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Long non-coding RNA CRNDE Involved in Resistance to EGFR tyrosine kinase inhibitor in EGFR-mutant Lung Cancer via eIF4A3/MUC1/EGFR Signal.

ABSTRACT: Long non-coding RNA CRNDE Involved in Resistance to EGFR tyrosine kinase inhibitor in EGFR-mutant Lung Cancer via eIF4A3/MUC1/EGFR Signal.

PROVIDER: PRJNA688205 | ENA |

REPOSITORIES: ENA

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Long non-coding RNA CRNDE Involved in Resistance to EGFR tyrosine kinase inhibitor in EGFR-mutant Lung Cancer via eIF4A3/MUC1/EGFR Signal.

Project description:Introduction: Overcoming of acquired resistance to EGFR-tyrosine kinase inhibitors (EGFR-TKIs) is an intractable obstacle for many clinical oncologists. The mechanisms of resistance to EGFR-TKIs are very complex. Long non-coding RNAs (lncRNAs) may play an important role in cancer development and metastasis. However, the biological process between lncRNAs and drug resistance to EGFR mutated lung cancer largely unknown. Methods: Osimertinib and afatinib-resistant EGFR-mutated lung cancer cells were established using by a stepwise method. Microarray analysis of non-coding and coding RNAs was performed using parental and resistant EGFR-mutant NSCLC cells. Results: Microarray analysis was evaluated by bioinformatics analysis through medical-industrial collaboration. CRNDE and DGCR5 lncRNAs were highly expressed in EGFR-TKIs-resistant cells. CRNDE binds to eIF4A3 protein, down-regulates eIF4A3 and MUC1 expression, and down-regulates p-EGFR expression. CRNDE inhibition activated the eIF4A3/MUC1/EGFR signaling pathway and apoptotic activity and restored sensitivity to EGFR-TKIs. Conclusions: We identified lncRNA CRNDE associated with resistance to EGFR-TKIs in EGFR-mutant NSCLC cells. CRNDE may be a novel therapeutic target for EGFR mutant NSCLC patients.

2021-04-28 | GSE163913 | GEO

Long Non-Coding RNA CRNDE Is Involved in Resistance to EGFR Tyrosine Kinase Inhibitor in EGFR-Mutant Lung Cancer via eIF4A3/MUC1/EGFR Signaling.

Project description: Not available

| S-EPMC8070547 | biostudies-literature

Host-dependent Phenotypic Resistance to EGFR Tyrosine Kinase Inhibitors

Project description:Host-dependent Phenotypic Resistance to EGFR Tyrosine Kinase Inhibitors

| PRJNA705946 | ENA

MUC1 triggers lineage plasticity of Her2 positive mammary tumor

Project description:The aberrant overexpression of mucin 1 (MUC1) and human epidermal growth factor receptor 2 (HER2) are often observed in breast cancer. However, the role of concomitant of MUC1/HERR2 in the development of breast cancer has not been fully illustrated. Following analysis public microarray datasets that revealed a correlation of double positive of MUC1 and HER2 to a worse clinical outcome, we generated a mouse model overexpressing both Her2 and MUC1 cytoplasmic domain (MUC1-CD) to investigate their interaction in mammary carcinogenesis. Coexpression of Her2 and MUC1-CD confers growth advantage and promotes the development of spontaneous mammary tumors. Genomic analysis uncovers that enforced expression of MUC1-CD and Her2 induces mammary tumor lineage plasticity which is supported by gene reprogramming and mammary stem cell enrichment. With gain- and loss-of function strategies, we show that coexpression of Her2 and MUC1-CD was associated with down-regulation of TCA cycle genes in tumors. Importantly, the reduction of TCA cycle genes induced by MUC1-CD is is significantly connected to the poor prognosis in HER2+ breast cancer patients. In addition, MUC1 augments Her2 signaling pathway by inducing Her2/Egfr dimerization. These findings collectively demonstrate the vital role of MUC1-CD/Her2 collaboration in shaping mammary tumor landscape and highlight the prognostic and therapeutic implication of MUC1 in patients with Her2+ breast cancer.

