Induction of Cell Cycle Arrest in MKN۴۵ Cells after Schiff Base Oxovanadium Complex Treatment Using Changes in Gene Expression of CdC۲۵ and P۵۳
محل انتشار: پنجمین کنگره بین المللی سرطان
سال انتشار: 1400
نوع سند: مقاله کنفرانسی
زبان: انگلیسی
مشاهده: 259
نسخه کامل این مقاله ارائه نشده است و در دسترس نمی باشد
- صدور گواهی نمایه سازی
- من نویسنده این مقاله هستم
استخراج به نرم افزارهای پژوهشی:
شناسه ملی سند علمی:
CANCERMED05_053
تاریخ نمایه سازی: 27 دی 1400
چکیده مقاله:
Introduction: Compounds containing heavy metals such as vanadium, nickel, and cobalt may be useful for the treatment of various diseases. Multiple studies have been carried out on the anticancer effects of vanadium-contained compounds on different cell types. Method: This study aimed to evaluate the role of schiff base oxovanadium complex ([N, N'-bis(۳-methoxy-salicylidene)-۱,۲-phenylenediamine] Vanadium(IV) Oxide Complex) on cell cycle arrest and different cell cycle phases in MKN۴۵ cell of gastric cancer. Schiff base oxovanadium complex was used to assessthe amount of cytotoxicity via cell viability test. PI color and flow cytometry technique were applied to evaluate the effects of vanadium synthetic compounds on cell cycle phases; subsequently, we analyzed the change rates of gene expression in P۵۳, GADD۴۵, and CDC۲۵ genes, which are involved in cell division phases. Results: The findings indicated that the vital activities of time-dependent and concentration-dependent MKN۴۵ cells with schiff base oxovanadium complex were significantly reduced; therefore, this complex is able to inhibit the migration of cancer cells and metastatic activities in a time-dependent mode. Cell cycle arrest was obtained after ۴۸ h of treatment in phase G۲/M at ۱ microgram/milliliter (μg/ml) concentration. Conclusion: This is probably attributed to the increased gene expression of P۵۳ and GADD۴۵ genes and reduced gene expression of CDC۲۵ gene. Compounds containing such heavy metals as vanadium decrease the growth, proliferation, and migration of MKN۴۵ cells. They arrest cell cycle in phase G۲/M via changing the controllers of cell division phases activated due to DNA damage.
کلیدواژه ها:
نویسندگان
Dorna Basir
Biochemistry Department, Faculty of Medicine, Semnan University of Medical Sciences, Semnan, Iran
Mahsa Iraji
Biochemistry Department, Faculty of Medicine, Semnan University of Medical Sciences, Semnan, Iran
Ali Khaleghian
Biochemistry Department, Faculty of Medicine, Semnan University of Medical Sciences, Semnan, Iran