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PRRX1 通过调节上皮-间充质转化促进胃癌的淋巴结转移。

PRRX1 promotes lymph node metastasis of gastric cancer by regulating epithelial-mesenchymal transition.

机构信息

Department of Surgical Oncology, Gansu Provincial Hospital, Lanzhou.

The First Clinical Medical College, Lanzhou University.

出版信息

Medicine (Baltimore). 2021 Feb 12;100(6):e24674. doi: 10.1097/MD.0000000000024674.

DOI:10.1097/MD.0000000000024674
PMID:33578599
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10545397/
Abstract

BACKGROUND

Gastric cancer has multiple metastasis pathways, of which lymph node metastasis plays a dominant role. However, the specific mechanism of lymph node metastasis is still not unclear.

METHODS

The bioinformatics technology was utilized to mine gene chip data related to gastric cancer and Epithelial-Mesenchymal Transition (EMT) in a high-throughput gene expression database (Gene Expression Omnibus, GEO), we screened out all genes that have differential expression levels in gastric cancer tissues and in adjacent normal gastric mucosa tissues. The corresponding function package of R language software were performed for gene annotation and cluster analysis, then enrichment analysis of genes with differential expression and protein interaction network diagram for correlation analysis were performed, we finally screened out the paired related homeobox 1 gene (PRRX1) related to EMT. Next, we collected 65 metastatic lymph node samples and 93 gastric cancer tissue samples. The expression levels of PRRX1 and EMT-related protein E-cadherin (E-ca) and vimentin (Vim) in gastric cancer tissues and metastatic lymph node tissues were determined by immunohistochemistry (IHC) staining of streptavidin-peroxidase (SP). The expression differences of PRRX1, E-ca and Vim in gastric cancer tissues and metastatic lymph node tissues as well as the correlation were analyzed by the experimental data, and the clinical significance was analyzed in combination with the clinicopathological data.

RESULTS

The PRRX1 expression levels in gastric cancer tissues are significantly higher than that in adjacent normal gastric mucosa tissues. The positive expression rates of PRRX1, Vim and E-ca in gastric cancer and in metastatic lymph node tissues were significantly different. Comparing with that in gastric cancer, expression of PRRX1 and Vim was significantly down-regulated, and E-ca expression was significantly up-regulated in metastatic lymph nodes.

CONCLUSION

PRRX1 may promote lymph node metastasis of gastric cancer by regulating EMT, and then affect the prognosis of patients. PRRX1 may be used as a new biological indicator to predict or prevent lymph node metastasis in gastric cancer.

摘要

背景

胃癌有多种转移途径,其中淋巴结转移起主导作用。然而,淋巴结转移的具体机制尚不清楚。

方法

利用生物信息学技术,从高通量基因表达数据库(Gene Expression Omnibus,GEO)中挖掘与胃癌和上皮间质转化(EMT)相关的基因芯片数据,筛选出胃癌组织与癌旁正常胃黏膜组织中差异表达的所有基因。使用 R 语言软件的对应功能包进行基因注释和聚类分析,然后对差异表达基因进行富集分析,并进行蛋白互作网络分析,最后筛选出与 EMT 相关的配对相关同源盒 1 基因(PRRX1)。接着,收集了 65 例转移性淋巴结样本和 93 例胃癌组织样本。采用链霉亲和素-过氧化物酶(SP)免疫组化染色法检测胃癌组织和转移性淋巴结组织中 PRRX1 及 EMT 相关蛋白 E-钙黏蛋白(E-ca)和波形蛋白(Vim)的表达水平。通过实验数据分析 PRRX1、E-ca 和 Vim 在胃癌组织和转移性淋巴结组织中的表达差异及相关性,并结合临床病理资料分析其临床意义。

结果

PRRX1 在胃癌组织中的表达水平明显高于癌旁正常胃黏膜组织。PRRX1、Vim 和 E-ca 在胃癌及转移性淋巴结组织中的阳性表达率差异有统计学意义。与胃癌相比,转移性淋巴结组织中 PRRX1 和 Vim 的表达明显下调,E-ca 的表达明显上调。

结论

PRRX1 可能通过调节 EMT 促进胃癌淋巴结转移,进而影响患者的预后。PRRX1 可作为预测或预防胃癌淋巴结转移的新的生物学指标。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05d2/10545397/a4a4815cb2c4/medi-100-e24674-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05d2/10545397/b5f6c4ab2696/medi-100-e24674-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05d2/10545397/0f8c17660bf3/medi-100-e24674-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05d2/10545397/dee680371424/medi-100-e24674-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05d2/10545397/87f52ad5a08d/medi-100-e24674-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05d2/10545397/1fb07ec7fe1f/medi-100-e24674-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05d2/10545397/d1fe8e4c2eeb/medi-100-e24674-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05d2/10545397/a4a4815cb2c4/medi-100-e24674-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05d2/10545397/b5f6c4ab2696/medi-100-e24674-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05d2/10545397/0f8c17660bf3/medi-100-e24674-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05d2/10545397/dee680371424/medi-100-e24674-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05d2/10545397/87f52ad5a08d/medi-100-e24674-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05d2/10545397/1fb07ec7fe1f/medi-100-e24674-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05d2/10545397/d1fe8e4c2eeb/medi-100-e24674-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05d2/10545397/a4a4815cb2c4/medi-100-e24674-g007.jpg

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