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Heat Shock Factor 1 (HSF1) acquires transcriptional competence under 17b-estradiol in ERa-positive breast cancer cells [ChIP-seq]

ABSTRACT: Heat Shock Transcription Factor 1 (HSF1) is a well-known regulator of gene expression during acute environmental stress that enables the cells to survive. Its high level in estrogen receptor-positive breast cancer patients correlated with a worse prognosis. Here, we demonstrated that 17β-estradiol (E2) as well as bisphenol A (BPA) and propyl pyrazole triol (PPT, ERα agonist) led to HSF1 phosphorylation on S326 in ERα positive mammary breast cancer cells, but not in ERα-negative ones. We showed that ERK1/2 signaling was involved in this process and down-regulation of ERα expression abrogated it. E2activated HSF1 was transcriptionally potent. Chip-Seq and RNA-Seq analyses revealed that it could modulate the expression of several genes known to be essential for breast cancer cells growth and/or ERα action, i.e. HSPB8, LHX4, PRKCE, WWC1, and GREB1. Our findings indicate that a positive feedback loop between ERα and HSF1 signaling may exist which support the growth of estrogen-dependent tumors.

ORGANISM(S): Homo sapiens

PROVIDER: GSE137558 | GEO | 2019/10/05

REPOSITORIES: GEO

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Heat Shock Factor 1 (HSF1) acquires transcriptional competence under 17b-estradiol in ERa-positive breast cancer cells [RNA-seq]

Project description:Heat Shock Transcription Factor 1 (HSF1) is a well-known regulator of gene expression during acute environmental stress that enables the cells to survive. Its high level in estrogen receptor-positive breast cancer patients correlated with a worse prognosis. Here, we demonstrated that 17β-estradiol (E2) as well as bisphenol A (BPA) and propyl pyrazole triol (PPT, ERα agonist) led to HSF1 phosphorylation on S326 in ERα positive mammary breast cancer cells, but not in ERα-negative ones. We showed that ERK1/2 signaling was involved in this process and down-regulation of ERα expression abrogated it. E2activated HSF1 was transcriptionally potent. Chip-Seq and RNA-Seq analyses revealed that it could modulate the expression of several genes known to be essential for breast cancer cells growth and/or ERα action, i.e. HSPB8, LHX4, PRKCE, WWC1, and GREB1. Our findings indicate that a positive feedback loop between ERα and HSF1 signaling may exist which support the growth of estrogen-dependent tumors.

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