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Exploring the Potential of Montmorillonite As an Antiproliferative Nanoagent Against Mda-Mb-231 and Mcf-7 Human Breast Cancer Cells Publisher Pubmed



Sabzevari AG1 ; Sabahi H2 ; Nikbakht M3 ; Azizi M1 ; Dianatmoghadam H4, 5 ; Amoozgar Z6
Authors
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Authors Affiliations
  1. 1. Department of Tissue Engineering and Biomaterials, Faculty of Advanced Medical Sciences and Technologies, Hamadan University of Medical Sciences, Hamadan, 6517838736, Iran
  2. 2. Department of Life Science Engineering, Faculty of New Sciences and Technologies, University of Tehran, Tehran, 1439957131, Iran
  3. 3. Hematology Oncology and Stem Cell Transplantation Research Center, Tehran University of Medical Sciences, Tehran, 1411713135, Iran
  4. 4. Department of Genetics and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, 8174673461, Iran
  5. 5. Pediatric Inherited Diseases Research Center, Isfahan University of Medical Sciences, Isfahan, 8174673461, Iran
  6. 6. Edwin L. Steele Laboratories for Tumor Biology, Department of Radiation Oncology, Massachusetts General Hospital, Harvard Medical School, Boston, 02114, MA, United States

Source: Cells Published:2024


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. © 2024 by the authors.