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Ginsenoside F4 inhibits colorectal cancer progression by boosting dendritic cell maturation and remodeling the tumor
Wei Xie1,2, Xue-Jian Li1,2, Yu-Sen Zhong1
1Key Laboratory of Experimental Animal and Safety Evaluation, Hangzhou Medical College, Hangzhou 310013, Zhejiang Province, China.
Background:
Immunotherapy that employs dendritic cells (DCs) to activate the patient's immune system has emerged as a promising therapeutic strategy to combat cancer; however, effective targeting agents are still limited. Ginsenoside F4, as a rare ginsenoside found in Panax ginseng, exhibits stronger antitumor and immunomodulatory activities than primary ginsenosides. However, its therapeutic effects on various diseases remain limited.
Aim:
To investigate the antitumor effect of Ginsenoside F4 and mechanism on the maturation of DCs in colorectal cancer (CRC).
Methods:
The changes in mature DC markers and cytokines generated after DCs were exposed to F4 were assessed using flow cytometry and enzyme-linked immunosorbent assay, respectively. The viability of CRC CT26 cells co-cultured with T lymphocytes was monitored by cell counting kit-8 assay. Furthermore, the histopathological characteristics and immune cell infiltration in tumor tissues of CT26-bearing mice were analyzed by hematoxylin-eosin and immunofluorescent staining. The expressions of apoptosis-relative proteins were detected by western blot assay.
Results:
Treatment with F4 promoted the maturation of DCs, elevated the expressions of cluster of differentiation (CD) 83 and CD86, increased the secretion of interleukin (IL)-2, IL-10, and IL-12 p70, and upregulated the expressions of phosphorylated phosphoinositide 3-kinase, phosphorylated protein kinase B, and nuclear factor kappa-B (NF-κB) phosphorylated p65 in DCs, which enhanced antigen-specific CD8+ T-cell responses. However, these benefits could be reversed by the sphingosine-1-phosphate 1 (S1PR1) inhibitor fingolimod hydrochloride. Furthermore, oral administration with F4 inhibited tumor growth and increased DC and CD8+ T-cell infiltration in the tumor tissues of CT26-bearing mice.
Conclusion:
The results demonstrated that F4 inhibited the growth of CRC by maturing DCs through activating S1PR1-mediated phosphoinositide 3-kinase/protein kinase B and NF-κB pathways, which triggered the antitumor effects of CD8+ T cells. Therefore, F4 could serve as an antitumor immunomodulator for CRC treatment.
Insights
Ginsenoside F4 promotes dendritic cell (DC) maturation and enhances CD8+ T-cell responses, inhibiting colorectal cancer (CRC) growth. This natural compound activates key signaling pathways, offering potential as an antitumor immunomodulator for CRC treatment.
Area of Science:
- Immunology
- Pharmacology
- Oncology
Background:
- Dendritic cells (DCs) are crucial for cancer immunotherapy, but effective targeting agents are limited.
- Ginsenoside F4, a rare ginsenoside from Panax ginseng, shows potent antitumor and immunomodulatory activities.
- Investigating Ginsenoside F4's mechanism in colorectal cancer (CRC) is vital for developing new treatments.
Purpose of the Study:
- To explore the antitumor effects of Ginsenoside F4 in colorectal cancer (CRC).
- To elucidate the mechanism by which Ginsenoside F4 influences DC maturation in CRC.
- To assess Ginsenoside F4's potential as an immunomodulator for CRC therapy.
Main Methods:
- Flow cytometry and ELISA were used to analyze DC maturation markers and cytokine secretion.
- Cell counting kit-8 assay monitored cancer cell viability upon co-culture with T lymphocytes.
- In vivo studies involved analyzing tumor tissues from CT26-bearing mice and western blot for apoptosis-related proteins.
Main Results:
- Ginsenoside F4 promoted DC maturation, upregulating CD83, CD86, IL-2, IL-10, and IL-12 p70.
- F4 treatment enhanced PI3K/Akt and NF-κB signaling in DCs, boosting CD8+ T-cell responses.
- Oral administration of F4 inhibited tumor growth and increased immune cell infiltration in a mouse CRC model.
Conclusions:
- Ginsenoside F4 inhibits CRC growth by maturing DCs via the S1PR1-mediated PI3K/Akt and NF-κB pathways.
- This DC maturation enhances CD8+ T-cell-mediated antitumor effects.
- Ginsenoside F4 demonstrates potential as an effective antitumor immunomodulator for colorectal cancer.
