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We began analyzing https://www.spandidos-publications.com/10.3892/or.2022.8355, but it redirected us to https://www.spandidos-publications.com/10.3892/or.2022.8355. The analysis below is for the second page.

Title[redir]:
Genome‑wide expression and methylation analyses reveal aberrant cell adhesion signaling in tyrosine kinase inhibitor‑resistant CML cells
Description:
Although chronic myeloid leukemia (CML) can be effectively treated using BCR‑ABL1 kinase inhibitors, resistance due to kinase alterations or to BCR‑ABL1 independent mechanisms remain a therapeutic challenge. For the latter, the underlying mechanisms are widely discussed; for instance, gene expression changes, epigenetic factors and alternative signaling pathway activation. In the present study, <em>in vitro</em>‑CML cell models of resistance against the tyrosine kinase inhibitors (TKIs) imatinib (0.5 and 2 µM) and nilotinib (0.1 µM) with biological replicates were generated to identify novel mechanisms of resistance. Subsequently, genome‑wide mRNA expression and DNA methylation were analyzed. While mRNA expression patterns differed largely between biological replicates, there was an overlap of 71 genes differentially expressed between cells resistant against imatinib or nilotinib. Moreover, all TKI resistant cell lines demonstrated a slight hypermethylation compared with native cells. In a combined analysis of 151 genes differentially expressed in the biological replicates of imatinib resistance, cell adhesion signaling, in particular the cellular matrix protein fibronectin 1 (FN1), was significantly dysregulated. This gene was also downregulated in nilotinib resistance. Further analyses showed significant FN1‑downregulation in imatinib resistance on mRNA (P<0.001) and protein level (P<0.001). SiRNA‑mediated FN1‑knockdown in native cells reduced cell adhesion (P=0.02), decreased imatinib susceptibility visible by higher Ki‑67 expression (1.5‑fold, P=0.04) and increased cell number (1.5‑fold, P=0.03). Vice versa, recovery of FN1‑expression in imatinib resistant cells was sufficient to partially restore the response to imatinib. Overall, these results suggested a role of cell adhesion signaling and fibronectin 1 in TKI resistant CML and a potential target for novel strategies in treatment of resistant CML.

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Keywords {🔍}

imatinib, cell, resistance, cells, resistant, expression, article, view, google, scholar, pubmedncbi, tki, genes, gene, methylation, nilotinib, adhesion, differentially, replicates, leukemia, native, chronic, fig, cml, lines, sublines, biological, compared, expressed, lowimr, myeloid, dna, drug, signaling, kinase, study, analysis, performed, analyses, total, bcrabl, lowim, highim, observed, analyzed, protein, cancer, line, data, methylated,

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bcr-abl-positive cell line bcr-abl1 kinase domain pre-warmed serum-free media ph chromosome-positive leukemia tyrosine kinase bcr-abl1 1021-335x online issn bcr-abl positive cells bcr‑abl1 kinase inhibitors conditions genome‑wide expression bcr-abl1 fusion protein recurrent genome-wide expression genome-wide methylation profile genome-wide gene expression genome‑wide mrna expression pselect–puromycin-mcs vector es/tools/venny/index bcr-abl1-independent mechanisms decreased microrna-30a levels mdr-cml cell lines university hospital schleswig-holstein excellence ‘precision medicine bcr-abl1 mutations sh-sy5y neuroblastoma cells intercept/tbs blocking solution imatinib-resistant cell lines microrna-212/abcg2-axis contributes published article bcr-abl1-kinase gov/geo/query/acc reverse transcription-quantitative pcr vitro‑cml cell models ruwen boehm im-resistant sublines compared tki-treated cml patients posttranscriptional micro-rna regulation home submit manuscript negative control transfection bcr-abl1 expression serum-free media supplementary information files abl tyrosine kinase bcr-abl activity analyzed normalizing im-treated treatment-naïve cells analyzing vitro-drug resistance models cell adhesion assay im-resistant k-562 cells clinical oncology experimental tyrosine kinase inhibitor sublines showed mutations

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Rumjanek VM, Vidal RS and Maia RC: Multidrug resistance in chronic myeloid leukaemia: How much can we learn from MDR-CML cell lines?

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