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N-acetyltransferase 10 drives cisplatin chemoresistance by enhancing ac4C-associated DNA repair in bladder cancer

ABSTRACT: N-acetyltransferase 10 drives cisplatin chemoresistance by enhancing ac4C-associated DNA repair in bladder cancer

PROVIDER: PRJNA824002 | ENA |

REPOSITORIES: ENA

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N-acetyltransferase 10 drives cisplatin chemoresistance by enhancing ac4C-associated DNA repair in bladder cancer

Project description:To explore the molecular mechanism underlying NAT10-mediated cisplatin resistance in bladdder cancer, a genome-wide RNA-sequencing was conducted to compare gene expression profiles of T24 and UM-UC-3 cells with NAT10 knockdown and control. And acRIP-seq was performed to identified the downstream targets of NAT10.

2022-04-07 | GSE200285 | GEO

Proteomic signature of neuroblastoma cells UKF-NB-4 reveals key role of lysosomal sequestration and the proteasome complex in acquiring chemoresistance to cisplatin

Project description:Cisplatin (CDDP) is a widely used agent in the treatment of neuroblastoma. Unfortunately, the development of acquired chemoresistance limits its clinical use. To gain a detailed understanding of the mechanisms underlying the development of such chemoresistance, we comparatively analysed established cisplatin-resistant neuroblastoma cell line (UKF-NB- 4CDDP) and its sensitive counterpart (UKF-NB-4). We confirmed the decreased sensitivity of tested cells to cisplatin and identified a cross-resistance to carboplatin and oxaliplatin. Among the proteins responsible for UKF-NB-4CDDP chemoresistance, ion channels transport family proteins, ABC superfamily proteins, SLC-mediated trans-membrane transporters, proteasome complex subunits and V-ATPases were identified. Moreover, we detected markedly higher proteasome activity in UKF-NB-4CDDP cells and a remarkable lysosomal enrichment that can be inhibited by bafilomycin A to sensitize UKF-NB-4CDDP to CDDP. Our results indicate that lysosomal sequestration and proteasome activity may be one of key mechanisms responsible for intrinsic chemoresistance of neuroblastoma to CDDP.

2019-01-02 | PXD012132 | Pride

transcriptome expression profiling of cisplatin chemoresistance 5-8F cells

Project description:transcriptome expression profiling of cisplatin chemoresistance 5-8F cells

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APIM-peptide targeting PCNA improves cisplatin therapy in a rat muscle-invasive bladder cancer model

Project description:High mortality rate of muscle-invasive bladder cancer (MIBC) and complexity of disease demand new multi-targeting treatment strategies. Targeting proliferating cell nuclear antigen (PCNA) with a peptide containing the AlkB homologue 2 PCNA interacting motif (APIM), is shown to impair multiple vital cellular stress responses and induce hypersensitivity against several chemotherapeutics in different pre-clinical models. This study examine the anti-cancer efficacy of the novel APIM-peptide drug when combined with cisplatin-based therapies (cisplatin, cisplatin/gemcitabine (GC) and methotrexate/vinblastine/adriamycin/cisplatin (MVAC)) in a panel of bladder cancer (BC) cells and with intravenous cisplatin-therapy in a rat MIBC-model. Furthermore, we explore the molecular mechanisms underlying the observed effects on a genomic, proteomic and metabolomic level using microarray, multiplexed inhibitor bead (MIB)-assay, and targeted mass spectrometric metabolite profiling. The APIM-peptide significantly increased the efficacy of all cisplatin-based therapies in all BC cell lines tested, including a cisplatin resistant cell line and reduced the tumor load in cisplatin treated MIBC-bearing rats. Genome and proteome analysis of APIM-peptide/cisplatin treated BC cells revealed reduced expression of multiple proteins frequently overexpressed in MIBC. Of notice, the EGFR/ERBB2, PI3K/Akt and MAPK signaling pathways and anti-apoptosis were downregulated. We suggest that the anti-cancer effect of the APIM-peptide is through the downregulation of several known oncogenic signaling pathways including anti-apoptosis. Together our results indicate that the APIM-peptide represents a potential improved treatment approach for patients with MIBC.

2018-09-10 | PXD008724 | Pride

Characterization of the difference of mRNA and lncRNA profiling between cisplatin-resistance and regular T24 bladder cancer cells

Project description:To investigate the difference of mRNA and lncRNA profiling between cisplatin-resistance and regular T24 bladder cancer cells, T24 cells were treated with a gradual increment (4, 8, 16, 32, 64 ug/ml cisplatin) with a discontinuous period until cells recover. 10^6 cells T24R and T24 cells were harvested for RNA-seq.

2019-11-11 | E-MTAB-7437 | biostudies-arrayexpress

Activation of cGAS-STING signal to inhibit the proliferation of bladder cancer: the immune effect of cisplatin

Project description:our findings indicated a cisplatin dependent cGAS-STING signal in bladder cancer. This signal could be enhanced by accumulation of dsDNA and chromatin dissociated cGAS and would finally recruit infiltration DCs and CD8+ T cells in bladder cancer bladder cancer tumor microenvironment. However, the specific role and effect of this signal towards bladder cancer tumor microenvironment need to be further clarified.

2021-03-31 | GSE165767 | GEO

Reprogrammed Lipid Metabolism in Bladder Cancer with Cisplatin Resistance

Project description:This study conducted comprehensive and comparative lipidomic profiling of two isogenic human T24 bladder cell lines, which are characterized as sensitive or resistant to the cisplatin-induced cell apoptosis.

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CircIPO7 Promotes Nasopharyngeal Carcinoma Metastasis and Cisplatin Chemoresistance by Regulating YBX1 Nuclear Localization

Project description:The development of therapeutic resistance and metastatic dissemination takes place in 20-30% patients with nasopharyngeal carcinoma (NPC), resulting in poor survival. Hence, a better understanding of the underlying molecular mechanisms will help improve clinical outcome. We have identified a novel circRNA, circIPO7, as a promoter of metastasis and cisplatin chemoresistance in NPC cells. Expression profiling and Genome binding/occupancy profiling by high throughput sequencing were performed to explore the underlying molecular mechanisms.

2022-07-26 | GSE189459 | GEO

Acquired semi-squamalization during chemotherapy suggests a differentiation therapy for bladder cancer

Project description:Cisplatin-based chemotherapy is the most common treatment for unresectable bladder cancers and also increasingly used as neoadjuvant treatments before or after surgery and radiotherapy. Unfortunately, though many patients respond to the treatment, most of them develop resistance quickly with unclear mechanisms and few further treatment options. Here, we report that semi-squamazation is acquired during chemo treatment in both mice and human. Multi-omics analyses show that cathepsin H (CTSH), a direct target of p63, is associated with chemoresistance and semi-squamation. Treatment with the cathepsin inhibitor E64 specifically restrains chemoresistant but not chemosensitive cancer. Mechanistically, cathepsin inhibition induces fully squamous differentiation of bladder cancer cells, which requires TNF receptor 1alpha and is associated with pyroptosis. Our study suggests that semi-squamazation would be a diagnosistic marker for chemoresistance and differentiation therapy by targeting CTSH might be a potential treatment for chemoresistant bladder cancer.

2022-07-09 | GSE192575 | GEO

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