FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W3085386072> ?p ?o ?g. }

• W3085386072 endingPage "483" @default.
• W3085386072 startingPage "471" @default.
• W3085386072 abstract "Although patients with non-small cell lung cancer harboring activating mutations in the epidermal growth factor receptor (EGFR) show good clinical response to EGFR tyrosine kinase inhibitors (TKIs), patients eventually develop acquired resistance. Previous studies have shown that several microRNAs (miRNAs) are involved in EGFR TKI resistance. Here, we aimed to investigate whether miR-146b-5p sensitizes the EGFR TKI-resistant lung cancer cells. Clinical analysis showed that miR-146b-5p expression in lung cancer cells isolated from pleural effusions of treatment-naive patients was significantly higher than that after acquiring resistance to EGFR TKI treatment. Ectopic expression of miR-146b-5p in EGFR TKI-resistant cells enhanced EGFR TKI-induced apoptosis. The same results were observed in EGFR-dependent and -independent osimertinib-resistant primary cancer cells (PE3479 and PE2988). Mechanically, miR-146b-5p suppressed nuclear factor κB (NF-κB) activity and NF-κB-related IL-6 and IL-8 production by targeting IRAK1. A negative correlation was observed between miR-146b-5p and IRAK1 in clinical specimens. In rescue experiments, restoration of IRAK1 expression reversed the effects of miR-146b-5p on EGFR TKI sensitivity and recovered NF-κB-regulated IL-6 and IL-8 production. In conclusion, miR-146b-5p/IRAK1/NF-κB signaling is important in promoting EGFR TKI resistance, and miR-146b-5p may be a useful tool for overcoming EGFR TKI resistance. Although patients with non-small cell lung cancer harboring activating mutations in the epidermal growth factor receptor (EGFR) show good clinical response to EGFR tyrosine kinase inhibitors (TKIs), patients eventually develop acquired resistance. Previous studies have shown that several microRNAs (miRNAs) are involved in EGFR TKI resistance. Here, we aimed to investigate whether miR-146b-5p sensitizes the EGFR TKI-resistant lung cancer cells. Clinical analysis showed that miR-146b-5p expression in lung cancer cells isolated from pleural effusions of treatment-naive patients was significantly higher than that after acquiring resistance to EGFR TKI treatment. Ectopic expression of miR-146b-5p in EGFR TKI-resistant cells enhanced EGFR TKI-induced apoptosis. The same results were observed in EGFR-dependent and -independent osimertinib-resistant primary cancer cells (PE3479 and PE2988). Mechanically, miR-146b-5p suppressed nuclear factor κB (NF-κB) activity and NF-κB-related IL-6 and IL-8 production by targeting IRAK1. A negative correlation was observed between miR-146b-5p and IRAK1 in clinical specimens. In rescue experiments, restoration of IRAK1 expression reversed the effects of miR-146b-5p on EGFR TKI sensitivity and recovered NF-κB-regulated IL-6 and IL-8 production. In conclusion, miR-146b-5p/IRAK1/NF-κB signaling is important in promoting EGFR TKI resistance, and miR-146b-5p may be a useful tool for overcoming EGFR TKI resistance." @default.
• W3085386072 created "2020-09-21" @default.
• W3085386072 creator A5009000893 @default.
• W3085386072 creator A5024780507 @default.
• W3085386072 creator A5036843957 @default.
• W3085386072 creator A5041294713 @default.
• W3085386072 creator A5048965137 @default.
• W3085386072 creator A5067347318 @default.
• W3085386072 creator A5072569999 @default.
• W3085386072 creator A5090446534 @default.
• W3085386072 date "2020-12-01" @default.
• W3085386072 modified "2023-10-18" @default.
• W3085386072 title "miR-146b-5p Enhances the Sensitivity of NSCLC to EGFR Tyrosine Kinase Inhibitors by Regulating the IRAK1/NF-κB Pathway" @default.
• W3085386072 cites W1489240871 @default.
• W3085386072 cites W1594203091 @default.
• W3085386072 cites W1648301895 @default.
• W3085386072 cites W1685156615 @default.
• W3085386072 cites W1753659383 @default.
• W3085386072 cites W1831549537 @default.