2022-03-10 | GSE198239 | GEO

eIF4A3 - Modified iCLIP

Project description:eIF4A3 - Modified iCLIP

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CD8+ T cell-1 dependent antitumor response boosted by dual blockade of PD-1 and VGFR2 following EGFR-tyrosine kinase inhibitors against lung cancer with Egfr mutation

Project description:We showed that CD8+ T cell-dependent antitumor response was induced by an EGFR-tyrosine kinase inhibitor (TKI) against syngeneic Egfr-mutant NSCLC tumors and that the effect was further pronounced by the sequential dual blockade of PD-1 and vascular endothelial growth factor receptor 2 (VEGFR2).

2023-02-22 | GSE197260 | GEO

Expression data for EGFR TKI resistant EGFR-mutated Cells

Project description:Intratumoral heterogeneity in EGFR mutant NSCLC results in divergent resistance mechanisms in response to EGFR tyrosine kinase inhibition We used microarrays to investigate the gene expression underlying EGFR TKI resistance with a mesenchymal phenotype.

2016-06-04 | GSE69181 | GEO

eIF4A3 interactome by IP-MS in mouse ESCs

Project description:RNA helicases are involved in multiple steps of RNA metabolism to direct their roles in gene expression, yet their functions in pluripotency control remain largely unexplored. Starting from an RNAi screen of RNA helicases, we identified that eIF4A3, a DEAD-box (Ddx) helicase component of the exon junction complex (EJC), is essential for the maintenance of embryonic stem cells (ESCs). We mapped the eIF4A3 interactomes in mouse ESCs, revealing that eIF4A3 is widely involved in the post-transcriptional regulation of gene expression. Mechanistically, we show that eIF4A3 post-transcriptionally controls the pluripotency-related cell cycle regulators and that its depletion causes cellular differentiation via cell cycle dysregulation. Specifically, eIF4A3 is required for the efficient nuclear export of Ccnb1 mRNA, which encodes Cyclin B1, a key component of the pluripotency-promoting pathway during cell cycle progression of ESCs. Our results reveal a previously unappreciated role of eIF4A3 and its associated EJC in the post-transcriptional cell cycle control in maintaining stem cell pluripotency.

2023-03-11 | PXD031362 | Pride

RNA-Seq of control and EJC factor (EIF4A3, RBM8A, MAGOH) knockdowns in part with EIF4A3 rescue in HeLa Tet-Off cells

Project description:The exon junction complex is involved in gene expression regulation on multiple co- and post-transcriptional levels. We aimed to investigate in HeLa Tet-Off cells which gene expression alterations can be observed upon knockdown of core EJC factors (EIF4A3, RBM8A and MAGOH) or upon EIF4A3 knockdown and rescue with EIF4A3 wild type construct by using RNA-Seq analyses. The rescue construct was stably integrated into the genome using the PiggyBac transposon system. As control Luciferase (Luc) siRNA was used.

2022-05-06 | E-MTAB-10771 | biostudies-arrayexpress

Sequencing the anti-MUC1 hybridoma antibody 139H2

Project description:Mucin 1 (MUC1) is a transmembrane mucin expressed at the apical surface of epithelial cells at different mucosal surfaces including breast and intestine. The MUC1 extracellular domain contains a variable number of tandem repeats (VNTR) of 20 amino acids, which are heavily O-linked glycosylated. Monoclonal antibodies against the MUC1 VNTR can be powerful tools because of their multiplicity of binding and possible applications in the diagnosis and treatment of MUC1-expressing cancers. One such antibody is the hybridoma mouse monoclonal 139H2 which is also widely used as a research tool to study non-cancer MUC1. Here we report direct mass spectrometry-based sequencing of hybridoma-derived 139H2 IgG, which enabled reverse engineering of a recombinant 139H2.

2024-03-18 | PXD043489 | Pride

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