Knockdown of TRIP13 inhibits gastric cancer stemness and cisplatin resistance by regulating FBXW7/ENO1 axis

• DOI: 10.4314/tjpr.v23i1.4
• Publication Date: 2024-02-08T13:46:27Z
• Authors: Jiayun Liu; Che Chen; Guannan Wu; Xuequan Yao; Fukun Liu; Shenlin Liu

Purpose: To explore the role of thyroid hormone receptor interactor 13 (TRIP13) in gastric cancer (GC) and associated mechanism.
 Methods: TRIP13 expression GC was found The Cancer Genome Atlas (TCGA) database siTRIP13 transfected cells order to generate cell lines with low expression. Cell proliferation determined by colony formation assay, while migration invasion were evaluated scratch test Transwell respectively. Sphere assay used assess stemness characteristics whereas half-inhibitory concentration (IC50) value Counting Kit-8 (CCK8). F-box WD repeat domain containing 7 (FBXW7) enolase 1 (ENO1) western-blot assay.
 Results: significantly expressed based on TCGA (p < 0.001) high predicted poor prognosis patients 0.05). Based findings function si-TRIP13 inhibited proliferation, migration, decreased IC50 value. Mechanically, knockdown ENO1 level stabilizing FBXW7.
 Conclusion: functions as an oncogene stimulates growth via FBXW7/ENO1 pathway GC. Thus, a potential therapeutic target for treatment is provided this study.