Knockdown of ASF1B inhibits cell proliferation, migration, invasion and cisplatin resistance in gastric cancer through the Myc pathway

• DOI: 10.3892/ol.2023.13828
• Publication Date: 2023-04-20T12:25:29Z
• Authors: Zao Zhang; Meiying Ning; Li Li; Zhuangzhuang Li; Yanrong Wang; Jing Zhao
• Keywords: Viability assay; Gentamicin protection assay

Gastric cancer (GC) is a prevalent malignancy in the digestive system that poses serious threat to human health. Anti-silencing function 1B (ASF1B) performs an important role progression of numerous tumors; however, its GC still requires further elucidation. Using data from The Cancer Genome Atlas, expression levels ASF1B tissues were analyzed and survival curve for high-ASF1B low-ASF1B groups was plotted using Kaplan-Meier method. Reverse transcription-quantitative PCR performed evaluate cells. Small interfering RNAs targeting transfected into HGC-27 AGS cells silence expression. Cell viability, proliferation, migration, invasion, apoptosis assessed cell counting kit-8 assay, colony formation wound healing Transwell assay flow cytometry, respectively. protein changes western blotting. Gene Set Enrichment Analysis (GSEA) used identify related pathways. results demonstrated increased compared with adjacent healthy normal (GES-1), high associated poor outcomes patients GC. Silencing inhibited formation, invasion cisplatin resistance, while also attenuating apoptotic capability GSEA showed could activate Myc-targets-v1 Myc-targets-v2 Moreover, silencing Myc pathway-related proteins Myc, minichromosome maintenance (MCM)4 MCM5. Overexpression reversed inhibitory effect on resistance. In conclusion, indicate knockdown may suppress migration promote sensitivity by modulating pathway, thereby offering novel possibilities reversing resistance