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YB-1 affects response to paclitaxel in TNBCs by modulation of EGR1

ABSTRACT: For patients with triple negative breast tumours (TNBCs), lacking receptors for oestrogen, progesterone or HER2 on their cell surface, chemotherapy is the main treatment. The taxanes, paclitaxel (PTX) and docetaxel, have become the most commonly-used chemotherapies for these kinds of breast cancer. Although several targeted therapies are currently undergoing clinical trials for TNBC, because of the heterogeneous nature of TNBCs, it is predicted that these may often be used in combination with chemotherapy. Therefore an understanding of the mechanisms of chemotherapy resistance will continue to be important for the treatment of these patients.

ORGANISM(S): Homo sapiens

PROVIDER: GSE60964 | GEO | 2015/09/02

SECONDARY ACCESSION(S): PRJNA260001

REPOSITORIES: GEO

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YB-1 affects response to paclitaxel in TNBCs by modulation of EGR1

Project description:For patients with triple negative breast tumours (TNBCs), lacking receptors for oestrogen, progesterone or HER2 on their cell surface, chemotherapy is the main treatment. The taxanes, paclitaxel (PTX) and docetaxel, have become the most commonly-used chemotherapies for these kinds of breast cancer. Although several targeted therapies are currently undergoing clinical trials for TNBC, because of the heterogeneous nature of TNBCs, it is predicted that these may often be used in combination with chemotherapy. Therefore an understanding of the mechanisms of chemotherapy resistance will continue to be important for the treatment of these patients. Given the pleiotropic nature of YB-1, the aim of this study was to understand whether there were mechanisms in addition to those discussed above, by which YB-1 controls response to PTX in TNBCs. We initially followed up two previously studied mechanisms, mediated by ABCB1/MDR1 and DUSP4. We then proceeded to use genomics to identify novel mechanisms by which YB-1 regulates the response of TNBCs to PTX. This analysis identified and experimentally validated EGR1, encoding the early growth response protein 1 (EGR1) as a previously undiscovered mechanism of YB-1-driven PTX resistance.

2015-09-02 | E-GEOD-60964 | biostudies-arrayexpress

Gene expression data of sensitive, Docetaxel resistant and Paclitaxel resistant MDA-MB-231 Cells

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.

2011-04-22 | GSE28784 | GEO

Proteomic analysis of extracellular vesicles (EVs) from 4T1 breast cancer cells upon paclitaxel treatment

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).

2019-01-02 | PXD010362 | Pride

Gene expression data of sensitive, Docetaxel resistant and Paclitaxel resistant MDA-MB-231 Cells

2011-04-22 | E-GEOD-28784 | biostudies-arrayexpress

Extracellular vesicle-derived VDAC1 protein promotes paclitaxel resistance through autophagy and mitophagy in gastric cancer

Project description:Gastric cancer (GC) is ranked as as the third most prevalent malignant tumor worldwide [1, 2]. Chemotherapy is considered the primary therapeutic approach for metastatic and unresectable GC [3]. Paclitaxel (PTX) is an anti-microtubule agent, and single therapy with PTX or PTX-based chemotherapy combined with other chemotherapy has demonstrated promising efficacy in clinical treatment in patients with advanced GC [4]. However, PTX-based chemotherapy is limited by acquired chemoresistance[5]. Mounting evidence have indicated that drug resistance in cancer cells is a major contributing factor for the failure of tumor treatment,resulting in the rapid recurrence, progression, and ultimately, patient mortality [6]. GC exhibits higher tissue heterogeneity and invasive behavior compared to other primary tumors [7]. Therefore, it is essential to promptly uncover the mechanisms underlying drug resistance in GC and meet unmet needs in GC treatment.

2024-10-17 | PXD056923 |

Transcriptional screening in MDA-231 cells treated with low-dose Paclitaxel for 24 and 48 hours

Project description:Paclitaxel is the most commonly used chemotherapeutic agent in breast cancer treatment. Notably, a comprehensive understanding of paclitaxelâs effects requires insight into the dose-specific activities of paclitaxel and their influence on the cancer cells and host microenvironment. The aim of our study is to reveal the gene transcriptional changes in response to low-Paclitaxel (PTX) treatment in breast cancer cells. For genome-wide gene expression analysis, MDA-MB-231 cells (high-invasive breast cancer cell line) were treated with 5 ng/ml PTX for 24 and 48 hours respectively and then the cell lysates were prepared by TRIzol reagent. Then the total RNA in each group was extracted and the genome-wide gene expressing profile was detected through the Human One Array (HOA) Microarray system (Phalanx Biotech Group, Taiwan).

2016-06-01 | E-GEOD-82048 | biostudies-arrayexpress

miR-1061 and miR-591 are involved in paclitaxel-resistance and their regulation increases the sensitivity to paclitaxel

Project description:MicroRNA expression in paclitaxel (PTX)-resistant SKpac sublines was compared to that of the PTX-sensitive, parental SKOV3 ovarian cancer cell line using microarray and real-time RT-PCR. The function of differentially expressed microRNAs in chemoresistant ovarian cancer was further evaluated by apoptosis, cell proliferation, and migration assays.

2013-01-17 | GSE43598 | GEO

Expression profiling and DNA methylation of TNBCs

Project description:Expression profiling and DNA methylation of TNBCs

| PRJNA483987 | ENA

Alleviating iatrogenic effects of paclitaxel-coated balloons via anti-inflammatory treatment

Project description:Background: Paclitaxel is touted as an essential medicine due to its extensive use as a chemotherapeutic for various cancers and an antiproliferative agent for restenosis. Due to recent concerns related to long-term mortality, paclitaxel (PTX)-based endovascular therapy is now surrounded by controversies. Objective: Examine the inflammatory mediators driven by the systemic administration of PTX and explore the means to suppress these effects. Methods: RNAseq analysis, cell and mouse models. Results: RNAseq analysis of primary human endothelial cells (ECs) treated with PTX demonstrated transcriptional perturbations of a set of pro-inflammatory mediators, including monocyte chemoattractant protein-1 (MCP-1) and CD137, which were validated in EC lysates. These perturbations were abrogated with dexamethasone, a prototypic anti-inflammatory compound. The media of ECs pre-treated with PTX showed a significant increase in MCP-1 levels, which were reverted to baseline levels with DEX treatment. A group of mice harvested at different time points after PTX injection were analyzed for immediate and delayed effects of PTX. A 3-fold increase in MCP-1 was noted in blood and aortic ECs after 12 hours of PTX treatment. Similar changes in CD137 and downstream mediators such as tissue factor, VCAM-1 and E-selectin were noted in aortic ECs. Conclusions: Our study shows that systemic PTX exposure upregulates atherothrombotic markers, and co-delivery of DEX can subdue the untoward toxic effects. Long-term studies are needed to probe the mechanisms driving systemic complications of PTX-based therapies and evaluate the clinical potential of DEX to mitigate risk.

2023-03-02 | GSE217550 | GEO

RNA-sequencing for the characterization of the transcriptome of SUM 159 parental and Paclitaxel (PTX) resistant breast cancer cells.

Project description:RNA-sequencing was performed in SUM 159 parental and PTX resistant breast cancer cells in an effort to identify novel regulators of chemoresistance that could potentially be targeted in Triple Negative Breast Cancer (TNBC). The bioinformatic analysis identified numerous differentially expressed genes including several known chemoresistance markers, as well as novel genes that may play an important role in breast cancer chemoresistant cells.

2022-09-20 | GSE206242 | GEO

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