PRSS2 regulates EMT and metastasis via MMP-9 in gastric cancer

IF 2.3 4区生物学 Q4 CELL BIOLOGY

Acta histochemica Pub Date : 2023-08-01 DOI:10.1016/j.acthis.2023.152071

Fei Wang , Jianfeng Yi , Yu Chen , Xiang Bai , Chunfeng Lu , Shichun Feng , Xiaojun Zhou

{"title":"PRSS2 regulates EMT and metastasis via MMP-9 in gastric cancer","authors":"Fei Wang , Jianfeng Yi , Yu Chen , Xiang Bai , Chunfeng Lu , Shichun Feng , Xiaojun Zhou","doi":"10.1016/j.acthis.2023.152071","DOIUrl":null,"url":null,"abstract":"<div>Serine protease 2 (PRSS2) is upregulated in gastric cancer tissues, correlates with poor prognosis and promotes migration and invasion of gastric cancer cells. However, the exact mechanism by which PRSS2 promotes metastasis in gastric cancer is unclear. We examined serum PRSS2 levels in healthy controls and gastric cancer patients by enzyme linked immunosorbent assay (ELISA) and analyzed the correlation between PRSS2 serum level with the clinicopathological characteristics of gastric cancer patients and matrix metalloproteinase-9 (MMP-9) expression. A lentiviral MMP-9 overexpression vector was constructed and used to transfect gastric cancer cells with stable silencing of PRSS2, and migration, invasion and epithelial-mesenchymal transition (EMT) of gastric cancer cells were examined. High serum PRSS2 levels were detected in gastric cancer patients and associated with lymphatic metastasis and TNM stage. Serum PRSS2 was positively correlated with serum MMP-9 level. PRSS2 silencing inhibited EMT, and knock-down of PRSS2 partially abrogated cell metastasis and EMT caused by overexpression of MMP-9. These results suggest that PRSS2 promotes the migration and invasion of gastric cancer cells through EMT induction by MMP-9. Our findings suggest that PRSS2 may be a potential early diagnostic marker and therapeutic target of gastric cancer.</div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":"125 6","pages":"Article 152071"},"PeriodicalIF":2.3000,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Acta histochemica","FirstCategoryId":"99","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0065128123000776","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"CELL BIOLOGY","Score":null,"Total":0}

引用次数: 1

Abstract

Serine protease 2 (PRSS2) is upregulated in gastric cancer tissues, correlates with poor prognosis and promotes migration and invasion of gastric cancer cells. However, the exact mechanism by which PRSS2 promotes metastasis in gastric cancer is unclear. We examined serum PRSS2 levels in healthy controls and gastric cancer patients by enzyme linked immunosorbent assay (ELISA) and analyzed the correlation between PRSS2 serum level with the clinicopathological characteristics of gastric cancer patients and matrix metalloproteinase-9 (MMP-9) expression. A lentiviral MMP-9 overexpression vector was constructed and used to transfect gastric cancer cells with stable silencing of PRSS2, and migration, invasion and epithelial-mesenchymal transition (EMT) of gastric cancer cells were examined. High serum PRSS2 levels were detected in gastric cancer patients and associated with lymphatic metastasis and TNM stage. Serum PRSS2 was positively correlated with serum MMP-9 level. PRSS2 silencing inhibited EMT, and knock-down of PRSS2 partially abrogated cell metastasis and EMT caused by overexpression of MMP-9. These results suggest that PRSS2 promotes the migration and invasion of gastric cancer cells through EMT induction by MMP-9. Our findings suggest that PRSS2 may be a potential early diagnostic marker and therapeutic target of gastric cancer.

查看原文本刊更多论文

PRSS2通过MMP-9调控胃癌的EMT和转移

丝氨酸蛋白酶2（PRSS2）在癌症组织中上调，与预后不良相关，并促进癌症细胞的迁移和侵袭。然而，PRSS2促进癌症转移的确切机制尚不清楚。采用酶联免疫吸附试验（ELISA）检测了健康对照组和癌症患者血清PRSS2水平，并分析了PRSS2与癌症患者临床病理特征和基质金属蛋白酶-9（MMP-9）表达的相关性。构建慢病毒MMP-9过表达载体，转染稳定沉默PRSS2的癌症细胞，检测癌症细胞的迁移、侵袭和上皮-间质转移（EMT）。癌症患者血清PRSS2水平升高，与淋巴结转移和TNM分期有关。血清PRSS2与血清MMP-9水平呈正相关。PRSS2沉默抑制EMT，并且PRSS2的敲除部分消除了由MMP-9过表达引起的细胞转移和EMT。这些结果表明，PRSS2通过MMP-9的EMT诱导促进癌症细胞的迁移和侵袭。我们的研究结果表明，PRSS2可能是癌症潜在的早期诊断标志物和治疗靶点。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Acta histochemica 生物-细胞生物学

CiteScore

4.60

自引率

4.00%

发文量

107

审稿时长

23 days

期刊介绍： Acta histochemica, a journal of structural biochemistry of cells and tissues, publishes original research articles, short communications, reviews, letters to the editor, meeting reports and abstracts of meetings. The aim of the journal is to provide a forum for the cytochemical and histochemical research community in the life sciences, including cell biology, biotechnology, neurobiology, immunobiology, pathology, pharmacology, botany, zoology and environmental and toxicological research. The journal focuses on new developments in cytochemistry and histochemistry and their applications. Manuscripts reporting on studies of living cells and tissues are particularly welcome. Understanding the complexity of cells and tissues, i.e. their biocomplexity and biodiversity, is a major goal of the journal and reports on this topic are especially encouraged. Original research articles, short communications and reviews that report on new developments in cytochemistry and histochemistry are welcomed, especially when molecular biology is combined with the use of advanced microscopical techniques including image analysis and cytometry. Letters to the editor should comment or interpret previously published articles in the journal to trigger scientific discussions. Meeting reports are considered to be very important publications in the journal because they are excellent opportunities to present state-of-the-art overviews of fields in research where the developments are fast and hard to follow. Authors of meeting reports should consult the editors before writing a report. The editorial policy of the editors and the editorial board is rapid publication. Once a manuscript is received by one of the editors, an editorial decision about acceptance, revision or rejection will be taken within a month. It is the aim of the publishers to have a manuscript published within three months after the manuscript has been accepted