Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA384367 | ENA |
REPOSITORIES: ENA
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Project description:In advanced malignancies, cancer cells have acquired capabilities to resist a variety of stress-inducing insults. We show that c-Jun N-terminal kinase (JNK) stress signaling is highly active in cancer cells from patients with late stage breast cancer and promotes tumor growth and metastasis in mouse models. Transcriptomic analysis revealed that JNK activity induces genes associated with extracellular matrix (ECM), wound healing and mammary stem cells. The ECM proteins and niche components osteopontin (SPP1) and tenascin C (TNC) are induced by JNK signaling and promote metastatic colonization of the lungs. Notably, treatment with chemotherapeutic drugs induces JNK activity in breast cancer cells, reinforcing the production of SPP1 and TNC. Inhibition of JNK or reduction of SPP1 or TNC expression sensitizes primary tumors and metastases in mice to chemotherapy. In order to investigate cancer cell-response to chemotherapy, we exposed MDA231-LM2 breast cancer cells to the chemotherapeutic agent paclitaxel and performed transcriptomic analysis using Affymetrix microarray.
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Project description:Gene expression data in MDA231-LM2 breast cancer cells cultured as oncospheres
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Project description:Genes regulated by JNK signaling in MDA231-LM2 breast cancer cells
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Project description:Purpose: To identify downstream signaling pathways that mediate functions of GALNT14 Methods: RNAs isolated from MDA231-LM2 cells expressing shCntr or shGALNT14 and MDA231-Par cells expressing pBabe-Hygro control vector or GALNT14 expression vector were analyzed by using an Illumina HiSeq 2500 Conclusions: Our study represents the first transcriptome profile of GALNT14-depleted MDA231-LM2 and GALNT14-overexpressing Par cells.
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Project description:In advanced malignancies, cancer cells have acquired capabilities to resist a variety of stress-inducing insults. We show that c-Jun N-terminal kinase (JNK) stress signaling is highly active in cancer cells from patients with late stage breast cancer and promotes tumor growth and metastasis in mouse models. Transcriptomic analysis revealed that JNK activity induces genes associated with extracellular matrix (ECM), wound healing and mammary stem cells. The ECM proteins and niche components osteopontin (SPP1) and tenascin C (TNC) are induced by JNK signaling and promote metastatic colonization of the lungs. Notably, treatment with chemotherapeutic drugs induces JNK activity in breast cancer cells, reinforcing the production of SPP1 and TNC. Inhibition of JNK or reduction of SPP1 or TNC expression sensitizes primary tumors and metastases in mice to chemotherapy. We used Affymetrix microarrays to analyze the transcriptomic output modulated by JNK activity in a lung metastatic derivative of the MDA-MB-231 breast cancer cell line, MDA231-LM2.
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Project description:Increasing pre-clinical data suggest that chemotherapy may elicit pro-metastatic responses in breast cancer models. Primary tumours release extracellular vesicles (EVs) that can facilitate the seeding and growth of metastatic cancer cells in distant organs, but the effects of chemotherapy on pro-metastatic EVs are poorly understood. The goal of the project was to analyse the protein content in EVs released by the mouse breast cancer cell line 4T1 after treatment with the chemotherapeutic agent paclitaxel (PTX) or its vehicle control cremophor (CREMO).
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Project description:The taxanes, namely Paclitaxel and Docetaxel, are important and widely used cancer chemotherapy drugs in the treatment of invasive and metastatic human breast cancer. Although treatment with the taxanes is beneficial to many patients, drug-responsive tumors in patients with metastatic breast cancer often display resistance to these drugs, either initially or over time following the continued administration of chemotherapy drugs. To investigate the patterns of cross-resistance with the taxane drugs and to identify potential mechanisms of resistance, we generated a series of MDA-MB-231 taxane resistant cell lines. We then used microarrays to determine gene expression differences between sensitive, Docetaxel and Paclitaxel resistant MDA-MB-231 cells. RNA isolated from three independent passages of sensitive, Docetaxel and Paclitaxel resistant cell lines and purified using the Qiagen RNeasy Mini Kit. Total RNA was processed and hybridized to Affymetrix Genechip HU133A arrays.
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Project description:CTCF, H2AFZ and FOXA1 genomic recruitment sites were determined using ChIP-chip while MeDIP-chip was used to monitor DNA methylation levels. Amplified and labeled DNA was hybridized to Affymetrix tiling arrays covering human chromosomes 8, 11 and 12. Cells used in this study are: MCF7 breast cancer cells, LNCaP prostate cancer cells, MDA-MB-231 breast cancer cells stably transfected with a FOXA1 expression vector (MDA231-FOXA1) or the empty control plasmid (MDA231-CTRL). H3K4me2 genomic distribution was determined using ChIP-chip. Amplified and labeled DNA was hybridized to Affymetrix tiling arrays covering human chromosomes 8, 11 and 12. Cells used in this study are MDA-MB-231 breast cancer cells stably transfected with a FOXA1 expression vector (MDA231-FOXA1) or the empty control plasmid (MDA231-CTRL).
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Project description:Expression data from paclitaxel and salinomycin-treated HMLER breast cancer cells
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