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Estrogen Receptor Alpha Signaling in Cervical Cancer Associated Fibroblasts

ABSTRACT: Cancer Associated Fibroblasts (CAFs) are crucial in the genesis and progression of tumors. Cervical CAFs (C-CAFs) are less well characterized. Estrogen (E2) is considered a cofactor in cervical carcinogenesis. We studied the molecular signature of exvivo cultured C-CAFs from 4 early International Federation of Gynaecology and Obstetrics (FIGO, IB2) and 2 late (IIIA) stage disease using gene expression microarray. We found C-CAFs to be both pro-tumorigenic and moderately inflammatory; late stage C-CAFs were more actively metabolizing, and cycling, but expressed fewer genes related to immune function. We investigated the expression of ERα in exvivo cultured C-CAFs and studied the role of E2 in their biology by gene expression microarray in the presence of two ERα antagonists: ICI 182,780 and Methyl Piperidino Pyrazole (MPP). Both modulated C-CAF function by down regulating genes associated with cell cycle and metabolism, affecting angiogenesis and cancer progression, though their transcriptomes differed. MPP also down regulated genes involved in Epithelial to Mesenchymal Transition. Thus, canonical ERα signaling is vital for C-CAF functioning. Interfering with paracrine signaling through fibroblast ERα may be worth exploiting as a targeted therapy in cervical cancer.

ORGANISM(S): Homo sapiens

PROVIDER: GSE65227 | GEO | 2015/04/03

SECONDARY ACCESSION(S): PRJNA273453

REPOSITORIES: GEO

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Estrogen Receptor Alpha Signaling in Cervical Cancer Associated Fibroblasts

Project description:Cancer Associated Fibroblasts (CAFs) are crucial in the genesis and progression of tumors. Cervical CAFs (C-CAFs) are less well characterized. Estrogen (E2) is considered a cofactor in cervical carcinogenesis. We studied the molecular signature of exvivo cultured C-CAFs from 4 early International Federation of Gynaecology and Obstetrics (FIGO, IB2) and 2 late (IIIA) stage disease using gene expression microarray. We found C-CAFs to be both pro-tumorigenic and moderately inflammatory; late stage C-CAFs were more actively metabolizing, and cycling, but expressed fewer genes related to immune function. We investigated the expression of ERα in exvivo cultured C-CAFs and studied the role of E2 in their biology by gene expression microarray in the presence of two ERα antagonists: ICI 182,780 and Methyl Piperidino Pyrazole (MPP). Both modulated C-CAF function by down regulating genes associated with cell cycle and metabolism, affecting angiogenesis and cancer progression, though their transcriptomes differed. MPP also down regulated genes involved in Epithelial to Mesenchymal Transition. Thus, canonical ERα signaling is vital for C-CAF functioning. Interfering with paracrine signaling through fibroblast ERα may be worth exploiting as a targeted therapy in cervical cancer. Gene expression microarray profiling of 4 early-stage E2 (estrogen) treated, 2 late-stage E2 treated, 2 early-stage ICI (ER-alpha antagonist) treated, 2 late-stage ICI treated and 2 early-stage MPP (ER-alpha antagonist) treated cervical cancer CAFs. E2 treated C-CAFs served as control.

2015-04-03 | E-GEOD-65227 | biostudies-arrayexpress

Comprehensive Analysis of a Competing Endogenous RNA Network Identifies Five-lncRNA Nomogram as a Prognostic Model for Cervical Cancer

Project description:LncRNAs have been found to regulate mRNA expression levels and serve an important role in cervix carcinogenesis. To explore the lncRNA expression profiles during the development and progression of cervical cancer, we performed microarray analysis with total RNA in with only Human papillomavirus (HPV) 16-positive, 7 stage IA-IIA SCC (following the International Federation of Gynecology and Obstetrics (FIGO) criteria (10)) and 7 matched normal controls (NC).

