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Allyl Isothiocyanate Exhibits No Anticancer Activity in MDA-MB-231 Breast Cancer Cells.

Abstract
It was reported recently that allyl isothiocyanate (AITC) could inhibit various types of cancer cell growth. In the present study, we further investigated whether AITC could inhibit the growth of human breast cancer cells. Unexpectedly, we found that AITC did not inhibit, rather slightly promoted, the proliferation of MDA-MB-231 breast cancer cells, although it did have inhibitory effect on MCF-7 breast cancer cells. Cytofluorimetric analysis revealed that AITC (10 µM) did not induce apoptosis and cell cycle arrest in MDA-MB-231 cells. In addition, AITC significantly (p < 0.05) increased the expression of BCL-2 and mTOR genes and Beclin-1 protein in MDA-MB-231 cells. No significant changes in expression of PRKAA1 and PER2 genes, Caspase-8, Caspase-9, PARP, p-mTOR, and NF-κB p65 proteins were observed in these AITC-treated cells. Importantly, AITC displayed cytotoxic effect on MCF-10A human breast epithelial cell line. These observations suggest that AITC may not have inhibitory activity in MDA-MB-231 breast cancer cells. This in vitro study warrants more preclinical and clinical studies on the beneficial and harmful effects of AITC in healthy and cancer cells.
AuthorsMd Abu Sayeed, Massimo Bracci, Veronica Ciarapica, Marco Malavolta, Mauro Provinciali, Ernesta Pieragostini, Simona Gaetani, Federica Monaco, Guendalina Lucarini, Venerando Rapisarda, Roberto Di Primio, Lory Santarelli
JournalInternational journal of molecular sciences (Int J Mol Sci) Vol. 19 Issue 1 (Jan 04 2018) ISSN: 1422-0067 [Electronic] Switzerland
PMID29300316 (Publication Type: Journal Article)
Chemical References
  • Antineoplastic Agents
  • Isothiocyanates
  • Neoplasm Proteins
  • allyl isothiocyanate
Topics
  • Antineoplastic Agents (pharmacology, therapeutic use)
  • Apoptosis (drug effects, genetics)
  • Breast Neoplasms (drug therapy, genetics)
  • Cell Cycle Checkpoints (drug effects)
  • Cell Line, Tumor
  • Cell Proliferation (drug effects)
  • Down-Regulation (drug effects, genetics)
  • Female
  • Gene Expression Regulation, Neoplastic (drug effects)
  • Humans
  • Isothiocyanates (pharmacology, therapeutic use)
  • Neoplasm Proteins (metabolism)
  • Up-Regulation (drug effects, genetics)

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