Delving into the Function of Ginsenoside Rh2 in the Develpoment of Breast Cancer

Delving into the Function of Ginsenoside Rh2 in the Develpoment of Breast Cancer



1. Introduction

According to the 2020 report of World Health Organization (WHO), there are approximately 2.3 million cases with breast cancer worldwide. Breast cancer has emerged as one of the most malignant tumor in females with significant incidence rate. Although great progress has made in improving the cure rate of early-stage breast cancer in recent years, advanced breast cancer is still hard to be cured.

How to reduce the risk of recurrence and metastasis of early-stage breast cancer as well as prolong the survival of patients with advanced breast cancer is still a challenge in the clinical treatment of breast cancer. Notably, ginsenoside Rh2 (GRh2) exerts prominent impacts on retarding the progression of breast cancer via strengthening the immune surveillance of natural killer (NK) cells, a kind of cytotoxic innate lymphocytes critical for tumor immune response.

2. The repressive role of GRh2 in the progression of breast cancer

GRh2 hinders the growth, proliferation and metastasis of breast cancer. Simply put, the body weight and tumor volume of model mice are markedly reduced post treatment of GRh2 (10 mg/kg and 20 mg/kg). In addition, the proliferating rate of breast cancer cells is repressed by GRh2 in a dose-dependent manner (5, 10 and 20 mg/kg). Upon the treatment of GRh2 (20 mg/kg), the loss of lung capacity is obviously reduced and the lung metastases formed by MDA-MB-231 tumor cells are strikingly mitigated as well, with no apparent liver metastatic nodules.

3. The enhanced killing effect of NK cells on breast cancer cells following GRh2 treatment

GRh2 exerts remarkable effects on retarding the progression of breast cancer via improving the killing ability of NK92MI cells. In a nutshell, the mRNA expression levels of killing mediators perforin and IFN-γ in NK92MI cell-breast cancer cell co-culture system are explicitly upregulated post GRh2 treatment. Strikingly, the reduced lung metastasis of breast cancer by GRh2 is almost counteracted upon the depletion of NK cells. Relative to that of the vehicle control, the amount of CD107a, a degranulation marker of NK cells, is overtly elevated in the presence of GRh2 (20 mg/kg), verifying the enhanced killing activity of NK cells on breast cancer. 

4. The underlying molecular mechanism of GRh2 on potentiating the NK cell activity against breast cancer

Breast cancer cells reduce the recognition by NKG2D through proteolytic shedding MICA mediated by ERp5 to escape NK cell surveillance. GRh2 interferes with the formation of soluble MICA (sMICA) by suppressing the expression of ERp5 to increase the contents of killing mediators from NK cells, thereby exerting striking effects on fighting against breast cancer.

5. Conclusion

GRh2 potentiates the cytotoxic effect of NK cells and enhances the immune surveillance function of NK cells to fight against breast cancer, which may be a potent drug candidate for the prevention and treatment of breast cancer.

Reference

[1] Sung H, Ferlay J, Siegel RL, et al. Global Cancer Statistics 2020: GLOBOCAN Estimates of Incidence and Mortality Worldwide for 36 Cancers in 185 Countries. CA Cancer J Clin. 2021;71(3):209-249. doi:10.3322/caac.21660
[2] Yang C, Qian C, Zheng W, et al. Ginsenoside Rh2 enhances immune surveillance of natural killer (NK) cells via inhibition of ERp5 in breast cancer. Phytomedicine. 2024;123:155180. doi:10.1016/j.phymed.2023.155180

Product advantages of BONTAC ginsenoside Rh2


BONTAC is the first enterprise worldwide that can provide national mass production of ginsenosides (Rh2) by enzymatic synthesis, with pure raw materials, higher conversion rate and higher content (up to 99%). One-stop service for customized product solution is available in BONTAC. With unique Bonzyme enzymatic synthesis technology, both S-type and R-type isomers can be accurately synthesized here, with stronger activity and precise targeting action. Our products are subjected to strict third-party self-inspection, which are worth of trustworthy.

Disclaimer

This article is based on the reference in the academic journal. The relevant information is provide for sharing and learning purposes only, and does not represent any medical advice purposes. If there is any infringement, please contact the author for deletion. The views expressed in this article do not represent the position of BONTAC. 
 

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