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UPK3A的高表达通过使p53通路失活促进胃癌细胞的进展。

High Expression of UPK3A Promotes the Progression of Gastric Cancer Cells by Inactivating p53 Pathway.

作者信息

Xu Deliang, Guo Jing, Xu Hongwei

机构信息

Department of Gastroenterology, Zaozhuang Municipal Hospital, Zaozhuang, Shandong 277100, China.

Department of Gastroenterology, Shandong Provincial Hospital, Jinan, Shandong 250000, China.

出版信息

Anal Cell Pathol (Amst). 2022 Jun 21;2022:6897561. doi: 10.1155/2022/6897561. eCollection 2022.

DOI:10.1155/2022/6897561
PMID:35774082
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9239834/
Abstract

BACKGROUND

Gastric cancer is a common gastrointestinal tract cancer and is a considerable health burden worldwide. TCGA analysis found Uroplakin 3A (UPK3A) was upregulated in gastric cancer tissues. Our study was designed to investigate the underlying mechanism of Uroplakin 3A (UPK3A) in gastric cancer.

METHODS

Data from TCGA database were used to assess the expression, and Kaplan-Meier plotter analysis was used to assess the prognosis value of UPK3A. Furthermore, there are effects of UPK3A silencing on the activity, proliferation, migration, and invasion of human gastric cancer cells (SNU-216 and HGC-27) using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), colony formation, wound healing, and Transwell assays. In addition, the expression of UPK3A, p53, KLF4, ZMAT3, MDM2, and SP1 was detected by qRT-PCR and Western blot assay.

RESULTS

UPK3A was markedly upregulated in gastric cancer tissues compared to that in normal tissues, and patients with high UPK3A level showed poor prognosis. UPK3A was highly expressed in human gastric cancer cell lines compared to that in a normal human gastric epithelial cell line. Silencing of UPK3A inhibited the proliferation, migration, and invasion of gastric cancer cells. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis revealed that UPK3A was involved in the p53 signaling pathway. UPK3A suppressed the activation of p53 signaling pathway, and treatment with Pifithrin- (an inhibitor of the p53 signaling pathway) or silencing of p53 significantly reversed the effect of UPK3A silencing on the expression of p53, KLF4, ZMAT3, MDM2, and SP1.

CONCLUSION

Our findings showed that UPK3A promotes the progression of gastric cancer by regulating the p53 signaling pathway and could be a potential therapeutic target for gastric cancer.

摘要

背景

胃癌是一种常见的胃肠道癌症，在全球范围内是一项相当大的健康负担。癌症基因组图谱（TCGA）分析发现，uroplakin 3A（UPK3A）在胃癌组织中上调。我们的研究旨在探讨uroplakin 3A（UPK3A）在胃癌中的潜在机制。

方法

使用来自TCGA数据库的数据评估UPK3A的表达，并使用Kaplan-Meier Plotter分析评估UPK3A的预后价值。此外，使用3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐（MTT）、集落形成、伤口愈合和Transwell实验，研究UPK3A沉默对人胃癌细胞（SNU-216和HGC-27）的活性、增殖、迁移和侵袭的影响。另外，通过qRT-PCR和蛋白质免疫印迹法检测UPK3A、p53、KLF4、ZMAT3、MDM2和SP1的表达。

结果

与正常组织相比，UPK3A在胃癌组织中显著上调，UPK3A水平高的患者预后较差。与正常人胃上皮细胞系相比，UPK3A在人胃癌细胞系中高表达。UPK3A沉默抑制了胃癌细胞的增殖、迁移和侵袭。京都基因与基因组百科全书（KEGG）通路富集分析显示，UPK3A参与p53信号通路。UPK3A抑制p53信号通路的激活，使用pifithrin-α（一种p53信号通路抑制剂）治疗或p53沉默可显著逆转UPK3A沉默对p53、KLF4、ZMAT3、MDM2和SP1表达的影响。

结论

我们的研究结果表明，UPK3A通过调节p53信号通路促进胃癌进展，可能是胃癌的一个潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8798/9239834/2fb75f164bd9/ACP2022-6897561.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8798/9239834/46c5d74050d9/ACP2022-6897561.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8798/9239834/d56ee03116cd/ACP2022-6897561.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8798/9239834/403d05ca77c7/ACP2022-6897561.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8798/9239834/4f5bab547298/ACP2022-6897561.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8798/9239834/50326ca36fbb/ACP2022-6897561.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8798/9239834/2fb75f164bd9/ACP2022-6897561.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8798/9239834/46c5d74050d9/ACP2022-6897561.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8798/9239834/d56ee03116cd/ACP2022-6897561.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8798/9239834/403d05ca77c7/ACP2022-6897561.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8798/9239834/4f5bab547298/ACP2022-6897561.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8798/9239834/50326ca36fbb/ACP2022-6897561.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8798/9239834/2fb75f164bd9/ACP2022-6897561.006.jpg

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