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Analysis of differentially expressed circRNAs after EGFR-TKI treatment

ABSTRACT: CircRNA-seq of H1975 cells treated with DMSO or Osi (500 nM) and PC9 cells treated with DMSO or Ge (100 nM) for 3 days

ORGANISM(S): Homo sapiens

PROVIDER: GSE211854 | GEO | 2022/08/26

REPOSITORIES: GEO

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3' UTR RNA-sequencing of human EGFR-mutant lung adenocarcinoma cell lines treated with trametinib or controls

Project description:Human EGFR-mutated lung adenocarcinoma cell lines HCC4006, HCC827 and PC9 were treated with trametinib or DMSO to assess the impact on transcription.

2021-07-19 | E-MTAB-9889 | biostudies-arrayexpress

Mechanisms of tolerance and resistance to EGFR inhibition in lung cancer [RNA-seq]

Project description:Purpose: Multiple mechanims have been proposed that lead to reduced effectiveness of EGFR tyrosine kinase inhibitors (TKIs) in lung cancer and yet resistance to osimertinib and gefitinib still remains a challenge in the clinic. The goals of this study are to identify key genes contributing to tolerance and resistance to EGFR inhibition. Methods: mRNA profiles of gefitinib and osimertinib tolerant cells in PC9 and HCC827 cells were generated by deep sequencing using Illumina. In addition, mRNA profiles of cells (AALE, PC9 and HCC827) overexpressing with miR-147b or miR-21 and mRNA profiles of cells (H1975 and PC9ER) with miR-147b and miR-21 knocking down were generated by deep sequencing. The mappable reads were aligned to the human transcripts using Bowtie2 and gene abundance was estimated using RSEM. Results: Upregulation of miR-147b and miR-21 expression is related to tolerance and resistance to gefitinib and osimertinib in lung cancer. The signaling pathways of transcripts by knocking down miR-147b or miR-21 in resistant cells (H1975 and PC9ER) and by overexpressing miR-147b or miR-21 in both sensistive cells (HCC827 and PC9) and immortalized lung epithelial cells (AALE) are consistent with the key signaling pathways shown in tolerant cells to gefitinib and osimertinib in HCC827 and PC9 cells (HCC827GTR/OTR vs HCC827 and PC9GTR/OTR vs PC9). Conclusions: Our work identifies key signaling pathways that mediate EGFR-TKI tolerance and resistance in lung cancer. Our study provides potential targets to improve the efficacy of EGFR-TKIs therapy in cancer pagtients.

2018-01-11 | GSE103350 | GEO

Mutant EGFR is a preferred SMURF2 substrate of ubiquitination: role in enhanced receptor stability and TKI sensitivity

Project description:We previously reported that differential protein degradation of TKI-sensitive [L858R, del(E746-A750)] and resistant (T790M) epidermal growth factor receptor (EGFR) mutants upon erlotinib treatment correlates with drug sensitivity. However, the molecular mechanism remains unclear. We also reported SMAD ubiquitination regulatory factor 2 (SMURF2) as a stabilizer of EGFR in a ligase (E3) activity-dependent manner. Here, using in vitro and in vivo ubiquitination assays, mass spectrometry, and super-resolution microscopy, we show SMURF2-EGFR functional interaction is critical in receptor stability and TKI sensitivity. We found that L858R/T790M EGFR is a preferred substrate of SMURF2-UBCH5 (an E3-E2) complex-mediated K63-linked polyubiquitination, which preferentially stabilizes mutant receptor. We identified three lysine (K) residues (K721, 1037 and 1164) as the sites of ubiquitination and replacement of K to acetylation-mimicking asparagine (Q) at K1037 position in L858R/T790M background converts the stable protein sensitive to erlotinib-induced degradation. Using STochastic Optical Reconstruction Microscopy (STORM) imaging, we show that SMURF2 presence allows longer membrane retention of activated EGFR upon EGF treatment, whereas, siRNA-mediated SMURF2 knockdown fastens receptor endocytosis and lysosome enrichment. In an erlotinib-sensitive PC9 cells, SMURF2 overexpression increased EGFR levels with improved erlotinib tolerance, whereas, SMURF2 knockdown decreased EGFR steady state levels in NCI-H1975 and PC9-AR cells to overcome erlotinib and AZD-9291 resistance respectively. Additionally, disruption of the SMURF2-UBCH5 complex destabilized EGFR. Together, we propose that SMURF2-mediated preferential polyubiquitination of L858R/T790M EGFR may be competing with acetylation-mediated receptor internalization to provide enhanced receptor stability and that disruption of the E3-E2 complex may be an attractive alternate to overcome TKI resistance

