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The anticancer effect of 2'-3'-dehydrosalannol on triple-negative breast cancer cells
Thiyagarajan Boopalan1, Arunkumar Arumugam, Chendil Damodaran
1Center of Excellence in Cancer Research, Department of Biomedical Sciences, Paul L. Foster School of Medicine, Texas Tech University Health Sciences Center, El Paso, TX, USA.
Background:
Triple-negative breast cancer (TNBC) accounts for 15-20% of all breast tumors and these breast tumors are usually aggressive and highly metastatic. Unfortunately, treatment options for TNBCs are limited; we have identified a novel molecule, 2'-3'-dehydrosalannol (DHS) and in this study we investigated the anticancer effect of DHS against TNBC cells.
Materials And Methods:
TNBC (MDA-MB 231; MDA-MB 468) cells were treated with DHS and its effect on cell viability, apoptosis and molecular mechanisms were analyzed.
Results:
DHS inhibited growth and induced apoptosis in TNBC cell lines. Molecular analysis suggested that DHS inhibited cathepsin-mediated pro-survival signaling [pAKT: phosphorylated protein kinase B; BCL-2: B-cell lymphoma 2 and cyclin D1] and induced pro-apoptotic markers such as BAX [BCL-2-associated X protein] and cleaved caspase-3.
Conclusion:
Our results demonstrate that DHS inhibits cathepsin-mediated pro-survival signaling which resulted in growth arrest of TNBC cells. These findings suggest that DHS may be a promising agent for the prevention and treatment of TNBC.
Insights
The novel molecule 2'-3'-dehydrosalannol (DHS) effectively inhibits triple-negative breast cancer (TNBC) cell growth and induces apoptosis. DHS targets pro-survival signaling pathways, showing promise for TNBC treatment.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Triple-negative breast cancer (TNBC) is an aggressive subtype with limited treatment options.
- TNBC is characterized by its high metastatic potential.
- Novel therapeutic agents are urgently needed for TNBC management.
Purpose of the Study:
- To investigate the anticancer effects of 2 -3 -dehydrosalannol (DHS) on TNBC cells.
- To elucidate the molecular mechanisms underlying DHS-induced cytotoxicity in TNBC.
- To evaluate DHS as a potential therapeutic agent for TNBC.
Main Methods:
- TNBC cell lines (MDA-MB 231, MDA-MB 468) were treated with varying concentrations of DHS.
- Cell viability assays were performed to assess the impact of DHS on cell proliferation.
- Apoptosis markers (BAX, cleaved caspase-3) and pro-survival signaling pathways (pAKT, BCL-2, cyclin D1) were analyzed.
Main Results:
- DHS significantly inhibited the growth of TNBC cell lines.
- DHS treatment induced apoptosis in TNBC cells.
- Molecular analysis revealed inhibition of cathepsin-mediated pro-survival signaling and induction of pro-apoptotic markers.
Conclusions:
- DHS demonstrates potent anticancer activity against TNBC by inhibiting pro-survival signaling.
- DHS induces growth arrest and apoptosis in TNBC cells.
- These findings highlight DHS as a promising candidate for the development of novel TNBC therapies.
