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Genome-wide characterization of platinum persister ovarian cancer (OC) cells with upregulation of Wnt pathway receptor, Frizzled 7 (FZD7)

ABSTRACT: The goal of this study is to define molecular signature of platinum persister OC cells characterized by FZD7, and investigate the functional role of FZD7 relative to stemness and chemo-responsiveness.

ORGANISM(S): Homo sapiens

PROVIDER: GSE148003 | GEO | 2020/10/22

REPOSITORIES: GEO

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Genome-wide characterization of platinum persister ovarian cancer (OC) cells with upregulation of Wnt pathway receptor, Frizzled 7 (FZD7)

Project description:Genome-wide characterization of platinum persister ovarian cancer (OC) cells with upregulation of Wnt pathway receptor, Frizzled 7 (FZD7)

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RNA-Seq of treatment response of platinum sensitive and platinum resistant ovarian cancer cells

Project description:Resistance to platinum-based chemotherapy is a clinical challenge in the treatment of ovarian cancer (OC) and limits survival. Therefore, innovative drugs against platinum-resistance are urgently needed. Our therapeutic concept is based on the conjugation of two chemotherapeutic compounds to a monotherapeutic pro-drug, which is taken up by cancer cells and cleaved into active cytostatic metabolites. Here, we explore the activity of the duplex-prodrug 5-FdU-ECyd, covalently linking 2'-deoxy-5-fluorouridine (5-FdU) and 3'-C-ethynylcytidine (ECyd), on platinum-resistant OC cells. RNA-Sequencing was used for characterization of 5-FdU-ECyd treated platinum-sensitive A2780 and isogenic platinum-resistant A2780cis.

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Molecular analysis of platinum-resistant and -sensitive ovarian cacner based on RNA-Seq analysis

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Differential and divergent activity of Insulin-like Growth Factor Binding Protein 6 (IGFBP6) in platinum-sensitive versus platinum-resistant high-grade serous ovarian carcinoma cell lines.

Project description:IGFBP6 is a secreted protein with a controversial role in human malignancies, being downregulated in the majority of human cancers, but upregulated in selected tumors. Ovarian carcinoma (OC) is a human malignancy characterized by IGFBP6 downregulation, even though the significance of its low expression during ovarian carcinogenesis is still poorly understood. IGFBP6 expression levels and the activation of its signaling pathway were evaluated in two matched OC cell lines derived from a high-grade serous ovarian cancer before and after platinum resistance (PEA1 and PEA2 cells,respectively). A whole genome gene expression analysis was comparatively performed in both cell lines upon IGFBP6 stimulation by Illumina technology. IGFBP6 gene expression in human OCs data were obtained from public datasets. Gene expression data from public datasets confirmed the downregulation of IGFBP6 from normal ovarian tissues to primary and metastatic OCs. The comparative analysis of platinum-sensitive (PEA1) and platinum-resistant (PEA2) cell lines showed quantitative and qualitative differences in the activation of IGFBP6 signaling. Indeed, IGFBP6 enhanced ERK1/2 phosphorylation only in PEA1 cells and induced a more evident and significant gene expression reprogramming in PEA1 compared to PEA2 cells. Furthermore, the analysis of selected genes modulated by IGFBP6 (i.e., FOS, JUN, TNF, IL6, IL8, and EGR1) showed an inverse regulation in PEA1 versus PEA2 cells, as well as selected hallmarks and IL-6 signaling were ositively regulated in PEA1, while inhibited in PEA2 cells.These data suggest that loss of IGFBP6 signaling may play a role in ovarian cancer progression, being likely associated to the development of platinum resistance.

2022-03-23 | GSE189717 | GEO

Expression data from human OC+BAP+ double positive versus OC-BAP- double negative cells

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Gene expression analysis of Mycobacterium tuberculosis high-persister (hip) mutants.

