Effects of Notoginsenoside R1 on Characteristics of Esophageal Squamous Cell Carcinoma KYSE150 Cells

Jinling XIAO; Ruiyan LIU; Xinyu LI; Junrun ZENG; Liping ZHANG; Yu GUO

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Jinling XIAO, Ruiyan LIU, Xinyu LI, Junrun ZENG, Liping ZHANG, Yu GUO. Effects of Notoginsenoside R1 on Characteristics of Esophageal Squamous Cell Carcinoma KYSE150 Cells[J]. Journal of Kunming Medical University.

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Effects of Notoginsenoside R1 on Characteristics of Esophageal Squamous Cell Carcinoma KYSE150 Cells

Department of Immunology，Xinjiang Second Medical University，Karamay Xinjiang 834000，China

Received Date: 2026-04-27

Abstract

Abstract

Objective To investigate the effects of Notoginsenoside R1 （NGR1）, an active monomer derived from the traditional Chinese medicine Panax notoginseng, on the proliferation, migration, invasion, cell cycle distribution, and apoptosis of esophageal squamous cell carcinoma （ESCC） KYSE150 cells, and to preliminarily predict its potential targets using bioinformatics mathods. Methods KYSE150 cells cultured in vitro were divided into a control group （complete medium containing an equal volume of DMSO）, a low-dose group （5.7 μg/mL NGR1）, a medium-dose group （28.8 μg/mL NGR1）, and a high-dose group （144.0 μg/mL NGR1）. Cell proliferation activity was detected by the CCK-8 assay; cell migration and invasion abilities were evaluated by wound healing assay and Transwell assay, respectively; cell cycle distribution and apoptosis rate were detected by flow cytometry; and network pharmacology and molecular docking were used to predict the potential core targets of NGR1 against esophageal cancer. Results Compared with the control group, NGR1 significantly inhibited KYSE150 cell proliferation in a dose-dependent manner （P < 0.05）. In the medium- and high-dose groups, the wound healing rate and the number of cells penetrating the Transwell membrane were significantly decreased, while the apoptosis rate was significantly increased （P < 0.05）. The proportion of cells in the G₀/G₁-phase was significantly increased in all dose groups, indicating cell cycle arrest at G₀/G₁ phase （P < 0.05）. Network pharmacology screening identified core targets such as STAT3, CDK1, MMPs （MMP2/7/9） and CASP3, and molecular docking results showed that NGR1 had good binding activity with the above target proteins. Conclusion NGR1 can effectively inhibit the proliferative capacity of esophageal cancer KYSE150 cells, significantly impede their migration and invasion, induce apoptosis, and arrest the cell cycle at the G0/G1 phase. Its mechanism may be related to coordinated regulation of multiple targets.
- Esophageal neoplasms,
- Notoginsenoside R1,
- Cell proliferation,
- Cell migration,
- Bioinformatics

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References(27)

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