Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA309709 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Targeting Taxane-Platin Resistant Lung Cancers with JumonjiC Lysine Demethylase Inhibitors
| PRJNA322313 | ENA
Project description:Targeting Taxane-Platin Resistant Lung Cancers with JumonjiC Lysine Demethylase Inhibitors (RNA-Seq)
| PRJNA322315 | ENA
Project description:Targeting Taxane-Platin Resistant Lung Cancers with JumonjiC Lysine Demethylase Inhibitors (ChIP-Seq)
| PRJNA322314 | ENA
Project description:While taxane-platin standard chemotherapy provides benefit in advanced and localized non-small cell lung cancer (NSCLC), the majority of patients relapse with drug resistant tumors. Mechanisms underlying NSCLC resistance to this standard doublet chemotherapy are still not fully understood, and treatment options for chemoresistant lung tumors are limited. The goals of this work were to establish new preclinical NSCLC models of resistance to taxane-platin doublet chemotherapy, identify mechanisms of resistance, and develop new rational pharmacologic approaches to target drug resistant NSCLCs.
2016-12-31 | GSE77209 | GEO
Project description:Characterization of histone 3 lysine 4 and lysine 27 trimethylation changes upon development of taxane-platin drug resistance in NSCLC cells and evaluation of these histone modifications after treatment with Jumonji KDM inhibitors, JIB-04 and GSK-J4.
2017-05-23 | GSE81688 | GEO
Project description:Targeting HuH7 cells with JumonjiC Lysine Demethylase Inhibitors and RAC1 inhibitors (RNA-Seq)
| PRJNA516661 | ENA
Project description:Characterization of gene expression changes upon development of taxane-platin drug resistance in NSCLC cells and further, upon treatment of these resistant cells with the Jumonji KDM inhibitor, GSK-J4.
2017-05-23 | GSE81687 | GEO
Project description:Purpose: Breast cancer is a genetically heterogenous disease with subtypes differing in prognosis and chemosensitivity. The basal-like breast cancer (BLBC) molecular subtype is associated with poorer outcomes, but is more responsive to taxane-based chemotherapy. We evaluated the role of kinesins, motor proteins interacting with microtubules, in influencing taxane resistance. Experimental Design: Kinesin (KIF) expression was studied in one local dataset comprising all taxane resistant breast cancers in relation to taxane resistance. Data in the NCI-60 cell line dataset (GSE5846) nd the MDACC dataset (GSE20194) is separately detailed. Results: In the local dataset, the kinesin KIF26B is overexpressed in taxane-resistant residual breast cancers post-chemotherapy. Conclusions: We show that kinesin overexpression correlates with taxane resistance in BLBC cell lines and tissue. Our results suggest a potential approach to overcoming taxane resistance through concurrent or sequential use of kinesin inhibitors, highlighting the ATP-binding domain as a drug development target. Kinesin (KIF) expression was studied in one local dataset comprising all taxane resistant breast cancers in relation to taxane resistance. Data in the NCI-60 cell line dataset (GSE5846) and the MDACC dataset (GSE20194) is separately detailed.
2012-12-01 | E-GEOD-22796 | biostudies-arrayexpress
Project description:Purpose: Breast cancer is a genetically heterogenous disease with subtypes differing in prognosis and chemosensitivity. The basal-like breast cancer (BLBC) molecular subtype is associated with poorer outcomes, but is more responsive to taxane-based chemotherapy. We evaluated the role of kinesins, motor proteins interacting with microtubules, in influencing taxane resistance. Experimental Design: Kinesin (KIF) expression was studied in one local dataset comprising all taxane resistant breast cancers in relation to taxane resistance. Data in the NCI-60 cell line dataset (GSE5846) nd the MDACC dataset (GSE20194) is separately detailed. Results: In the local dataset, the kinesin KIF26B is overexpressed in taxane-resistant residual breast cancers post-chemotherapy. Conclusions: We show that kinesin overexpression correlates with taxane resistance in BLBC cell lines and tissue. Our results suggest a potential approach to overcoming taxane resistance through concurrent or sequential use of kinesin inhibitors, highlighting the ATP-binding domain as a drug development target.
2012-12-01 | GSE22796 | GEO
Project description:Drug resistance in patients remains a significant obstacle to successful treatment, even with improvements in cancer treatment strategies. Resistance to taxanes, such as docetaxel (Dtx) and cabazitaxel (Cbz), frequently emerges in Castration Resistant Prostate Cancer (CR-PCa). Through pulse selection of the parental cells (Du145), we established Dtx- and Cbz-resistant CR-PCa cell models and integrated different omic approaches, including transcriptomics and proteomics, to determine the molecular signatures underlying taxane resistance. Interestingly, several genes were regulated in the same direction (up- or down-regulation) at both the gene and protein expression levels in resistant cells compared to parental cells, suggesting that alterations primarily occur at the transcriptional level and manifest at the protein level. Among the differentially regulated genes, CRIP2, a gene associated with tumor suppressor function, has been found to be the most downregulated in taxane-resistant cells. Conversely, NNMT exhibited top-ranked significant upregulation and has been validated in the context of taxane resistance. Its overexpression was shown to promote taxane resistance, whereas depletion via siRNA or gRNA has resensitized the cells. RNA-sequencing of NNMT-knockout cells has indicated involvement of TGFβ signaling, and suppressing this pathway has further increased the taxane sensitivity. EMT was another pathway depleted upon knockout, and subsequent analysis revealed a significant correlation between NNMT and EMT-related genes (VIM, CDH2, FN1, TGFB1, and ZEB2) in both the cell line panel (CCLE) and patient data. Additionally, in cancers other than PCa, NNMT has been observed to predict treatment outcomes, and notably, among the patients with a high EMT signature, elevated NNMT levels were associated with decreased overall survival. More importantly, NNMT-high patients were found to be non-responders to taxane-containing chemotherapy regimens. Collectively, our findings suggest that targeting NNMT and the pathways it affects, such as TGFβ, offers a viable approach for addressing taxane-resistant PCa.
2026-04-30 | GSE279444 | GEO