A platform for research: civil engineering, architecture and urbanism
A platform for research: civil engineering, architecture and urbanism
Sodium arsenite inhibited genomic estrogen signaling but induced pERα (Ser118) via MAPK pathway in breast cancer cells
Arsenic (As) is considered a major environmental health threat worldwide due to its widespread contamination in drinking water. Recent studies reported that arsenic is a potential xenoestrogen as it interfered with the action of estrogen (E2) and estrogen receptor (ER) signaling. The present study investigated the effects of sodium arsenite (NaAsO 2 ) on estrogen signaling in human breast cancer cells. The results demonstrated that NaAsO 2 dose‐dependently increased viability of hormone‐dependent breast cancer MCF‐7 and T47D cells expressing both ERα and ERβ but not hormone‐independent MDA‐MB‐231 cells expressing ERβ. These suggested ERα contribution to NaAsO 2 ‐stimulated breast cancer cells growth. NaAsO 2 induced down‐regulation of ERα but up‐regulation of ERβ protein expressions in T47D cells. Moreover, NaAsO 2 dose‐dependently inhibited E2‐induced ER transcriptional activity as it decreased E2‐mediated ERE‐luciferase transcription activation and PgR mRNA transcription but increased pS2 mRNA transcription. However, NaAsO 2 induced both rapid and sustained activation of ERK1/2 and increased in phosphorylation of ERα at serine 118 residue, c‐fos and c‐myc protein expressions. These results indicated that NaAsO 2 interferes the genomic estrogen‐signaling pathway but induces activation of a rapid nongenomic signal transduction through ERK1/2 pathway which may contribute to its proliferative effect on hormone‐dependent breast cancer cells. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1133–1146, 2016.
Sodium arsenite inhibited genomic estrogen signaling but induced pERα (Ser118) via MAPK pathway in breast cancer cells
Arsenic (As) is considered a major environmental health threat worldwide due to its widespread contamination in drinking water. Recent studies reported that arsenic is a potential xenoestrogen as it interfered with the action of estrogen (E2) and estrogen receptor (ER) signaling. The present study investigated the effects of sodium arsenite (NaAsO 2 ) on estrogen signaling in human breast cancer cells. The results demonstrated that NaAsO 2 dose‐dependently increased viability of hormone‐dependent breast cancer MCF‐7 and T47D cells expressing both ERα and ERβ but not hormone‐independent MDA‐MB‐231 cells expressing ERβ. These suggested ERα contribution to NaAsO 2 ‐stimulated breast cancer cells growth. NaAsO 2 induced down‐regulation of ERα but up‐regulation of ERβ protein expressions in T47D cells. Moreover, NaAsO 2 dose‐dependently inhibited E2‐induced ER transcriptional activity as it decreased E2‐mediated ERE‐luciferase transcription activation and PgR mRNA transcription but increased pS2 mRNA transcription. However, NaAsO 2 induced both rapid and sustained activation of ERK1/2 and increased in phosphorylation of ERα at serine 118 residue, c‐fos and c‐myc protein expressions. These results indicated that NaAsO 2 interferes the genomic estrogen‐signaling pathway but induces activation of a rapid nongenomic signal transduction through ERK1/2 pathway which may contribute to its proliferative effect on hormone‐dependent breast cancer cells. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1133–1146, 2016.
Sodium arsenite inhibited genomic estrogen signaling but induced pERα (Ser118) via MAPK pathway in breast cancer cells
2016
Article (Journal)
English