Zinc oxide nanoparticles enhance expression of maspin in human breast cancer cells

• Published in: Environmental science and pollution research international 2020-10, Vol.27 (30), p.38300-38310
• Main Authors: Khorsandi, Layasadat, Farasat, Maryam
• Format: Article
• Language: English
• Subjects: 17β-Estradiol; Annexin V; Apoptosis; Aquatic Pollution; Atmospheric Protection/Air Quality Control/Air Pollution; BAX protein; Bcl-2 protein; Breast cancer; Cell migration; Cell survival; Cell viability; Earth and Environmental Science; Ecotoxicology; Environment; Environmental Chemistry; Environmental Health; Environmental science; Estrogen receptors; Estrogens; Evaluation; Gene expression; Metastases; Nanoparticles; p53 Protein; Protease inhibitors; Proteinase inhibitors; Proteins; Research Article; Serine; Serine proteinase; Sex hormones; Tumor suppressor genes; Tumors; Waste Water Technology; Water Management; Water Pollution Control; Western blotting; Zinc oxide; Zinc oxides
• ISSN: 0944-1344; 1614-7499
• DOI: 10.1007/s11356-020-09986-5

Toxic and apoptotic impacts of zinc oxide nanoparticle (ZNP) on different cancer cells have been reported. Maspin (a mammary serine protease inhibitor) as a tumor suppressor gene can inhibit tumor growth and metastasis. The expression of maspin is modulated by p53, Bcl-2 family genes, and estrogen receptor α (ER-α). This study aimed to assess the ZNP effects on maspin expression in MCF-7 cells (a breast cancer cell). Experimental groups (ZNP5, ZNP10, and ZNP20) received 5, 10, and 20 μM/mL ZNP for 48 h, respectively. 17-β-estradiol (E2) was used to evaluate the role of ER-α in the anticancer impact of ZNP. Cell viability, Annexin V, migration assay, gene expression, and western blotting methods were applied to evaluate ZNP effects on the MCF-7 cells. ZNP at the concentrations of 10 and 20 μM/mL could significantly decrease the viability and migration rate, and significantly increase apoptosis percentage in the MCF-7 cells. ZNP significantly enhanced mRNA expression and protein level of maspin in MCF-7 cells in a concentration-dependent way. ZNP concentration-dependently elevated mRNA expression and protein level of p53 and Bax while reduced the expression of Bcl-2 and ER-α. E2 promoted cancer cell growth by enhancing survival and migration rates. E2 treatment reduced mRNA expression and protein level of maspin and p53, and elevated Bcl-2 expression. ZNP considerably changed these events induced by E2 in the MCF-7 cells. It is concluded that the maspin overexpression is one of the toxic mechanisms of the ZNP on the ER-α-positive breast cancer cells, and can suppress the migration of these cells.