TMT-based quantitative proteomic analysis of spheroid cells of endometrial cancer possessing cancer stem cell properties
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE222599 | GEO | 2023/01/14
REPOSITORIES: GEO
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Project description:TMT-based quantitative proteomic analysis of spheroid cells of endometrial cancer possessing cancer stem cell properties
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Project description:The goal of this study is to compare transcriptome profiling of SF3B1 depleted Ishikawa endometrial cancer cells by RNA-sequencing Methods: SF3B1 depleted mRNA profiles of control siRNA treated and SF3B1 siRNA treated Ishikawa endometrial cancer cells were generated by deep sequencing, in triplicate using Illumina HiSeq 3000 sequencers with 2×150 paired-end reads. Basecalls and demultiplexing were performed with Illumina’s RTA version 1.9 and bcl2fastq2 software with a maximum of one mismatch in the indexing read. RNA-seq reads were then aligned to the Ensembl release 76 primary assembly with STAR version 2.0.4b. qRT–PCR validation was performed using TaqMan assays Results: Using a 2.5-fold cutoff and Benjamini-Hochberg false discovery rate (FDR) of <0.01 threshold for inclusion, we identified 1,992 differentially expressed genes (DEGs) between Control and SF3B1 depleted Ishikawa cells Conclusions: Our study represents the first detailed analysis of SF3B1 depleted Ishikawa endometrial cancer cells transcriptomes, with biologic replicates, generated by RNA-seq technology.
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Project description:To investigate the role of ARID1A in estrogen receptor positive endometrial cancers, we performed RNAseq in control and ARID1A-knockdown Ishikawa cells treated with DMSO,E2 and E2+Fulvestrant for 8 hours.
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Project description:Every year more than 42,000 women die of endometrial cancer, mainly due to recurrent or metastatic disease. The presence of tumor infiltrating lymphocytes (TILs) as well as progesterone receptor (PR) positivity has been correlated with improved prognosis. This study describes two mechanisms by which progesterone inhibits metastatic spread of endometrial cancer: by stimulating T-cell infiltration and by inhibiting epithelial-to-mesenchymal cell transition (EMT). Paraffin sections from patients with (n=9) or without (n=10) progressive endometrial cancer (recurrent or metastatic disease) were assessed for the presence of CD4+ (helper), CD8+ (cytotoxic) and Foxp3+ (regulatory) T-lymphocytes and PR expression. Progressive disease was observed to be associated with significant loss of TILs and loss of PR expression. Frozen tumor samples, used for genome-wide expression analysis, showed significant regulation of pathways involved in immunosurveillance, EMT and metastasis. For a number of genes, such as CXCL14, DKK1, DKK4 and WIF1, quantitive RT-PCR was performed to verify down regulation in progressive disease. To corroborate the role of progesterone in regulating invasion, Ishikawa (IK) endometrial cancer cell lines stably transfected with PRA (IKPRA), PRB (IKPRB) and PRA+PRB (IKPRAB) were cultured in the presence/absence of progesterone (MPA) and used for genome-wide expression analysis, Boyden- and wound healing migration assays, and IHC for known EMT makers. IKPRB and IKPRAB cell lines showed MPA induced inhibition of migration and loss of the mesenchymal marker vimentin at the invasive front of the wound healing assay. Furthermore, pathway analysis of significantly MPA-regulated genes showed significant down regulation of important pathways involved in EMT, immunesuppression and metastasis: such as IL6-, TGF-β and Wnt/β-catenin signalling. Intact progesterone signaling in non-progressive endometrial cancer seems to be an important factor stimulating immunosurveillance and inhibiting transition from an epithelial to a more mesenchymal, more invasive phenotype. The PRA- and PRB-expressing Ishikawa endometrial cancer cell line (IKPRAB36) was cultured for 48h in the absence or presence of 1nM MPA (n = 3). The RNA was isolated and used for hybridization on Affymetrix microarrays. Cells cultured in the presence of MPA were compared with cells cultured in the absence of MPA.
