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Ginsenoside compound K inhibits the proliferation, migration and invasion of Eca109 cell via VEGF-A/Pi3k/Akt pathway
Jianhou Huang1, Dinglong Pan2, Feng Liu3
1Department of Pharmacy, Quanzhou First Hospital Affiliated to Fujian Medical University, Quanzhou, China.
Objective:
Esophageal cancer, one of the most common cancers in the upper digestive tract and is one of the leading cancer-related mortality worldwide. Accumulating studies found that Ginsenoside compound K (CK) has significantly anti-tumor effects, especially in the suppression of proliferation, migration, as well as invasion in various human cancers. While the effects of Ginsenoside CK in esophageal cancer have not been well studied. In our present study, we aim to explore the functions and mechanisms of Ginsenoside CK in the progression of esophageal cancer cells (Eca109).
Methods:
Cell Counting Kit-8 (CCK-8), wound healing, transwell and flow cytometry assays were applied to analyze the effects of Ginsenoside CK in the progression of Eca109 cell, western blot assay was used to investigate the potential downstream signaling pathway after Ginsenoside CK treatment.
Results:
Our study found that Ginsenoside CK can suppress cell proliferation, migration and invasion of Eca109 cell. Furthermore, the flow cytometry showed that Ginsenoside CK increased of apoptosis rates in Eca109 cell. The western blot results indicated that Ginsenoside CK decreased the expression of VEGF-A, P-Pi3k and P-Akt proteins. Moreover, the knockdown of VEGF-A gene could suppress cell proliferation, migration, invasion and induce apoptosis in Eca109 cell, and the expression of P-Pi3k and P-Akt proteins were significantly downregulated.
Conclusions:
Our study suggests that Ginsenoside CK inhibits the proliferation, migration, invasion, and induced apoptosis of Eca109 cell by blocking VEGF-A/Pi3k/Akt signaling pathway.
Insights
Ginsenoside compound K (CK) inhibits esophageal cancer cell growth, migration, and invasion. It also induces apoptosis by blocking the VEGF-A/Pi3k/Akt signaling pathway.
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Esophageal cancer is a major cause of cancer mortality worldwide.
- Ginsenoside compound K (CK) exhibits anti-tumor properties in various cancers.
- The role of CK in esophageal cancer progression remains understudied.
Purpose of the Study:
- To investigate the anti-cancer effects of Ginsenoside CK on esophageal cancer cells (Eca109).
- To elucidate the underlying molecular mechanisms of CK's action in esophageal cancer.
Main Methods:
- Cell Counting Kit-8 (CCK-8), wound healing, and Transwell assays were used to assess cell proliferation, migration, and invasion.
- Flow cytometry was employed to analyze apoptosis rates.
- Western blot was utilized to examine protein expression in signaling pathways.
Main Results:
- Ginsenoside CK significantly suppressed Eca109 cell proliferation, migration, and invasion.
- CK treatment led to increased apoptosis rates in Eca109 cells.
- CK decreased the expression of VEGF-A, p-Pi3k, and p-Akt proteins, suggesting pathway inhibition.
Conclusions:
- Ginsenoside CK demonstrates potent anti-cancer activity against esophageal cancer cells.
- The mechanism involves the inhibition of the VEGF-A/Pi3k/Akt signaling pathway.
- CK holds potential as a therapeutic agent for esophageal cancer.
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