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In Vivo Antitumor Effects of MK615 Led by PD-L1 Downregulation
Masashi Yanaki1, Masayuki Kobayashi1, Atsushi Aruga1
11 Tokyo Women's Medical University, Tokyo, Japan.
Background/Aim:
MK615 extracted from Prunus mume was reported to have anti-inflammatory effects. In this article, we examined the in vivo antitumor effect of MK615 (an extract from Japanese apricot) using mouse tumor xenografts and focusing on the downregulation of PD-L1 (programmed death-ligand 1), a ligand of programmed cell death-1, a surface protein of activated T cells.
Materials And Methods:
B16/BL6 melanoma cells were injected into C57BL/6 or BALB/c-nu/nu mice to establish lung metastasis. BALB/c-nu/nu mice (nude mice) were used as a T cell-deficient model. The mice were given MK615 or saline orally every other day for approximately 8 weeks, and their survival was observed. NF-κB (nuclear factor-κB) and PD-L1 expressions of metastatic lung tissues were also examined.
Results:
The survival rate was improved only in the MK615-treated C57BL/6 mice ( P < .05), not in the saline-given control mice or BALB/c-nu/nu mice. The downregulations of NF-κB and PD-L1 were observed in both MK615-treated C57BL/6 and BALB/c-nu/nu mice. These results suggest that the antitumor effects of MK615 are associated with T cell-mediated immunity activated by MK-615-induced PD-L1 downregulation in tumor cells.
Conclusion:
MK615 is beneficial for a prolonged host survival time in the B16/BL6 melanoma xenograft model associated with T cell-mediated antitumor immunity.
Insights
MK615, a Japanese apricot extract, prolonged survival in a mouse melanoma model by downregulating PD-L1 and activating T cell immunity. This extract shows potential for T cell-mediated antitumor effects.
Area of Science:
- Immunology
- Pharmacology
- Oncology
Background:
- MK615, derived from Prunus mume, exhibits anti-inflammatory properties.
- Programmed death-ligand 1 (PD-L1) is a key regulator of T cell-mediated immune responses.
- PD-L1 is expressed on activated T cells and tumor cells, influencing immune evasion.
Purpose of the Study:
- To investigate the in vivo antitumor effect of MK615.
- To determine the role of PD-L1 downregulation in MK615's antitumor activity.
- To explore the association between MK615 and T cell-mediated immunity.
Main Methods:
- B16/BL6 melanoma lung metastasis model established in C57BL/6 and T cell-deficient BALB/c-nu/nu mice.
- Mice treated orally with MK615 or saline for approximately 8 weeks.
- Survival rates, NF-κB, and PD-L1 expression in metastatic lung tissues were analyzed.
Main Results:
- MK615 significantly improved survival in C57BL/6 mice but not in nude mice.
- Downregulation of NF-κB and PD-L1 was observed in both mouse models treated with MK615.
- These findings suggest a T cell-dependent mechanism for MK615's antitumor effects.
Conclusions:
- MK615 demonstrates a T cell-mediated antitumor effect in a melanoma xenograft model.
- The antitumor activity of MK615 is linked to the downregulation of PD-L1.
- MK615 administration prolongs host survival by modulating immune responses.
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