In Vitro Evaluation of the Antitumor Effect of Bismuth Lipophilic Nanoparticles (BisBAL NPs) on Breast Cancer Cells

Overview

Journal Int J Nanomedicine

Publisher Dove Medical Press

Specialty Biotechnology

Date 2018 Oct 17

PMID 30323596

Citations 12

Authors

Rene Hernandez-Delgadillo

Claudia Maria Garcia-Cuellar

Yesennia Sanchez-Perez

Nayely Pineda-Aguilar

Marco Antonio Martinez-Martinez

Eyra Elvyra Rangel-Padilla

Sergio Eduardo Nakagoshi-Cepeda

Juan Manuel Solis-Soto

Rosa Isela Sanchez-Najera

Maria Argelia Akemi Nakagoshi-Cepeda

Shankararaman Chellam

Claudio Cabral-Romero

Affiliations

Soon will be listed here.

Abstract

Aim: The objective of this study was to evaluate the antitumor activity of lipophilic bismuth nanoparticles (BisBAL NPs) on breast cancer cells.

Materials And Methods: The effect of varying concentrations of BisBAL NPs was evaluated on human MCF-7 breast cancer cells and on MCF-10A fibrocystic mammary epitheliocytes as noncancer control cells. Cell viability was evaluated with the MTT assay, plasma membrane integrity was analyzed with the calcein AM assay, genotoxicity with the comet assay, and apoptosis with the Annexin V/7-AAD assay.

Results: BisBAL NPs were spherical in shape (average diameter, 28 nm) and agglomerated into dense electronic clusters. BisBAL NP induced a dose-dependent growth inhibition. Most importantly, growth inhibition was higher for MCF-7 cells than for MCF-10A cells. At 1 µM BisBAL NP, MCF-7 growth inhibition was 51%, while it was 11% for MCF-10A; at 25 µM BisBAL NP, the growth inhibition was 81% for MCF-7 and 24% for MCF-10A. With respect to mechanisms of action, a 24-hour exposure of 10 and 100 µM BisBAL NP caused loss of cell membrane integrity and fragmentation of tumor cell DNA. BisBAL NPs at 10 µM were genotoxic to and caused apoptosis of breast cancer cells.

Conclusion: BisBAL NP-induced growth inhibition is dose dependent, and breast cancer cells are more vulnerable than noncancer breast cells. The mechanism of action of BisBAL NPs may include loss of plasma membrane integrity and a genotoxic effect on the genomic DNA of breast cancer cells.

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