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

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.