

机构信息

Department of Diagnostic Pathology, School of Basic Medical Sciences, Weifang Medical University, Shandong Province, China.

Department of Surgical Oncology, Weifang People's Hospital, Weifang Medical University, Shandong Province, China.

出版信息

J Cancer. 2021 Mar 1;12(8):2412-2421. doi: 10.7150/jca.52426. eCollection 2021.

DOI:10.7150/jca.52426
PMID:33758617
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7974898/
Abstract

Scavenger receptor class A member 5 (SCARA5) has been reported to be implicated in several types of cancer. However, its biological roles and mechanism of SCARA5 in gastric cancer (GC) have not been elucidated. In the present study, SCARA5 expression was found to be downregulated in GC which was associated with promoter methylation. The protein level of SCARA5 was negatively associated with aggressive clinicopathological characteristics, as well as poor prognosis. Moreover, SCARA5 overexpression markedly suppressed the growth, migration and invasion of GC cell lines . Furthermore, upregulation of SCARA5 inhibited gastric tumor growth and metastasis in a xenograft model. Mechanistic analysis revealed that SCARA5 suppressed the migration and invasion of GC cells via inhibiting epithelial-mesenchymal transition (EMT) and inactivating MMP-2 and MMP-9. Taken together, these results demonstrated that SCARA5 might play vital roles in the GC genesis and progression and could serve as a potential biomarker for diagnosis and therapeutic target of GC.

摘要

据报道,清道夫受体A类成员5(SCARA5)与多种类型的癌症有关。然而,SCARA5在胃癌(GC)中的生物学作用和机制尚未阐明。在本研究中,发现SCARA5在GC中表达下调,这与启动子甲基化有关。SCARA5的蛋白水平与侵袭性临床病理特征以及不良预后呈负相关。此外,SCARA5过表达显著抑制了GC细胞系的生长、迁移和侵袭。此外,SCARA5的上调抑制了异种移植模型中的胃肿瘤生长和转移。机制分析表明,SCARA5通过抑制上皮-间质转化(EMT)以及使基质金属蛋白酶-2(MMP-2)和基质金属蛋白酶-9(MMP-9)失活来抑制GC细胞的迁移和侵袭。综上所述,这些结果表明SCARA5可能在GC的发生和发展中起重要作用,并可作为GC诊断的潜在生物标志物和治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da75/7974898/cf6fed11b8b6/jcav12p2412g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da75/7974898/947b59d331d4/jcav12p2412g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da75/7974898/4b6d04a533bd/jcav12p2412g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da75/7974898/cf6fed11b8b6/jcav12p2412g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da75/7974898/947b59d331d4/jcav12p2412g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da75/7974898/4345a3966e92/jcav12p2412g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da75/7974898/b474e0e4918c/jcav12p2412g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da75/7974898/cf1255dd8f68/jcav12p2412g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da75/7974898/4b6d04a533bd/jcav12p2412g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da75/7974898/cf6fed11b8b6/jcav12p2412g006.jpg

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New insights into the mechanisms of epithelial-mesenchymal transition and implications for cancer.
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