核心蛋白聚糖、甲磺酸伊马替尼、苹果酸舒尼替尼对胃肠道 间质瘤细胞恶性表型的影响.

唐珊; 贾钧凯; 马鸿滢; 赵滢; 张天彪

Objective To investigate the effects and molecular mechanisms of decorin (DCN), imatinib mesylate, and sunitinib malate on the malignant phenotype of gastrointestinal stromal tumor cells. Methods Western blotting was used to detect changes in the expression of DCN and its downstream proteins after DCN overexpression and treatment with imatinib mesylate and sunitinib malate alone or in combination in gastrointestinal stromal tumor cells (GIST-882) . Cell counting kit-8, scratch, and Transwell assays were performed to validate the changes in cell proliferation, migration, and invasion abilities after DCN overexpression and treatment with imatinib mesylate and sunitinib malate alone or in combination in GIST-882 cells. Results Compared with the control group, DCN overexpression and treatment with imatinib mesylate and sunitinib malate alone or in combination in GIST-882 cells increased the expression levels of DCN protein, decreased the expression levels of epidermal growth factor receptor (EGFR), phosphorylated EGFR (p-EGFR), extracellular signal-regulated kinase 1/2 (ERK1/2), and phosphorylated ERK1/2 (p-ERK1/2) proteins, and significantly reduced cell proliferation, migration, and invasion abilities. Conclusion DCN overexpression and treatment with imatinib mesylate and sunitinib malate alone or in combination affect the MAPK signaling pathway by downregulating the expression of EGFR, thereby regulating the proliferation, migration, and invasion abilities of gastrointestinal stromal tumor cells.

EPIDERMAL growth factor receptors; GASTROINTESTINAL stromal tumors; SUNITINIB; STROMAL cells; IMATINIB

Journal of China Medical University, 2024, Vol 53, Issue 11, p961

0258-4646

Academic Journal

10.12007/j.issn.0258‐4646.2024.11.001