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靶向NCAPD3基因可激活EGFR和ASNS，这两者是胃癌进展的两个关键因素。

Targeting the NCAPD3 gene activates EGFR and ASNS as two pivotal contributors to gastric cancer progression.

作者信息

Bandarian Fatemeh, Razi Farideh, Jahani-Sharafat Somayeh, Rostami Nejad Mohammad, Arjmand Babak, Farahani Masoumeh

机构信息

Endocrinology and Metabolism Research Center, Endocrinology and Metabolism Clinical Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran.

Diabetes Research Center, Endocrinology and Metabolism Clinical Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran.

出版信息

Gastroenterol Hepatol Bed Bench. 2024;17(4):400-408. doi: 10.22037/ghfbb.v17i4.3031.

DOI:10.22037/ghfbb.v17i4.3031
PMID:40406431
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12094513/
Abstract

AIM

This study was conducted to discover the effect of NCAPD3 knockdown on the gene expression profile of gastric cancer.

BACKGROUND

Gastric cancer, a potentially fatal disease, requires thorough evaluation for targeted interventions. Through the post-analysis of microarray data, it is crucial to further examine the impact of NCAPD3 (Non-SMC condensin II complex subunit D3) inhibition in gastric cancer, emphasizing the need for a more comprehensive analysis of this knockdown.

METHODS

The use of Cytoscape and its plug-ins for protein-protein interaction network analysis enables the identification of genes that significantly affect network stability. These hub-bottlenecks are regulated due to the NCAPD3 inhibition and some of them act as compensators in this condition. The hub-bottlenecks pathways identified by ClueGO indicate their relationships in underlying mechanisms of knockdown. These identified central differentially expressed genes could be considered eligible targets for therapeutic interventions. Some of them play compensative roles while others are regulated in NCAPD3 knockdown.

RESULTS

It can be concluded that some of the hub-bottlenecks contribute to compensation mechanisms including NPM1, PTEN, EGFR, HSPA5, and ASNS, while the other ones including HSPA4, DHX9, CAV1, MAP1LC3B, and SRSF1 are among the regulated genes.

CONCLUSION

In particular, the up-regulation of EGFR and ASNS genes in the knockdown scenario could significantly impact and deteriorate cancer treatment outcomes after comprehensive validation studies.

摘要

目的

本研究旨在探究NCAPD3基因敲低对胃癌基因表达谱的影响。

背景

胃癌是一种潜在的致命疾病，需要进行全面评估以制定针对性干预措施。通过对微阵列数据的事后分析，进一步研究NCAPD3（非SMC凝聚素II复合体亚基D3）抑制在胃癌中的作用至关重要，这凸显了对这种基因敲低进行更全面分析的必要性。

方法

利用Cytoscape及其插件进行蛋白质-蛋白质相互作用网络分析，能够识别出显著影响网络稳定性的基因。这些枢纽瓶颈因NCAPD3抑制而受到调控，其中一些在这种情况下起到补偿作用。通过ClueGO识别出的枢纽瓶颈通路表明了它们在基因敲低潜在机制中的关系。这些确定的核心差异表达基因可被视为治疗干预的合适靶点。其中一些发挥补偿作用，而另一些在NCAPD3基因敲低时受到调控。

结果

可以得出结论，一些枢纽瓶颈促成了包括NPM1、PTEN、EGFR、HSPA5和ASNS在内的补偿机制，而其他一些基因包括HSPA4、DHX9、CAV1、MAP1LC3B和SRSF1则属于受调控基因。

结论

特别是，在经过全面验证研究后，基因敲低情况下EGFR和ASNS基因的上调可能会对癌症治疗结果产生显著影响并使其恶化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6e5/12094513/0d765acc643d/GHFBB-17-400-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6e5/12094513/aa62ebc812e9/GHFBB-17-400-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6e5/12094513/3c502c91e894/GHFBB-17-400-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6e5/12094513/ebf07a8849e8/GHFBB-17-400-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6e5/12094513/e6e1347d37da/GHFBB-17-400-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6e5/12094513/0d765acc643d/GHFBB-17-400-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6e5/12094513/aa62ebc812e9/GHFBB-17-400-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6e5/12094513/3c502c91e894/GHFBB-17-400-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6e5/12094513/ebf07a8849e8/GHFBB-17-400-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6e5/12094513/e6e1347d37da/GHFBB-17-400-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6e5/12094513/0d765acc643d/GHFBB-17-400-g005.jpg

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Front Pharmacol. 2024 Apr 22;15:1341039. doi: 10.3389/fphar.2024.1341039. eCollection 2024.
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