• W3085386072 cites W1917389599 @default.
• W3085386072 cites W1967394241 @default.
• W3085386072 cites W1985538305 @default.
• W3085386072 cites W1996869482 @default.
• W3085386072 cites W2012942268 @default.
• W3085386072 cites W2013995112 @default.
• W3085386072 cites W2027744584 @default.
• W3085386072 cites W2028950794 @default.
• W3085386072 cites W2040575339 @default.
• W3085386072 cites W2044246917 @default.
• W3085386072 cites W2047146433 @default.
• W3085386072 cites W2051224169 @default.
• W3085386072 cites W2059862833 @default.
• W3085386072 cites W2066027374 @default.
• W3085386072 cites W2071011329 @default.
• W3085386072 cites W2087955215 @default.
• W3085386072 cites W2096639900 @default.
• W3085386072 cites W2099099087 @default.
• W3085386072 cites W2099354673 @default.
• W3085386072 cites W2105493915 @default.
• W3085386072 cites W2109597203 @default.
• W3085386072 cites W2141903666 @default.
• W3085386072 cites W2146625800 @default.
• W3085386072 cites W2171488801 @default.
• W3085386072 cites W2188371844 @default.
• W3085386072 cites W2235523093 @default.
• W3085386072 cites W2260138955 @default.
• W3085386072 cites W2288686633 @default.
• W3085386072 cites W2590032828 @default.
• W3085386072 cites W2624019929 @default.
• W3085386072 cites W2724633001 @default.
• W3085386072 cites W2736048163 @default.
• W3085386072 cites W2747965175 @default.
• W3085386072 cites W2754970987 @default.
• W3085386072 cites W2778885300 @default.
• W3085386072 cites W2783677708 @default.
• W3085386072 cites W2792821195 @default.
• W3085386072 cites W2795708883 @default.
• W3085386072 cites W2799866623 @default.
• W3085386072 cites W2802402246 @default.
• W3085386072 cites W2885224353 @default.
• W3085386072 cites W2887298079 @default.
• W3085386072 cites W2891909134 @default.
• W3085386072 cites W2902539135 @default.
• W3085386072 cites W2910933849 @default.
• W3085386072 cites W2911188881 @default.
• W3085386072 cites W2922022182 @default.
• W3085386072 cites W2946572522 @default.
• W3085386072 cites W2948846381 @default.
• W3085386072 doi "https://doi.org/10.1016/j.omtn.2020.09.015" @default.
• W3085386072 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7554328" @default.
• W3085386072 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/33230450" @default.
• W3085386072 hasPublicationYear "2020" @default.
• W3085386072 type Work @default.
• W3085386072 sameAs 3085386072 @default.
• W3085386072 citedByCount "26" @default.
• W3085386072 countsByYear W30853860722021 @default.
• W3085386072 countsByYear W30853860722022 @default.
• W3085386072 countsByYear W30853860722023 @default.
• W3085386072 crossrefType "journal-article" @default.
• W3085386072 hasAuthorship W3085386072A5009000893 @default.
• W3085386072 hasAuthorship W3085386072A5024780507 @default.
• W3085386072 hasAuthorship W3085386072A5036843957 @default.
• W3085386072 hasAuthorship W3085386072A5041294713 @default.
• W3085386072 hasAuthorship W3085386072A5048965137 @default.
• W3085386072 hasAuthorship W3085386072A5067347318 @default.
• W3085386072 hasAuthorship W3085386072A5072569999 @default.
• W3085386072 hasAuthorship W3085386072A5090446534 @default.
• W3085386072 hasBestOaLocation W30853860721 @default.
• W3085386072 hasConcept C104317684 @default.
• W3085386072 hasConcept C121608353 @default.
• W3085386072 hasConcept C126322002 @default.
• W3085386072 hasConcept C145059251 @default.
• W3085386072 hasConcept C170493617 @default.
• W3085386072 hasConcept C184235292 @default.
• W3085386072 hasConcept C190283241 @default.
• W3085386072 hasConcept C2776256026 @default.
• W3085386072 hasConcept C2777626846 @default.
• W3085386072 hasConcept C2778087573 @default.

• next