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Gene expression profiles of ovarian endometriotic cyst stromal cells treated with tucidinostat

ABSTRACT: We previously demonstrated that the expression of histone deacetylase (HDAC) 10 is elevated in ovarian endometriotic cyst stromal cells (ECSCs) compared to normal endometrial stromal cells (NESCs). HDAC10 inhibitor, tucidinostat (10 μM) inhibited the cell proliferation of ECSCs and induced the apoptosis and G0/G1 cell cycle arrest of these cells. GThe objective of this study to unveil the role of HDAC10 in the pathogenesis of endometriosis. We cultured ECSCs with an HDAC10 inhibitor, tucidinostat (10 μM), isolated the total RNAs, and subjected to next-generation RNA sequencing to identify the target genes of HDAC10. Gene Ontology analysis identified upregulated genes. We will introduce these genes into endometriosis stromal cells and examine whether they induce cell proliferation inhibition and apoptosis promotion similar to HDAC10 inhibitors. This will help us evaluate whether HDAC10 inhibitors are promising candidates for endometriosis treatment. We found that somatostatin receptor 2 (SSTR2), dachshund homolog 11 (DACH1), and interferon regulatory factor 6 (IRF6) are the possible target genes of HDAC10.

ORGANISM(S): Homo sapiens

PROVIDER: GSE309027 | GEO | 2025/12/29

REPOSITORIES: GEO

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Project description:Eutopic endometrium in endometriosis has molecular evidence of resistance to progesterone (P4) and activation of the PKA pathway in the stromal compartment. To investigate global and temporal responses of eutopic endometrium to P4, we compared early (6-h), intermediate (48-h), and late (14-day) transcriptomes, signaling pathways, and networks of human endometrial stromal fibroblasts (hESFs) from women with endometriosis (hESFendo) to hESFs from women without endometriosis (hESFnonendo). Endometrial biopsy samples were obtained from subjects with and without mild peritoneal endometriosis (n = 4 per group), and hESFs were isolated and treated with P4 (1 μM) plus estradiol (E2) (10 nM), E2 alone (10 nM), or vehicle for up to 14 days. Total RNA was subjected to microarray analysis using a Gene 1.0 ST (Affymetrix) platform and analyzed by using bioinformatic algorithms, and data were validated by quantitative real-time PCR and ELISA. Results revealed unique kinetic expression of specific genes and unique pathways, distinct biological and molecular processes, and signaling pathways and networks during the early, intermediate, and late responses to P4 in both hESFnonendo and hESFendo, although a blunted response to P4 was observed in the latter. The normal response of hESF to P4 involves a tightly regulated kinetic cascade involving key components in the P4 receptor and MAPK signaling pathways that results in inhibition of E2-mediated proliferation and eventual differentiation to the decidual phenotype, but this was not established in the hESFendo early response to P4. The abnormal response of this cell type to P4 may contribute to compromised embryonic implantation and infertility in women with endometriosis. We compared early (6-h), intermediate (48-h), and late (14-day) in vitro whole-genome responses of hESF from women with endometriosis (hESFendo) to hESF from women without endometriosis (hESFnonendo) treated with P4 plus E2 (E2P4), E2 alone, or vehicle alone. Using this experimental paradigm, the data demonstrate unique phenotypes, gene expression processes, biochemical and signaling pathways, and networks suggestive of early, intermediate, and late responses of hESFnonendo and hESFendo to P4, giving insights into the complexity of events occurring normally in response to P4 and in the setting of endometriosis.

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Gene expression profiles of ovarian endometriotic cyst stromal cells treated with tucidinostat

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