PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 26166037-0 2015 Homoharringtonine induces apoptosis and inhibits STAT3 via IL-6/JAK1/STAT3 signal pathway in Gefitinib-resistant lung cancer cells. Gefitinib 93-102 interleukin 6 Homo sapiens 59-63 25760537-5 2015 Pre-treatment with IL-6 enhanced the cytotoxic effects of gefitinib and paclitaxel. Gefitinib 58-67 interleukin 6 Homo sapiens 19-23 31507089-0 2019 Reciprocal regulation of miR-206 and IL-6/STAT3 pathway mediates IL6-induced gefitinib resistance in EGFR-mutant lung cancer cells. Gefitinib 77-86 interleukin 6 Homo sapiens 37-41 33416163-7 2021 Furthermore, addition of IL-6 to ZA-pretreated gefitinib-resistant cell lines abrogated the effect of ZA and restored the cellular resistance to tyrosine kinase inhibitors. Gefitinib 47-56 interleukin 6 Homo sapiens 25-29 32441799-9 2020 In addition, silencing the expression of CYLD resulted in increase of the expression level of IL-6, TGF-beta and TNF-alpha, which may contribute to acquired resistance of PC-9 cells to gefitinib. Gefitinib 185-194 interleukin 6 Homo sapiens 94-98 34693451-5 2021 However, gefitinib treatment results in the feedback activation of signal transducer and activator of transcription 3 (STAT3) induced by interleukin 6 (IL-6) secretion. Gefitinib 9-18 interleukin 6 Homo sapiens 137-150 34693451-5 2021 However, gefitinib treatment results in the feedback activation of signal transducer and activator of transcription 3 (STAT3) induced by interleukin 6 (IL-6) secretion. Gefitinib 9-18 interleukin 6 Homo sapiens 152-156 34693451-7 2021 Western blot analysis demonstrates that stattic treatment in gefitinib-treated OS abrogates the IL-6-induced STAT3 activation and subsequently further restrains the activities of EGFR, Akt, and ERK pathways in tumor cells. Gefitinib 61-70 interleukin 6 Homo sapiens 96-100 34693451-8 2021 This study confirms that the EGFR inhibitor of gefitinib has moderate anti-tumor effects on OS through IL-6 secretion-mediated STAT3 activation. Gefitinib 47-56 interleukin 6 Homo sapiens 103-107 31507089-0 2019 Reciprocal regulation of miR-206 and IL-6/STAT3 pathway mediates IL6-induced gefitinib resistance in EGFR-mutant lung cancer cells. Gefitinib 77-86 interleukin 6 Homo sapiens 65-68 31507089-3 2019 However, whether miR-206 may overcome IL6-induced gefitinib resistance in EGFR-mutant lung cancer remains elusive. Gefitinib 50-59 interleukin 6 Homo sapiens 38-41 31507089-4 2019 In this study, we investigated the role of miR-206 in IL6-induced gefitinib-resistant EGFR-mutated lung cancer cell lines. Gefitinib 66-75 interleukin 6 Homo sapiens 54-57 31507089-5 2019 We showed that forced miR-206 expression restored gefitinib sensitivity in IL6-induced gefitinib-resistant EGFR-mutant lung cancer cells by inhibiting IL6/JAK1/STAT3 pathway. Gefitinib 50-59 interleukin 6 Homo sapiens 75-78 31507089-5 2019 We showed that forced miR-206 expression restored gefitinib sensitivity in IL6-induced gefitinib-resistant EGFR-mutant lung cancer cells by inhibiting IL6/JAK1/STAT3 pathway. Gefitinib 50-59 interleukin 6 Homo sapiens 151-154 31507089-5 2019 We showed that forced miR-206 expression restored gefitinib sensitivity in IL6-induced gefitinib-resistant EGFR-mutant lung cancer cells by inhibiting IL6/JAK1/STAT3 pathway. Gefitinib 87-96 interleukin 6 Homo sapiens 75-78 31507089-5 2019 We showed that forced miR-206 expression restored gefitinib sensitivity in IL6-induced gefitinib-resistant EGFR-mutant lung cancer cells by inhibiting IL6/JAK1/STAT3 pathway. Gefitinib 87-96 interleukin 6 Homo sapiens 151-154 31507089-8 2019 Taken together, our findings reveal a direct role of miR-206 in regulating IL-6/STAT3 pathway and contrarily activated IL-6/STAT3 signalling mediates the miR-206 maturation process in gefitinib-resistant EGFR-mutant lung cancer cells. Gefitinib 184-193 interleukin 6 Homo sapiens 119-123 28927099-0 2017 Interleukin-6 identified as an important factor in hypoxia- and aldehyde dehydrogenase-based gefitinib adaptive resistance in non-small cell lung cancer cells. Gefitinib 93-102 interleukin 6 Homo sapiens 0-13 31523190-10 2019 Meanwhile IL-6 induced gefitinib resistance and increased migration. Gefitinib 23-32 interleukin 6 Homo sapiens 10-14 29789542-6 2018 We identified that the ERK reactivation occurs via the function of cytokines, such as IL-6, whose expression is transcriptionally induced in a gefitinib-dependent manner by RNF25-mediated NF-kappaB signals. Gefitinib 143-152 interleukin 6 Homo sapiens 86-90 28927099-6 2017 RNA-seq analysis revealed that interleukin-6 (IL-6) is an important common factor in hypoxia and ALDH-based gefitinib resistance, supported by inflammation-associated tumor necrosis factor, nuclear factor-kappaB and Janus kinase-signal transducer and activator of transcription signaling pathway enrichment. Gefitinib 108-117 interleukin 6 Homo sapiens 31-44 28927099-6 2017 RNA-seq analysis revealed that interleukin-6 (IL-6) is an important common factor in hypoxia and ALDH-based gefitinib resistance, supported by inflammation-associated tumor necrosis factor, nuclear factor-kappaB and Janus kinase-signal transducer and activator of transcription signaling pathway enrichment. Gefitinib 108-117 interleukin 6 Homo sapiens 46-50 28927099-7 2017 Furthermore, exposure of PC9 and HCC827 cells to IL-6 increased gefitinib adaptive resistance. Gefitinib 64-73 interleukin 6 Homo sapiens 49-53 28115165-5 2017 We found that IL-6 signaling via phosphorylated Stat3 induced gefitinib resistance as repressing transcription of Smad3, whereas TGF-beta enhanced gefitinib sensitivity as activating transcription of Smad3 in HCC827 cells with gefitinib-sensitizing EGFR mutation. Gefitinib 62-71 interleukin 6 Homo sapiens 14-18 28260924-7 2017 In addition, circulating interleukin (IL)-6 was significantly decreased, especially in patients sensitive to gefitinib (P<0.001). Gefitinib 109-118 interleukin 6 Homo sapiens 25-43