Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MicroRNA and mRNA regulatory network in ALK-rearranged lung adenocarcinoma [mRNA]

ABSTRACT: MicroRNA and mRNA regulatory network in ALK-rearranged lung adenocarcinoma [mRNA]

PROVIDER: PRJNA527107 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

MicroRNA and mRNA regulatory network in ALK-rearranged lung adenocarcinoma [mRNA]

Project description:We examined microarray data of miRNAs and mRNAs from 77 cases of lung adenocarcinoma, including 42 ALK-rearranged cases. a multistep bioinformatics approach to build a miRNA–mRNA regulatory network in ALK-rearranged lung adenocarcinoma.

2022-03-14 | GSE128309 | GEO

MicroRNA and mRNA regulatory network in ALK-rearranged lung adenocarcinoma [miRNA]

2022-03-14 | GSE128310 | GEO

MicroRNA and mRNA regulatory network in ALK-rearranged lung adenocarcinoma

Project description:MicroRNA and mRNA regulatory network in ALK-rearranged lung adenocarcinoma

| PRJNA527104 | ENA

MicroRNA and mRNA regulatory network in ALK-rearranged lung adenocarcinoma [miRNA]

Project description:MicroRNA and mRNA regulatory network in ALK-rearranged lung adenocarcinoma [miRNA]

| PRJNA527106 | ENA

Single-cell transcriptomic analysis uncovers intratumoral heterogeneity and drug-tolerant persister in ALK-rearranged lung adenocarcinoma

Project description:Acquired drug resistance is the major therapeutic obstacle to maintenance treatment of advanced-stage non-small cell lung cancer. Lung adenocarcinoma (ADC) harboring driver mutations also showed poor response to immune checkpoint inhibitors (ICIs). Underlying mechanisms of how drug insensitivity evolves remain unclear. Here we explored the intratumoral heterogeneity of tyrosine kinase inhibitor (TKI)-resistant anaplastic lymphoma kinase (ALK)-rearranged lung ADC organoids using single-cell RNA-sequencing (scRNA-seq) transcriptomic analysis. IL-17 signaling pathway was found highly induced in a subpopulation of pre-existing ALK-TKI-resistant cells. These drug-tolerant persister (DTP) cells, also found to have high surface intracellular adhesion molecule 1 (ICAM-1) expression level, were more resistant towards ALK-TKI and expressed a higher level of cancer-stem cell transcriptional factors. Moreover, tumor cells with high ICAM-1 expression were found spatially correlated with RORɣt+ Th17 infiltration in ALK-rearranged NSCLC resected tumor tissues. In conclusion, our data revealed marked intratumoral heterogeneity in ALK-rearranged tumor, and pre-existing DTP cells may contribute to the development of drug insensitivity in ALK-rearranged lung ADC.

2023-08-09 | GSE223779 | GEO

Spatial evaluation of transcriptomic and proteomic data in ALK rearranged lung cancer - a pilot study

Project description:Spatial evaluation of transcriptomic and proteomic data in ALK rearranged lung cancer - a pilot study

2022-04-20 | MSV000089286 | MassIVE

MicroRNA and mRNA regulatory network in ALK-rearranged lung adenocarcinoma

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-03-14 | GSE128311 | GEO

Transcriptome profiling of ALK-rearranged lung cancer cells upon STAT3 inhibition.

Project description:DNA microarray analysis of ALK-rearranged lung cancer cells (H3122) comparing control untreated cells with cells treated by YHO-1701 (STAT3 inhibitor) for 24h.

2022-01-21 | GSE193858 | GEO

Fibroblast growth factor receptor 3 overexpression mediates ALK inhibitor resistance in ALK-rearranged non-small cell lung cancer

Project description:The rearrangement of anaplastic lymphoma kinase (ALK) occurs in 3%-5% of patients with non-small cell lung cancer (NSCLC) and confers sensitivity to ALK-tyrosine kinase inhibitors (TKIs). For the treatment of patients with ALK-rearranged NSCLC, various additional ALK-TKIs have been developed. Ceritinib is a second-generation ALK-TKI and has shown great efficacy in the treatment of patients with both newly diagnosed and crizotinib, a first-generation ALK-TKI, refractory ALK-rearranged NSCLC. However, tumors can also develop ceritinib resistance. This may result from secondary ALK mutations, but other mechanisms responsible for this have not been fully elucidated. In this study, we explored the mechanisms of ceritinib resistance by establishing ceritinib-resistant, echinoderm microtubule-associated protein-like 4 (EML4)-ALK-positive H3122 cells and ceritinib-resistant patient-derived cells. We identified a mechanism of ceritinib resistance induced by bypass signals that is mediated by the overexpression and activation of fibroblast growth factor receptor 3 (FGFR3). FGFR3 knockdown by small hairpin RNA or treatment with FGFR inhibitors was found to resensitize the resistant cells to ceritinib in vitro and in vivo. FGFR ligands from either human serum or fetal bovine serum were able to activate FGFR3 and induce ceritinib resistance. A detailed analysis of ceritinib-resistant patient-derived specimens confirmed that tyrosine-protein kinase Met (cMET) amplification induces ceritinib resistance. Amplified cMET counter-activated EGFR and/or Her3, and induced ceritinib resistance. These results reveal multiple ceritinib resistance mechanisms and suggest that ceritinib resistance might be able to overcome by identifying precise resistance mechanisms.

2022-08-14 | GSE77764 | GEO

Upregulation of E-cadherin Promotes Spheroid Formation in Crizotinib-Resistant ALK-rearranged Lung Cancer

Project description:The anaplastic lymphoma kinase (ALK) gene fusion functions as a potent oncogene in lung cancer. The development of ALK tyrosine kinase inhibitors has improved patient outcomes. However, cancer progression commonly occurs even after treatment. Chemoresistance arises mostly by the acquisition of gatekeeper mutations in ALK as well as by off-target bypass mechanisms arising during chemotherapy. To investigate these bypass mechanisms, we studied crizotinib resistance in ALK-rearranged lung cancer by using 2D and 3D cell line models and longitudinal human biopsy samples. We found that crizotinib-resistant H2228 cells exhibited increased tumor cell clustering and spheroid formation, with elevated E-cadherin levels. Notably, depletion of E-cadherin profoundly disrupted spheroid formation and restored drug sensitivity. Transcriptomic profiling revealed the upregulation of tissue morphology-related genes; in particular, EpCAM was highly expressed in the protrusive regions of spheroids. Remarkably, longitudinal biopsy analysis also demonstrated enhanced expression of E-cadherin and EpCAM in patients with ALK-rearranged lung cancer during chemotherapy. We propose that off-target resistance is mediated by the upregulation of morphogenic genes, which drive cell clustering and spheroid formation during tumor evolution. To overcome chemoresistance, it is crucial to monitor tumor evolution during treatment. Tracking the collective migration of cells may present a novel therapeutic target.

2026-03-11 | GSE284648 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data