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Antagonizing miR-128 abrogates chemoresistance-associated metastasis and is therapeutic in non-small cell lung cancer [miRNA]

ABSTRACT: This experiment is designed to screen miRNAs that are deregulated during chemoresistance-associated metastasis of lung cancer cells. Chemoresistant metastatic in vivo tumor model of A549-luc-Vector cells was established after four rounds of cisplatin (CDDP) treatments compared to corresponding control solvent treatments. Upon examining profiles of miRNA expression differential between tumor-derived cultured cells from the Ctrl-4th and CDDP-4th treatments, most markedly upregulated and downregulated miRNAs in chemoresistant, metastatic A549-luc-CDDP-4th cells were identified. In order to establish a chemoresistant in vivo tumor model, after inoculation of A549-luc-Vector cells, cisplatin (CDDP) or control solvent was intraperitoneally (i.p.) injected six rounds in a two-week period and cells were isolated from corresponding resultant tumors, cultured and re-transplanted into syngeneic mice to receive the next round of treatment. In our experimental model, human lung cancer xenografts developed chemoresistance in the third round of CDDP treatment (CDDP-3rd) and chemoresistance-associated metastases following the fourth round of treatment. Tumor-derived cultured cells from Ctrl-4th and CDDP (cisplatin)-4th treatment were subjected to miRNA array (Agilent-031181 human miRNA (8*60k) V16.0) analysis, with two biological replications for each treatment.

ORGANISM(S): Homo sapiens

SUBMITTER: junchao Cai

PROVIDER: E-GEOD-67727 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Similar Datasets

Antagonizing miR-128 abrogates chemoresistance-associated metastasis and is therapeutic in non-small cell lung cancer [miRNA]

Project description:This experiment is designed to screen miRNAs that are deregulated during chemoresistance-associated metastasis of lung cancer cells. Chemoresistant metastatic in vivo tumor model of A549-luc-Vector cells was established after four rounds of cisplatin (CDDP) treatments compared to corresponding control solvent treatments. Upon examining profiles of miRNA expression differential between tumor-derived cultured cells from the Ctrl-4th and CDDP-4th treatments, most markedly upregulated and downregulated miRNAs in chemoresistant, metastatic A549-luc-CDDP-4th cells were identified.

2015-04-10 | GSE67727 | GEO

Antagonizing miR-128 abrogates chemoresistance-associated metastasis and is therapeutic in non-small cell lung cancer

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-04-10 | E-GEOD-67729 | biostudies-arrayexpress

microRNA expression profiling of xenografted tumors derived from human esophageal squamous cell carcinoma model treated with cisplatin

Project description:The plasticity of cancer stem cells (CSCs)/tumor-initiating cells (T-ICs) indicates that multiple CSC/T-IC subpopulations exist within a tumor and multiple oncogenic pathways collaborate to maintain the CSC/T-IC state. Here, we aimed to enrich for T-ICs from clinical ESCC tissues. A chemoresistant human esophageal squamous cell carcinoma (ESCC) patient-derived xenograft model was employed to identify miRNA(s) that contribute to ESCC aggressiveness. We used microarrays to demenstrate the microRNA expression underlying different pretreated conditions. NOG mice bearing subcutaneous tumor xenografts derived from clinical ESCC cells were intraperitoneally treated with CDDP or PBS twice weekly for three weeks. Tumor cells were then isolated and re-inoculated subcutaneously into NOG mice for the next round of treatment. In the 4th round of treatment, the volume of tumors in both CDDP- and PBS-treated groups were approximately the same, suggesting that the cells in CDDP-treated tumors were becoming resistant to CDDP. microRNA expression was measured by RNA extraction from cisplatin-treated tumors (EC-CR) or PBS-treated tumors(EC-UT) after 4 round of treatment,two microarrays were performed for each sample.