2020-07-29 | PXD018324 | Pride

Microrna expression (Agilent McroRNA Array)

Project description:MicroRNA profiling of 3 Human NSCLC cell lines (PC9,PC9R,H1975)

2013-10-01 | E-MTAB-1327 | biostudies-arrayexpress

PIPseq on Gefitinib sensitive and resistant cell lines

Project description:We used PIP-seq single cell RNA-sequencing to study the response of PC9 and H1975 to Gefitinib

2023-01-12 | GSE202234 | GEO

Next generation sequencing facilitates quantitative analysis of PC9 and MTAC-P (EGFR-TKI resistant cell line derived from PC9)

Project description:The goals of this study are to compare the different transcriptome signiture between PC9 and MTAC-P with NGS-derived retinal transcriptome profiling (RNA-seq).

2019-10-29 | GSE79763 | GEO

Comprehensive analysis of circular RNA profiling in AZD9291-resistant non-small cell lung cancer cell lines

Project description:Considering the important role of circular RNAs (circRNAs) in cancers, we established AZD9291-resistant NSCLC cell lines (H1975/AZDR and HCC827/AZDR) and used microarray analysis to determine the circRNA expression profiles of the cells. The H1975/AZDR and HCC827/AZDR cell lines were induced by gradually increasing the drug concentration. CircRNA microarray expression profiles were obtained from H1975, HCC827, H1975/AZDR, and HCC827/AZDR cells and validated by quantitative reverse transcription PCR. Expression data were analyzed bioinformatically.

2024-04-05 | GSE263003 | GEO

Next generation sequencing quantitative analysis of C3H10T1/2 cells treated with purmorphamine, DMSO, purmorphamine and Picoberin or DMSO and Picoberin for 24h, 48h, 96h or 7 days

Project description:Purpose: Analysis of the differential gene expression of C3H10T1/2 cells undergoing Hedgehog (Hh) induced osteoblast differentiation compared to unstimulated (DMSO treated) cells and investigation of the differential gene expression caused by Picoberin, a highly potent inhibitor of Hh induced osteoblast differentiation (Comparison of purmorphamin + Picoberin treated C3H10T1/2 cells with purmorphamin + DMSO treated cells) Methods: 80 % confluent C3H10T1/2 cells were treated either with 1.5 µM purmorphamine + DMSO, only DMSO, 1.5 µM purmorphamine + 1 nM Picoberin, 1.5 µM purmorphamine +100 nM Picoberin or DMSO + 100 nM Picoberin for 24h, 48h, 96h or 7 days. Results: Picoberin inhibits osteoblast differentiation

2022-11-30 | GSE197970 | GEO

Erastin induced protein expression change in H1975 cells

Project description:H1975 cells were treated with DMSO and erastin, respectively. Protein was extracted and separated using SDS-PAGE electrophoresis. MS analysis was performed and protein was identified and quantified using Proteome Discoverer™ 1.3 software using the SEQUEST® search engine.

2021-09-09 | PXD020205 | Pride

Overcoming TKI resistance in a lung xenograft model

Project description:Bulk RNA-Seq of PC9 xenograft tumors in different stages of response and resistance to Erlotinib treatment. A combination treatment is proposed in order to overcome Erlotinib drug resistance.

2020-11-17 | GSE161584 | GEO

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