The Role of Cuproptosis Key Factor FDX1 in Gastric Cancer

癌症 癌细胞 癌症研究 生物 转染 恶性转化 细胞生长 细胞培养 免疫学 医学 内科学 遗传学
作者
Qiqi Zhao,Miao Yu,Xueqin Du,Yuan Li,Juantao Lv,Xianglai Jiang,Xiaomei Chen,Anqi Wang,Xiaojun Yang
出处
期刊:Current Pharmaceutical Biotechnology [Bentham Science]
卷期号:25 被引量:1
标识
DOI:10.2174/0113892010301997240527162423
摘要

Background: Gastric cancer is a common malignant tumor of the digestive tract, both domestically and internationally. It has high incidence and mortality rates, posing a significant threat to human health. The levels of blood copper are elevated in patients with gastric cancer. However, the exact relationship between copper overload and the malignant phenotype of gastric cancer is still unclear. This study aims to investigate the role of the Cuproptosis-related factor FDX1 in the conversion of gastric cancer to a malignant phenotype. Methods: Firstly, the relative mRNA and protein expression levels of FDX1 in gastric cancer were detected. Secondly, lentiviral transfection of gastric cancer cell lines was performed, and the effects of FDX1 functional intervention on the proliferation, invasion and migration of gastric cancer cells were assessed by CCK-8, colony formation, EdU proliferation, cell scratch and Transwell assays. Thirdly, the differential alteration of genes after overexpression of FDX1 was also analyzed by transcriptome sequencing. Finally, we assessed the tumour-forming capacity in vivo by the xenograft model. Results: FDX1 is significantly upregulated in gastric cancer. The inhibition of FDX1 function results in the suppression of malignant phenotypic transformation in gastric cancer cells. Conversely, overexpression of FDX1 function leads to alterations in tumor-related signaling pathways and the tumor microenvironment. method: First, the relative mRNA and protein expression levels of FDX1 in gastric cancer were detected; Subsequently, lentiviral transfection of gastric cancer cell lines is performed, followed by various experiments such as CCK-8, colony formation, EdU proliferation, cell scratch, and Transwell assays to assess the effects of FDX1 functional intervention on the proliferation, invasion, and migration of gastric cancer cells. Xenograft tumors are utilized to examine changes in tumor-forming ability in vivo. Finally, transcriptome sequencing is employed to further explore the relevant molecular mechanisms. Conclusion: FDX1 plays a significant role in the malignant phenotypic transformation of gastric cancer cells. Further investigation into the regulatory mechanism of FDX1 in the malignant transformation of gastric cancer will enhance our understanding of the involvement of Cuproptosis in gastric cancer.
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