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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Ai Liu

PROVIDER: E-GEOD-83362 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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.

2016-06-16 | GSE83362 | GEO

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. 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.

2015-04-10 | E-GEOD-67727 | biostudies-arrayexpress

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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.

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2013-12-31 | E-GEOD-38551 | biostudies-arrayexpress

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.

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Cyr61 promotes CD204 expression and migration of macrophages via MEK/Erk pathway in the microenvironment of human esophageal squamous cell carcinoma

Project description:The authors previously suggested that CD204 was a useful marker for tumor-associated macrophages (TAMs) of esophageal squamous cell carcinoma (ESCC). In this study, they discovered that within ESCC microenvironment not only cancer cells but also TAMs expressed cysteine-rich, angiogenic inducer, 61 (Cyr61), induced by conditioned media of ESCC cells. Levels of Cyr61 expression were associated with CD204+ macrophage infiltration in ESCC tissue. Cyr61 promoted CD204 expression and migration of macrophages via MEK/Erk pathway in vitro. To identify the molecules specifically upregulated in TAM-like THP-1 cells, we performed a cDNA microarray analysis using RNAs from THP-1 stimulated with 200 nM TPA or with 200 nM TPA followed by 50% TE-8CM. THP-1 human acute monocytic leukemia cell line was treated with 200 nM 12-O-tetradecanoylphorbol-13-acetate (TPA) for 2 days to induce macrophage-like differentiation, then exposed to 50%Conditioned medium of TE-8 ESCC cell line (TE-8CM) for 2 days. Differentially expressed genes between MM-NM-&-like and TAM-like THP-1 cells were analysed by cDNA microarray. TE-8CM was prepared by plating 5 M-CM-^W 106 tumor cells in 10 mL complete medium in 100-mm dishes for 24 hr, thereafter changing the medium to complete DMEM supplemented with 10% human AB serum instead of fetal bovine serum. After 2M-bM-^@M-^S3 days, the supernatants were harvested, centrifuged and stored in aliquots at M-bM-^HM-^R80M-BM-0C.

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

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

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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.

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