TY - JOUR
T1 - Breast cancer proliferation and deterioration-associated metabolic heterogeneity changes induced by exposure of bisphenol S, a widespread replacement of bisphenol A
AU - Zhao, Chao
AU - Yong, Ting
AU - Zhang, Yinbin
AU - Xiao, Yu
AU - Jin, Yaofeng
AU - Zheng, Chang
AU - Nirasawa, Takashi
AU - Cai, Zongwei
N1 - The work was supported by the National Natural Science Foundation of China ( 91843301 ), the National Key Research Program of China ( 2017YFC1600505 and 2017YFE0191000 ), Sanming Project of Medicine in Shenzhen of China ( SZSM201811070 ), and General Research Fund from Hong Kong Research Grants Council ( 12303320 ).
Publisher Copyright:
© 2021 Elsevier B.V.
PY - 2021/7/15
Y1 - 2021/7/15
N2 - Exposure to bisphenol A (BPA) is considered to be associated with the increased incidence of breast cancer. As a widespread replacement of BPA, the effect of bisphenol S (BPS) on breast tumor programming has not been studied. We reported that BPS exposure significantly promoted proliferation and deterioration of breast tumor by nonmonotonic dose response. The mechanisms were investigated by molecular biology and mass spectrometry-based lipidomics, proteomics and imaging. BPS exposure induced the spatially intratumor heterogeneity of morphology-driven lipids and proteins. The more significant proliferation resulted from BPS-10 (10 μg/kg body weight /day) exposure was evidenced by the variations of spatial distribution of lipids related to ceramide-sphingomyelin signaling pathway, proteins related to chromosomal stability and cell proliferation in central necrotic regions of breast tumor. In contrast, the BPS-100 exposure obviously accelerated deterioration of breast tumor by the variations of spatial distribution of proteins that were associated with the stability of nucleic acid structure in peripheral neoplastic regions. Accordingly, dysregulation of metabolism and protein function as well as DNA methylation and hypoxic tumor microenvironment could be applied to predict the possibility of tumorigenesis, proliferation and metastasis that might be caused by other bisphenol analogs.
AB - Exposure to bisphenol A (BPA) is considered to be associated with the increased incidence of breast cancer. As a widespread replacement of BPA, the effect of bisphenol S (BPS) on breast tumor programming has not been studied. We reported that BPS exposure significantly promoted proliferation and deterioration of breast tumor by nonmonotonic dose response. The mechanisms were investigated by molecular biology and mass spectrometry-based lipidomics, proteomics and imaging. BPS exposure induced the spatially intratumor heterogeneity of morphology-driven lipids and proteins. The more significant proliferation resulted from BPS-10 (10 μg/kg body weight /day) exposure was evidenced by the variations of spatial distribution of lipids related to ceramide-sphingomyelin signaling pathway, proteins related to chromosomal stability and cell proliferation in central necrotic regions of breast tumor. In contrast, the BPS-100 exposure obviously accelerated deterioration of breast tumor by the variations of spatial distribution of proteins that were associated with the stability of nucleic acid structure in peripheral neoplastic regions. Accordingly, dysregulation of metabolism and protein function as well as DNA methylation and hypoxic tumor microenvironment could be applied to predict the possibility of tumorigenesis, proliferation and metastasis that might be caused by other bisphenol analogs.
KW - Bisphenol S
KW - Imaging mass spectrometry
KW - In situ imaging of protein and lipid
KW - Tumor proliferation
UR - http://www.scopus.com/inward/record.url?scp=85101611699&partnerID=8YFLogxK
U2 - 10.1016/j.jhazmat.2021.125391
DO - 10.1016/j.jhazmat.2021.125391
M3 - Journal article
C2 - 33652221
AN - SCOPUS:85101611699
SN - 0304-3894
VL - 414
JO - Journal of Hazardous Materials
JF - Journal of Hazardous Materials
M1 - 125391
ER -