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Calcium Sulfide (CaS) Nanostructure Treatment on Non‐Small Cell Lung Cancer
Author(s) -
Forti Kevin Muñoz,
Figueroa Maria,
Torres Bryan,
Bernard Faviola,
Rivera Daniel,
Castro Miguel E,
Suarez Edu B
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.1099.4
Subject(s) - apoptosis , cancer research , etoposide , cancer cell , medicine , programmed cell death , lung cancer , cancer , cell growth , cell , calcium , cell cycle , chemotherapy , chemistry , biochemistry
Lung cancer is the number one cause of death among deaths due to cancer in the United States independent of gender. Current treatments focus on surgical removal of tumors and surround tissue, chemotherapy and radiation therapy. Side effects of the aforementioned treatments have been shown to be detrimental to a patient's health and wellbeing and are capable of causing secondary neoplasms. Recently, nanotechnology has shown promise in providing safer and more efficient therapy options for cancer patients. Our colleagues from the University of Puerto Rico at Mayagüez synthesized nanostructures composed of calcium sulfide (CaS). Due to both calcium and sulfur being incorporated in numerous biological pathways with the former being a mediator in apoptosis, we expect these nanostructures to be biocompatible and with low side effects. In this study, we evaluated the effect of CaS nanostructures on pulmonary adenocarcinoma cells by incubating ATCC CRL‐2124 cell line in the presence of CaS nanostructures [3.8 μM], Etoposide [10 μM], and DMSO (vehicle) for 24‐, 48‐, and 72‐hours after a single dose at time 0. We hypothesized that CaS nanostructures would suppress the cells’ proliferation by interfering with their cell cycle phases and increasing apoptosis. We performed cell‐based assays to study the cell cycle and apoptosis‐mediated cell death. There were no statistically significant observations after 24 hours in non‐cancerous cells (MRC5). Our results showed that at 48‐hours post treatment the progress of malignant cells from Sub‐G 1 into G0/G1 was suppressed along with an increase in apoptosis (p≤0.05). After initial treatment with CaS nanoclusters we observed a built up of malignant cells in S phase at 24‐hours (p≤0.05). These results provide a platform for elucidating the mechanism of action of CaS interfering with proliferation, which may lead to new alternative therapies for lung cancer. Currently we are studying apoptosis mediators and calcium‐dependent pathways believed to be influenced by CaS in cancerous cells. Support or Funding Information This work was supported by: UPR‐PRISE Program NIH Grant #R25GM096955