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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

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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.

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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

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Microrna expression (Agilent McroRNA Array)

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

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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

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