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• W4309316918 endingPage "e202201499" @default.
• W4309316918 startingPage "e202201499" @default.
• W4309316918 abstract "The role of the alternate G protein–coupled estrogen receptor 1 (GPER1) in colorectal cancer (CRC) development and progression is unclear, not least because of conflicting clinical and experimental evidence for pro- and anti-tumorigenic activities. Here, we show that low concentrations of the estrogenic GPER1 ligands, 17β-estradiol, bisphenol A, and diethylstilbestrol cause the generation of lagging chromosomes in normal colon and CRC cell lines, which manifest in whole chromosomal instability and aneuploidy. Mechanistically, (xeno)estrogens triggered centrosome amplification by inducing centriole overduplication that leads to transient multipolar mitotic spindles, chromosome alignment defects, and mitotic laggards. Remarkably, we could demonstrate a significant role of estrogen-activated GPER1 in centrosome amplification and increased karyotype variability. Indeed, both gene-specific knockdown and inhibition of GPER1 effectively restored normal centrosome numbers and karyotype stability in cells exposed to 17β-estradiol, bisphenol A, or diethylstilbestrol. Thus, our results reveal a novel link between estrogen-activated GPER1 and the induction of key CRC-prone lesions, supporting a pivotal role of the alternate estrogen receptor in colon neoplastic transformation and tumor progression." @default.
• W4309316918 created "2022-11-26" @default.
• W4309316918 creator A5001510553 @default.
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• W4309316918 creator A5031887894 @default.
• W4309316918 creator A5038895890 @default.
• W4309316918 creator A5049673246 @default.
• W4309316918 date "2022-11-16" @default.
• W4309316918 modified "2023-10-10" @default.
• W4309316918 title "GPER1 links estrogens to centrosome amplification and chromosomal instability in human colon cells" @default.
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