Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA384366 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Gene expression data in MDA231-LM2 breast cancer cells exposed to paclitaxel chemotherapy
| PRJNA384367 | ENA
Project description:Genes regulated by JNK signaling in MDA231-LM2 breast cancer cells
| PRJNA384365 | ENA
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.
2019-08-22 | GSE72111 | GEO
Project description:miR-126 over-expression in highly metastatic LM2 breast cancer cells.
| PRJNA133187 | ENA
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).
2011-01-06 | GSE21513 | GEO
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.
2018-08-26 | GSE98238 | GEO
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.
2018-08-26 | GSE98237 | GEO
Project description:Transcriptional profiling of human breast cancer cell line LM2, a subline of MDA-MB-231 highly metastatic to lung when injected to nude mice, to identify the genes that are regulated after the metastasis gene metadherin is knocked down. Keywords: Genetic modification Empty pSuper vector control cells were compared to the cells transfected with the MTDH knockdown shRNA construct. Two cultured conditions were studied: the LM2 cancer cells were cultured alone or on top of a monolayer of human lung endothelial HMVEC-L cells. Three arrays for each sample.
2010-05-26 | E-GEOD-9187 | biostudies-arrayexpress
Project description:To investigate downstream targets of PRRX1, we used MDA-MB-231 (MDA231) breast cancer cells which express low level of PRRX1 to generate a stable cell line where human PRRX1 was ectopically overexpressed (MDA231-PRRX1), and performed comparative microarray analyses. Interestingly, we found many miRNAs that were upregulated in MDA231-PRRX1 cells.
2019-10-18 | GSE138078 | GEO