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Exploring the Potential of Montmorillonite as an Antiproliferative Nanoagent against MDA-MB-231 and MCF-7 Human
Alireza Ghannad Sabzevari1, Hossein Sabahi2, Mohsen Nikbakht3
1Department of Tissue Engineering and Biomaterials, Faculty of Advanced Medical Sciences and Technologies, Hamadan University of Medical Sciences, Hamadan 6517838736, Iran.
Abstract:
Unlike MCF-7 cells, MDA-MB-231 cells are unresponsive to hormone therapy and often show resistance to chemotherapy and radiotherapy. Here, the antiproliferative effect of biocompatible montmorillonite (Mt) nanosheets on MDA-MB-231 and MCF-7 human breast cancer cells was evaluated by MTT assay, flow cytometry, and qRT-PCR. The results showed that the Mt IC50 for MDA-MB-231 and MCF-7 cells in a fetal bovine serum (FBS)-free medium was ~50 and ~200 µg/mL, and in 10% FBS medium ~400 and ~2000 µg/mL, respectively. Mt caused apoptosis in both cells by regulating related genes including Cas-3, P53, and P62 in MDA-MB-231 cells and Bcl-2, Cas-8, Cas-9, P53, and P62 in MCF-7 cells. Also, Mt arrested MCF-7 cells in the G0/G1 phase by altering Cyclin-D1 and P21 expression, and caused sub-G1 arrest and necrosis in both cells, possibly through damaging the mitochondria. However, fewer gene expression changes and more sub-G1 arrest and necrosis were observed in MDA-MB-231 cells, confirming the higher vulnerability of MDA-MB-231 cells to Mt. Furthermore, MDA-MB-231 cells appeared to be much more vulnerable to Mt compared to other cell types, including normal lung fibroblast (MRC-5), colon cancer (HT-29), and liver cancer (HepG2) cells. The higher vulnerability of MDA-MB-231 cells to Mt was inferred to be due to their higher proliferation rate. Notably, Mt cytotoxicity was highly dependent on both the Mt concentration and serum level, which favors Mt for the local treatment of MDA-MB-231 cells. Based on these results, Mt can be considered as an antiproliferative nanoagent against MDA-MB-231 cells and may be useful in the development of local nanoparticle-based therapies.
Insights
Biocompatible montmorillonite (Mt) nanosheets exhibit antiproliferative effects on human breast cancer cells, particularly MDA-MB-231 cells, inducing apoptosis and cell cycle arrest. Mt shows promise as a local nanoparticle-based therapy agent for resistant breast cancer.
Area of Science:
- Nanotechnology
- Biomaterials
- Cancer Biology
Background:
- MDA-MB-231 cells are resistant to standard therapies like hormone therapy, chemotherapy, and radiotherapy.
- There is a need for novel therapeutic agents targeting drug-resistant cancer cell lines.
- Montmorillonite (Mt) nanosheets are biocompatible nanomaterials with potential therapeutic applications.
Purpose of the Study:
- To evaluate the antiproliferative effects of montmorillonite (Mt) nanosheets on MDA-MB-231 and MCF-7 human breast cancer cells.
- To investigate the mechanisms underlying Mt-induced cytotoxicity, including apoptosis and cell cycle regulation.
- To assess the potential of Mt as a nanoagent for local nanoparticle-based therapies.
Main Methods:
- Cell viability was assessed using MTT assays.
- Apoptosis and cell cycle distribution were analyzed by flow cytometry.
- Gene expression related to apoptosis and cell cycle was quantified using qRT-PCR.
Main Results:
- Mt exhibited dose-dependent cytotoxicity, with lower IC50 values for MDA-MB-231 cells compared to MCF-7 cells, especially in serum-free conditions.
- Mt induced apoptosis in both cell lines by regulating key genes (e.g., Cas-3, P53, Bcl-2).
- Mt caused cell cycle arrest (G0/G1 in MCF-7) and sub-G1 arrest/necrosis in both cell types, with greater impact on MDA-MB-231 cells, suggesting higher vulnerability.
Conclusions:
- Montmorillonite (Mt) nanosheets demonstrate significant antiproliferative activity against MDA-MB-231 and MCF-7 breast cancer cells.
- MDA-MB-231 cells are more vulnerable to Mt cytotoxicity, likely due to their higher proliferation rate.
- Mt's efficacy is influenced by concentration and serum levels, supporting its potential for local nanoparticle-based therapies against resistant breast cancers.