2016-06-16 | E-GEOD-83362 | biostudies-arrayexpress

Proteome dynamics during cisplatin exposure in sensitive and resistant human lung cancer cells

Project description:Lung cancer is the leading cause of cancer-related deaths and its treatment is based in chemotherapy using platinum containing compounds, mainly cisplatin (CDDP). Many patients show resistance to CDDP leading to treatment failure. To understand the mechanisms involved in CDDP resistance in lung cancer, we used CDDP-sensitive (A549) and –resistant (A549/CDDP) cells to identify newly synthesized proteins in response to CDDP treatment using BONCAT technique. In addition the steady-state proteome of A549 and A549/CDDP cells was also evaluated. It was identified 70 and 69 proteins upregulated by CDDP in A549 and A549/CDDP cells, respectively. The set of proteins upregulated by CDDP in both cells are associated to GO terms related to proteostasis, telomere maintenance cell, RNA processing, cytoskeleton and response to oxidative stress. Interestingly, the profile of biological processes enriched in A549 cells after CDDP treatment is very similar to those identified in the steady-state proteome of A549/CDDP cells, suggesting their positive selection in CDDP-resistant cells development. Therefore, this study of proteomic response to CDDP is relevant to the identification of potential protein targets to development of therapeutic strategies to block drug resistance pathways.

2023-03-10 | PXD021779 | Pride

Noncoding RNA expression profiling of cisplatin-resistant cells derived from the A549 lung cell line (lncRNA and mRNA)

Project description:To determine the signaling networks that are dysregulated in cisplatin-resistant non-small cell lung cancer, noncoding RNA expression data were obtained from, and compared between, the lung adenocarcinoma cell line, A549, and its cisplatin-resistant derivative, A549/CDDP. Noncoding RNA expression data from a cisplatin-sensitive lung adenocarcinoma cancer cell line (A549) were collected and compared to noncoding RNA expression data from a cisplatin-resistant cell line (A549/CDDP). 3 independent experiments were completed for both the sensitive and resistant cell lines.

2013-01-15 | E-GEOD-43493 | biostudies-arrayexpress

Noncoding RNA expression profiling of cisplatin-resistant cells derived from the A549 lung cell line (miRNA)

2013-01-15 | E-GEOD-43249 | biostudies-arrayexpress

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

IGR_Michels_PARP

Project description:Non-small cell lung cancer (NSCLC) is often treated with cisplatin (CDDP). Here, we report that two distinct poly(ADP-ribose) polymerase (PARP) inhibitors exhibited a hyperadditive combination effect with CDDP to kill NSCLC cells. A majority of CDDP-resistant cell lines and clones exhibited constitutively increased PARP expression and enzymatic activity. Cells with hyperactivated PARP initiated a DNA damage response and the intrinsic pathway of apoptosis in response to pharmacological PARP inhibition or PARP1-targeting siRNAs. Transcriptome analysis depicted an unsupervised hierarchical clustering of NSCLC cells and CDDP resistant counterparts regarding to their response to PARP inhibitors. PARP-overexpressing tumors displayed elevated levels of intracellular poly(ADP-ribose) (PAR), which predicted the response to PARP inhibitors in vitro and in vivo more accurately than PARP expression itself. Thus, CDDP-resistant cancer cells develop a dependency to PARP, becoming susceptible to PARP inhibitor-induced apoptosis.

2013-10-31 | E-MTAB-1353 | biostudies-arrayexpress

CDDP treatment of U2OS cells with NCOR and SMRT knock-down

Project description:We detected an interaction between checkpoint kinase Chk2 and some members of the NCOR/SMRT co-repressor complex. In order to study the role of gene repression in the checkpoint response to DNA damage, we performed RNA profiling in NCOR or SMRT knockdown cells after treztment with cisplatin. U2OS cells were transfected with siRNAs for NCOR or SMRT, grown for 2 days in complete medium, and then treated with 100 microM cisplatin (CDDP) for 6h. Biological duplicates were used for RNa profiling

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Identification of proteome changes in apoptotic NSCLC cells

Project description:Here, we used an unbiased, functional target-discovery platform to identify immunogenic proteins from primary non-small cell lung cancer (NSCLC) cells that had been induced to apoptosis by cisplatin (CDDP) treatment in vitro, as compared with their live counterparts. Among the multitude of proteins identified, some of them were represented as fragmented proteins in apoptotic tumor cells, and acted as non-mutated neoantigens. Only the fragmented proteins elicited effective multi-specific T cell responses, upon a chemotherapy protocol including CDDP. Importantly, these responses further increased significantly upon anti-PD-1 therapy, and correlated with patients’ survival and decreased PD-1 expression.

2020-05-27 | PXD016997 | Pride

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