2022-11-22 | GSE218460 | GEO

The exponential slope from absolute lymphocyte counts during radiochemotherapy can predict an aggressive course of cervical cancer.

Project description:We sequenced plasma exosomal RNA obtained from 24 blood samples from 12 cervical cancer patients treated with concurrent chemoradiotherapy (CCRT) followed by intracavitary brachytherapy. The patients with 2018 International Federation of Gynecology and Obstetrics [FIGO] stage IB-3C2 at diagnosis were included. The 12 cervical cancer patients had two blood samples for each patient drawn before and after CCRT. Next generation sequencing data from plasma exosome included small RNAs, long non-coding RNAs, and mRNAs, of which miRNAs and mRNAs were used for analysis. The log2 fold change values were calculated between the two samples from each patient to detect mRNAs as predictors of slope of function estimated from ALCs and survival. We selected several potential exosomal mRNAs associated with clinical results.

2023-08-13 | E-MTAB-12187 | biostudies-arrayexpress

Transcriptomic analysis of CAFs with silencing of ANKRD1.

Project description:Stromal cell senescence plays a crucial role in activating cancer-associated fibroblasts (CAFs). The Androgen receptor (AR) function oversees cellular senescence and CAF activation. Here, we identify the mesenchymal-specific transcriptional coregulator ANKRD1 as a key driver of CAF conversion. ANKRD1 is strongly upregulated in CAFs and under direct negative control of AR, and its loss impairs the pro-tumorigenic potential of CAFs. ANKRD1 controls a CAF-specific gene expression program and is associated with poorer survival of HNSCC, lung, and cervical SCC patients. Mechanistically, ANKRD1 binds to the chromatin on CAF gene regulatory regions in a complex with the AP1 transcription factor family. We show that ANKRD1 enhances the AP1 DNA binding activity to CAF gene promoters. Targeting ANKRD1 with the FANA antisense oligonucleotides reverts CAFs into a normal fibroblast, disrupts AP1 complex formation, and blocks CAF’s pro-tumorigenic potential in an orthotopic model of SCC, thus representing an exciting target for stroma-oriented cancer therapy.

2023-11-10 | GSE218214 | GEO

ChIP-seq analysis of primary human dermal fibroblasts overexpressing ANKRD1 in human dermal fibroblasts (HDFs)

2023-11-10 | GSE218204 | GEO

Transcriptomic analysis of human dermal fibroblasts overexpressing ANKRD1.

2023-11-10 | GSE218198 | GEO

RNA seq from plasma exosome before and after chemoradiotherapy for cervical cancer patients

Project description:We sequenced plasma exosomal RNA obtained from 58 blood samples from 29 cervical cancer patients treated with concurrent chemoradiotherapy (CCRT) followed by intracavitary brachytherapy. The patients with 2018 International Federation of Gynecology and Obstetrics [FIGO] stage IB-IVB at diagnosis were included. The 29 cervical cancer patients had two blood samples for each patient drawn before and after CCRT. Next generation sequencing data from plasma exosome included small RNAs, long non-coding RNAs, and mRNAs, of which miRNAs and mRNAs were used for analysis. The log2 fold change values were calculated between the two samples from each patient to detect miRNAs as predictors of early progression and metastasis. We analysed their biological functions through miRNA-mRNA network analysis after selecting several potential exosomal miRNAs associated with clinical results.

2021-05-23 | E-MTAB-10215 | biostudies-arrayexpress

Estrogen receptor α-mediated signaling inhibits type I interferon response to promote breast cancer

Project description:To investigate the molecular mechanisms by which estrogen receptor α (ERα) inhibits type I IFN-induced signaling. We identified genes induced by ERα signaling using data obtained from RNA-seq of MCF7 cells treated or untreated with selective ERα agonist propyl pyrazole triol (PPT).

2022-05-18 | GSE203058 | GEO

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

2019-10-05 | GSE137558 | GEO

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