Project description:Bacterial persister cells are phenotypic variants of regular cells that are tolerant to antibiotics. High-persister (hip) mutants of Mycobacterium tuberculosis produce 10- to 1,000-fold more persister cells than the wild type strain when challenged with various antibiotics. Comparison of gene expression pattern of the hip mutants may provide clues as to the genetic mechanisms underlying persister formation. Transcriptome analysis will provide information on what differentiates M. tuberculosis hip strains from regular strains, which will be useful in the development of anti-persister therapy for persister cell eradication. Twelve independent M. tuberculosis hip mutants and the wild type strain were grown to stationary phase in duplicate. To avoid analyzing the drug effect, total RNA was extracted from the cultures prior to the addition of antibiotic for hybridization to Affymetrix microarrays. Data analysis was performed by comparing the hip mutants to the wild type control.

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Expression data from human OC+BAP+ double positive versus OC-BAP- double negative cells

2013-05-17 | E-GEOD-47060 | biostudies-arrayexpress

Resistance of Ovarian Cancer Cells to Platinum Requires Exogenous Cholesterol, Scavenger Receptor Class B Type 1, and Glutathione Peroxidase 4

Project description:Essentially, all patients diagnosed with ovarian cancer (OC) are treated with platinum (Pt); however, Pt resistance (Pt-R) rapidly develops. We show OC cells resistant to Pt increase intracellular cholesterol by increasing expression of the high-density lipoprotein (HDL) receptor, scavenger receptor class B type 1 (SR-B1). Expression of SR-B1 was associated with chemoresistance in OC cells and tumors. SR-B1 blockade using synthetic cholesterol-poor HDL-like nanoparticles (HDL NPs) diminished cholesterol uptake leading to cell death of Pt-R OC cells in vitro and suppressed Pt-R OC tumor growth in vivo. Reduced cholesterol accumulation in Pt-R OC cells induced lipid oxidative stress through reduction of glutathione peroxidase 4 (GPx4) expression leading to ferroptosis. Reduction of GPx4 expression in OC cells re-sensitized Pt-R cells to Pt by reducing cholesterol uptake and enhancing the accumulation of lipid reactive oxygen species (L-ROS). Mechanistically, GPx4 knockdown in OC cells was associated with reduced expression of the histone acetyltransferase EP300, leading to reduced H3K27 acetylation around the SREBP2 promoter suppressing its expression. As SREBP2 regulates SR-B1 transcription, these data demonstrate chemoresistance and cancer cell survival under high ROS burden obligates high GPx4 and SR-B1 expression through SREBP2. Targeting SR-B1 to modulate cholesterol uptake inhibits this axis and causes ferroptosis in vitro and in vivo in Pt-R OC.

2024-06-01 | GSE234404 | GEO

EIF6 conditions drug-tolerant persister-like transdifferentiation in small cell lung carcinoma (eIF6_KD)

Project description:Drug-tolerant persister cells withstand treatments by adapting their identity through lineage-dependent plasticity during systemic anti-cancer therapies. This phenomenon is evident in small-cell lung carcinoma (SCLC), a lethal neuroendocrine cancer initially responsive (60-80%) to platinum-based chemotherapy but succumbing to resistance within 6 months in advanced stages. This resistance associates with the transdifferentiation of residual tumour cells into a non-neuroendocrine state, a process intricately tied to SCLC's chemotolerance, yet molecular mechanisms governing this lineage conversion remain completed understood. Here we use paired cytoplasmic RNA-seq and polysomal RNA-seq to compare gene expression between NE and non-NE SCLC cell lines on both transcriptional and translational level. We report that first-line chemotherapy induces translation initiation factor eIF6 in drug-tolerant persister-like cells in SCLC, correlating with the non-neuroendocrine state in SCLC. Intervening eIF6 inhibits non-neuroendocrine transdifferentiation, thus enhancing SCLC responsiveness to chemotherapy. This study sheds light on eIF6's potential therapeutic interventions to mitigate treatment resistance in SCLC.

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