Effect of Interaction between Chromium(VI) with 17β-Estradiol and Its Metabolites on Breast Cancer Cell Lines MCF-7/WT and MDA-MB-175-VII: Preliminary Study.
Ewa SawickaJulita KulbackaMałgorzata Drąg-ZalesińskaArkadiusz WoźniakAgnieszka PiwowarPublished in: Molecules (Basel, Switzerland) (2023)
The number of factors initiating and stimulating the progression of breast cancer are constantly increasing. Estrogens are a risk factor for breast adenocarcinoma, the toxicity of which increases as a result of metabolism and interaction with other factors. Due to the presence of environmental exposure to estrogens and metalloestrogens, we investigated how interactions between estrogens and toxic chromium(VI)[Cr(VI)] affect breast cancer lines and investigated whether estrogens play a protective role. The aim of the study was to investigate the effect of 17β-estradiol and its metabolites: 2-methoxyestradiol (2-MeOE2), 4-hydroxyestradiol (4-OHE2), and 16α-hydroxyestrone (16α-OHE1) in exposure to Cr(VI) on cell viability and DNA cell damage. Two estrogen-dependent breast cancer cell lines, MCF 7/WT and MDA-MB-175-VII, were examined. In addition, the expression of Cu-Zn superoxide dismutase (SOD1) was determined immunocytochemically to elucidate the mechanism of oxidative stress. The effects of single substances and their mixtures were tested in the model of simultaneous and 7-day estrogen pre-incubation. As a result, the viability of MCF-7 and MDA-MB-175-VII cells is lowered most by Cr(VI) and least by 17β-E2. In the combined action of estrogens and metalloestrogens, we observed a protective effect mainly of 17β-E2 against Cr(VI)-induced cytotoxicity. The highest expression of SOD1 was found in MCF-7/WT cells exposed to 17β-E2. Moreover, high apoptosis was caused by both Cr(VI) itself and its interaction with 4-OHE2 and 2-MeOE2. The direction and dynamics of changes in viability are consistent for both lines.
Keyphrases
- breast cancer cells
- cell cycle arrest
- oxidative stress
- induced apoptosis
- cell death
- poor prognosis
- estrogen receptor
- pi k akt
- diabetic rats
- endoplasmic reticulum stress
- ischemia reperfusion injury
- dna damage
- squamous cell carcinoma
- young adults
- radiation therapy
- binding protein
- mass spectrometry
- atomic force microscopy
- signaling pathway
- amyotrophic lateral sclerosis
- bone marrow
- endothelial cells
- cell proliferation
- stem cells
- ionic liquid
- breast cancer risk
- metal organic framework
- cell free