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Project description:Microarrays were used to analyze differential gene expression and to help determine the efficacy of Iressa (gefitinib), a tyrosine kinase inhibitor, on endometrial cancer cells. Type I Ishikawa H and type II Hec50co endometrial carcinoma cells both express EGFR and sEGFR, but differ markedly in their responsiveness to the EGFR inhibitor gefitinib. This difference is paralleled by differences in the expression of sEGFR and EGFR, as well as in their transcriptional response following treatment with either EGFor gefitinib. The small cluster of differently regulated genes reported here in these type I vs. type II endometrial cancer-derived cell lines may identify candidate biomarkers useful for predicting sensitivity to EGFR blockade. Type I (Ishikawa H cells) and type II (Hec50co) derived endometrial carcinomas, were dosed with either EGF(epidermal growth factor) or Iressa (gefitinib) for 12 or 24 hours and gene expression was examined.
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Project description:Most endometrial cancers are driven by excess estrogen signaling and express the hormone receptor estrogen receptor alpha (ER). Evaluation of the estrogen response in endometrial cancer cells has been limited by the availability of hormonally responsive in vitro models, with one cell line, Ishikawa, being used in most studies. Here, we describe a novel, adherent endometrioid endometrial cancer (EEC) cell line model, HCI-EC-23. We show that HCI-EC-23 retains ER expression and that ER functionally responds to 17b-estradiol (E2) induction over a range of passages. We also demonstrate that this cell line retains paradoxical activation of ER by tamoxifen, which is also observed in Ishikawa and is consistent with clinical data. The mutational landscape shows that HCI-EC-23 is mutated at many of the commonly altered genes in EEC, has relatively few copy-number alterations, and is microsatellite instable high (MSI-high). In vitro proliferation of HCI-EC-23 is modestly enhanced by E2 but is strongly reduced upon combination E2 and progesterone (P4) treatment. HCI-EC-23 exhibit strong E2 dependence for tumor growth in vivo and tumor size is reduced by combination E2 + P4 treatment. Molecular characterization of E2 induction in HCI-EC-23 revealed hundreds of estrogen-responsive genes that significantly overlapped with those regulated in Ishikawa. Analysis of ER genome binding identified similar patterns in HCI-EC-23 and Ishikawa, although ER exhibited more bound sites in Ishikawa. This study demonstrates that HCI-EC-23 is estrogen-responsive and can be used to study the hormonal aspects of endometrial cancer.
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Project description:Most endometrial cancers are driven by excess estrogen signaling and express the hormone receptor estrogen receptor alpha (ER). Evaluation of the estrogen response in endometrial cancer cells has been limited by the availability of hormonally responsive in vitro models, with one cell line, Ishikawa, being used in most studies. Here, we describe a novel, adherent endometrioid endometrial cancer (EEC) cell line model, HCI-EC-23. We show that HCI-EC-23 retains ER expression and that ER functionally responds to 17b-estradiol (E2) induction over a range of passages. We also demonstrate that this cell line retains paradoxical activation of ER by tamoxifen, which is also observed in Ishikawa and is consistent with clinical data. The mutational landscape shows that HCI-EC-23 is mutated at many of the commonly altered genes in EEC, has relatively few copy-number alterations, and is microsatellite instable high (MSI-high). In vitro proliferation of HCI-EC-23 is modestly enhanced by E2 but is strongly reduced upon combination E2 and progesterone (P4) treatment. HCI-EC-23 exhibit strong E2 dependence for tumor growth in vivo and tumor size is reduced by combination E2 + P4 treatment. Molecular characterization of E2 induction in HCI-EC-23 revealed hundreds of estrogen-responsive genes that significantly overlapped with those regulated in Ishikawa. Analysis of ER genome binding identified similar patterns in HCI-EC-23 and Ishikawa, although ER exhibited more bound sites in Ishikawa. This study demonstrates that HCI-EC-23 is estrogen-responsive and can be used to study the hormonal aspects of endometrial cancer.
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