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. 2023 Feb 17;11(6):252. doi: 10.21037/atm-22-6346

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2023 Annals of Translational Medicine. All rights reserved.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0.

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CircRBM33 may regulate resistance to osimertinib in H1975-OR cells through DNMT1/IL-6 axis. Sh-circRBM33 and sh-PLVX cells were transcriptome sequenced and all differentially expressed genes were obtained after analysis, respectively. (A,B) Showing the results of GO and KEGG enrichment of all differentially expressed genes. (C) The red part shows the proteins that interacted with circRBM33 in the mass spectrometry result, and the blue part shows the key genes associated with EGFR-TKI resistance obtained by RNA-seq after knocking down circRBM33 in H1975-OR cells. The link between the two parts of the results is shown by the Cytoscape visualization network. H1975-OR, H1975 osimertinib-resistant; GO, Gene Ontology; BP, biological process; MF, molecular function; KEGG, Kyoto Encyclopedia of Genes and Genomes; EGFR-TKI, epidermal growth factor receptor tyrosine kinase inhibitors.