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Anti-Cancer Effects of an Optimised Combination of Ginsenoside Rg3 Epimers on Triple Negative Breast Cancer Models
Maryam Nakhjavani1,2, Eric Smith1,2, Helen M Palethorpe3
1Molecular Oncology, Basil Hetzel Institute, The Queen Elizabeth Hospital, Woodville South, SA 5011, Australia.
Abstract:
Key problems of chemotherapies, as the mainstay of treatment for triple-negative breast cancer (TNBC), are toxicity and development of tumour resistance. Using response surface methodology, we previously optimised the combination of epimers of ginsenoside Rg3 (Rg3) for anti-angiogenic action. Here, we show that the optimised combination of 50 µM SRg3 and 25 µM RRg3 (C3), derived from an RSM model of migration of TNBC cell line MDA-MB-231, inhibited migration of MDA-MB-231 and HCC1143, in 2D and 3D migration assays (p < 0.0001). C3 inhibited mammosphere formation efficiency in both cell lines and decreased the CD44+ stem cell marker in the mammospheres. Molecular docking predicted that Rg3 epimers had a better binding score with IGF-1R than with EGFR, HER-2 or PDGFR, and predicted an mTOR inhibitory function of Rg3. C3 affected the signalling of AKT in MDA-MB-231 and HCC1143 mammospheres. In a mouse model of metastatic TNBC, an equivalent dose of C3 (23 mg/kg SRg3 + 11 mg/kg RRg3) or an escalated dose of 46 mg/kg SRg3 + 23 mg/kg RRg3 was administered to NSG mice bearing MDA-MB-231-Luc cells. Calliper and IVIS spectrum measurement of the primary and secondary tumour showed that the treatment shrunk the primary tumour and decreased the load of metastasis in mice. In conclusion, this combination of Rg3 epimers showed promising results as a potential treatment option for TNBC patients.
Insights
This study optimized a combination of ginsenoside Rg3 epimers to treat triple-negative breast cancer (TNBC). The treatment effectively inhibited TNBC cell migration and metastasis in preclinical models, offering a promising new therapeutic avenue.
Area of Science:
- Oncology
- Pharmacology
- Biochemistry
Background:
- Chemotherapy for triple-negative breast cancer (TNBC) faces challenges with toxicity and drug resistance.
- Ginsenoside Rg3 (Rg3) epimers have shown potential for anti-cancer effects.
- Optimizing Rg3 epimer combinations is crucial for developing effective TNBC treatments.
Purpose of the Study:
- To evaluate the efficacy of an optimized combination of SRg3 and RRg3 (C3) against TNBC.
- To investigate the effects of C3 on TNBC cell migration, stemness, and molecular signaling pathways.
- To assess the in vivo anti-metastatic potential of C3 in a TNBC mouse model.
Main Methods:
- Response surface methodology (RSM) was used to optimize the Rg3 epimer combination.
- In vitro assays included 2D and 3D cell migration, mammosphere formation, and stem cell marker analysis (CD44+).
- Molecular docking predicted interactions with key signaling proteins (IGF-1R, EGFR, HER-2, PDGFR, mTOR).
- In vivo studies utilized a metastatic TNBC mouse model (MDA-MB-231-Luc) with caliper and IVIS measurements.
Main Results:
- The optimized C3 combination significantly inhibited MDA-MB-231 and HCC1143 cell migration in vitro.
- C3 reduced mammosphere formation efficiency and decreased CD44+ stem cell markers.
- Molecular docking suggested Rg3 epimers target IGF-1R and inhibit mTOR.
- C3 treatment affected AKT signaling in TNBC cells.
- In vivo, C3 treatment shrunk primary tumors and reduced metastatic burden in mice.
Conclusions:
- The optimized Rg3 epimer combination (C3) demonstrates significant anti-migratory and anti-metastatic effects against TNBC.
- C3 targets key signaling pathways involved in TNBC progression and stemness.
- This Rg3 epimer combination represents a promising therapeutic strategy for TNBC patients.
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