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人参皂苷Rg3通过JAK3/STAT5信号通路对结肠癌细胞增殖和迁移的抑制作用。

The inhibitory efficacy of Ginsenoside Rg3 on proliferation and migration of colonic carcinoma cells through the JAK3/STAT5 signaling pathway.

作者信息

Sun Xiumei, Bi Han, Gao Feng, Zhao Xiaoyu, Feng Xinyu, Bo Qifu, Liu Jin, Wang Wenhao

机构信息

Department of Comprehensive Oncology, Affiliated Hospital of Shandong Second Medical University, Kuiwen District, No.2428, Yuhe Road, Weifang, 261041, China.

Department of Oncology, Heze Municipal Hospital, No.2888, Caozhouxi Road, Heze, 274031, China.

出版信息

Discov Oncol. 2024 Nov 1;15(1):608. doi: 10.1007/s12672-024-01476-1.

Abstract

OBJECTIVE

To elucidate the efficacy of Ginsenoside Rg3 on the reproduction and immigration of HCT-116 cells and its molecular mechanism.

METHODS

Analysis of the cell cycle along with the colony formation assay, and MTT test were performed to detect the effect of Ginsenoside Rg3 (GRg3) on proliferation of HCT-116 cells. Transwell assay and Cell scratch wound method were carried out to determine the impact on the immigration. The differential expressed genes obtained by RNA-sequencing were intersected with the predicted target genes of GRg3, and PPI was constructed to analyze hub genes. The key target gene expression and its downstream genes were evaluated by western blot assay.

RESULTS

The GRg3 can inhibit the reproduction and immigrating ability of colonic carcinoma cells, decrease the ability of colony formation in HCT-116 cells, and arrest the G2 phase. JAK3 was identified as a key target gene. Western blot assay revealed decreased levels of p-STAT5 and JAK3 post-treatment with RG3, while STAT5a and STAT5b did not change significantly.

CONCLUSION

The GRg3 inhibits the phosphorylation of STAT5 but not the expression of total protein by inhibiting the expression of JAK3, and then inhibits the proliferation and migration of HCT-116 cells.

摘要

目的

阐明人参皂苷Rg3对HCT-116细胞增殖和迁移的影响及其分子机制。

方法

通过细胞周期分析、集落形成实验和MTT实验检测人参皂苷Rg3(GRg3)对HCT-116细胞增殖的影响。采用Transwell实验和细胞划痕实验确定其对迁移的影响。将RNA测序获得的差异表达基因与GRg3的预测靶基因进行交集分析,并构建蛋白质-蛋白质相互作用(PPI)网络以分析枢纽基因。通过蛋白质免疫印迹法评估关键靶基因表达及其下游基因。

结果

GRg3可抑制结肠癌细胞的增殖和迁移能力,降低HCT-116细胞的集落形成能力,并使细胞停滞于G2期。JAK3被鉴定为关键靶基因。蛋白质免疫印迹法显示,RG3处理后p-STAT5和JAK3水平降低,而STAT5a和STAT5b无明显变化。

结论

GRg3通过抑制JAK3的表达来抑制STAT5的磷酸化,但不影响其总蛋白表达,进而抑制HCT-116细胞的增殖和迁移。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a16/11530417/ec84e75ac87b/12672_2024_1476_Fig1_HTML.jpg

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