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Mitochondrial Mediated Apoptosis Evaluation of Myristicin on Triple Negative Breast Cancer Model Via Bcl2/Bid Pathway
Sudhina Sufina Nazar1,2, Aswathy Vadakkumkattle Ajaykumar3, Janeesh Plakkal Ayyappan1,2
1Translational Nanomedicine and Lifestyle Disease Research Laboratory, Department of Biochemistry, University of Kerala, Kariavattom campus, Thiruvananthapuram, Kerala, India.
Abstract:
Among 15-20 cases of breast cancer, triple-negative breast cancer (TNBC) is the deadliest form of the disease. The most effective form of treatment for this type of cancer is still targeted chemotherapy because it lacks hormone receptors. Myristicin, an active aromatic compound with anticancer properties, is mostly found in nutmeg. Antitumor, antioxidant, and antimicrobial activity are among few of the numerous properties of myristicin. On TNBC cells, the exact modes of action are mostly unidentified. This study shows that myristicin triggered the mitochondria-mediated apoptosis in MDA-MB-231 cells. The MTT assay assessed the anti-proliferative potential of myristicin on TNBC cells (IC50 0.65 mM ± 0.98). Flow cytometry analysis was used to evaluate the myristicin's effects on cell apoptosis using annexin V/PI (46.4 ± 2.31%). After evaluating the protein expression, myristicin significantly decreased the expression of Bcl2 and HSP60 while enhancing the expression of proteins such as caspase 9, caspase 3, bid, bad, caspase 7, P53, cytochrome c, and SDHA. Furthermore, our research confirmed that myristicin has a lower toxicological profile and greater in vivo therapeutic efficacy. In BALB/c mice, 4T1 cells were injected subcutaneously to develop breast tumors, and the mice subsequently received myristicin. According to in vivo results, myristicin treatment reduced tumor weight and volume when compared to the breast cancer control group. Besides, the enzyme analysis, gene, and protein expression showed significant apoptotic properties on myristicin treated group. According to these results, myristicin may be used as a therapeutic approach for the management of TNBC.
Insights
Myristicin, a compound from nutmeg, effectively triggers cancer cell death in triple-negative breast cancer (TNBC) models. This natural compound shows promise for TNBC treatment with reduced toxicity and enhanced therapeutic efficacy in vivo.
Area of Science:
- Biochemistry
- Pharmacology
- Oncology
Background:
- Triple-negative breast cancer (TNBC) is an aggressive subtype lacking hormone receptors, necessitating novel therapeutic strategies.
- Myristicin, a natural compound found in nutmeg, possesses known anticancer properties, but its specific mechanisms against TNBC remain largely unelucidated.
- Targeted chemotherapy is currently the primary treatment for TNBC, highlighting the need for alternative or complementary approaches.
Purpose of the Study:
- To investigate the anti-proliferative and apoptosis-inducing effects of myristicin on TNBC cells.
- To elucidate the molecular mechanisms underlying myristicin's action in TNBC, focusing on apoptotic pathways.
- To evaluate the in vivo therapeutic efficacy and toxicological profile of myristicin in a preclinical TNBC model.
Main Methods:
- In vitro studies utilized MTT assays for proliferation assessment and flow cytometry with Annexin V/PI staining for apoptosis analysis in MDA-MB-231 TNBC cells.
- Western blot analysis was performed to examine the expression levels of key proteins involved in apoptosis, including Bcl2, HSP60, caspases, P53, and cytochrome c.
- In vivo efficacy was assessed in BALB/c mice bearing 4T1 tumors, with myristicin treatment compared to a control group, evaluating tumor weight, volume, and apoptotic markers.
Main Results:
- Myristicin demonstrated significant anti-proliferative activity against TNBC cells with an IC50 of 0.65 µM.
- Flow cytometry revealed that myristicin induced apoptosis in 46.4% of TNBC cells.
- Myristicin modulated the expression of apoptosis-related proteins, decreasing Bcl2 and HSP60 while increasing pro-apoptotic proteins like caspases, P53, and cytochrome c.
- In vivo studies showed that myristicin treatment significantly reduced tumor weight and volume in mice, accompanied by enhanced apoptotic markers.
Conclusions:
- Myristicin effectively induces mitochondria-mediated apoptosis in TNBC cells through the modulation of key apoptotic proteins.
- Myristicin exhibits a favorable toxicological profile and demonstrates significant in vivo therapeutic efficacy against TNBC.
- Myristicin presents a potential therapeutic candidate for the management of triple-negative breast cancer.
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