PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 30863492-7 2019 Conversely, addition of RTK ligands HGF and NRG1 induced cetuximab resistance in CC cells, which could be blocked by addition of crizotinib. Crizotinib 129-139 hepatocyte growth factor Homo sapiens 36-39 31280674-5 2019 Conclusion: Target compound 10b can be considered as a leading drug candidate due to its lower IC50 values than crizotinib in both HGF-induced proliferation and c-Met kinase inhibition assays. Crizotinib 112-122 hepatocyte growth factor Homo sapiens 131-134 33497758-2 2021 Agents targeting MET and its ligand hepatocyte growth factor (HGF) including small molecules such as crizotinib, tivantinib and cabozantinib or antibodies including rilotumumab and onartuzumab have proven their values in different tumors. Crizotinib 101-111 hepatocyte growth factor Homo sapiens 36-60 33497758-2 2021 Agents targeting MET and its ligand hepatocyte growth factor (HGF) including small molecules such as crizotinib, tivantinib and cabozantinib or antibodies including rilotumumab and onartuzumab have proven their values in different tumors. Crizotinib 101-111 hepatocyte growth factor Homo sapiens 62-65 32111984-6 2020 In addition, SOX13 was shown to be a direct target of HGF/STAT3 signaling, and the c-MET inhibitor crizotinib blocked the HGF/STAT3/SOX13/c-MET axis, significantly inhibiting SOX13-mediated CRC migration, invasion and metastasis. Crizotinib 99-109 hepatocyte growth factor Homo sapiens 54-57 32111984-6 2020 In addition, SOX13 was shown to be a direct target of HGF/STAT3 signaling, and the c-MET inhibitor crizotinib blocked the HGF/STAT3/SOX13/c-MET axis, significantly inhibiting SOX13-mediated CRC migration, invasion and metastasis. Crizotinib 99-109 hepatocyte growth factor Homo sapiens 122-125 32111984-9 2020 In summary, SOX13 is a promising prognostic biomarker in patients with CRC, and blocking the HGF/STAT3/SOX13/c-MET axis with crizotinib could be a new therapeutic strategy to prevent SOX13-mediated CRC metastasis. Crizotinib 125-135 hepatocyte growth factor Homo sapiens 93-96 30333869-10 2018 Application of HGF activated MET and the downstream AKT signaling pathways, decreased apoptotic events and restored cell proliferation, which were reversed by MET inhibition via crizotinib or siRNA knockdown. Crizotinib 178-188 hepatocyte growth factor Homo sapiens 15-18 30412912-14 2019 Additionally, crizotinib completely blocked HGF induced cell migration. Crizotinib 14-24 hepatocyte growth factor Homo sapiens 44-47 28819999-8 2017 HGF-independent Met phosphorylation was prevented by inhibition of integrin alpha5beta1, Met inhibitor crizotinib, Src inhibitors PP2 and SU5565, but not by EGFR inhibitor AG1478. Crizotinib 103-113 hepatocyte growth factor Homo sapiens 0-3 29125233-6 2017 Moreover, HGF stimulated the proliferation of NUGC4 cells, that was inhibited by crizotinib, which has anti-MET activity. Crizotinib 81-91 hepatocyte growth factor Homo sapiens 10-13 28075018-2 2017 Several approaches have been developed for targeting HGF and/or c-Met, and one of them, crizotinib (dual c-Met/ALK inhibitor), is recently been approved by FDA for lung-cancers with ALK-rearrangement. Crizotinib 88-98 hepatocyte growth factor Homo sapiens 53-56 28498406-9 2017 Taken together, crizotinib may be a potent drug for treating peritoneal dissemination of pancreatic cancer by inhibiting cancer cell proliferation and invasion, at least in part through the suppression of HGF/MET signaling and RhoA activation. Crizotinib 16-26 hepatocyte growth factor Homo sapiens 205-208 28474864-7 2017 A cell-based in vitro assay revealed that HGF/MET inhibition, induced either by MET inhibitors (crizotinib and golvatinib), or by siRNA-mediated knockdown of HGF or MET, constrained growth of chemoresistant SCLC cells through the inhibition of ERK and AKT signals. Crizotinib 96-106 hepatocyte growth factor Homo sapiens 42-45 24828661-6 2014 RESULTS: Crizotinib and TAS-115 inhibited Met phosphorylation and reversed erlotinib resistance and VEGF production triggered by HGF in PC-9 and HCC827 cells in vitro. Crizotinib 9-19 hepatocyte growth factor Homo sapiens 129-132 26345996-2 2015 EXPERIMENTAL DESIGN: Met TKI inhibitor PF-2341066 alone, or in combination with cisplatin, was investigated for its ability to block HGF-induced signaling and biological effects in vitro and in vivo. Crizotinib 39-49 hepatocyte growth factor Homo sapiens 133-136 25775951-7 2015 Higher HGF secretion activated Akt signaling pathway, which was reversed by HGF receptor inhibitor (crizotinib). Crizotinib 100-110 hepatocyte growth factor Homo sapiens 7-10 26496080-10 2015 The HGF-induced bypass of canertinib was reversed by addition of crizotinib. Crizotinib 65-75 hepatocyte growth factor Homo sapiens 4-7 24722154-3 2014 However, the deregulation of MET/HGF pathway in NSCLC harboring ALK gene rearrangement (ALK[+]), which is sensitive to dual ALK and MET inhibitor Crizotinib, has not been reported. Crizotinib 146-156 hepatocyte growth factor Homo sapiens 33-36 23962905-7 2013 In vivo, the combination therapy with crizotinib and gefitinib also markedly suppressed the growth of gefitinib-resistant mouse xenografts established by injecting HCC827 cells mixed with HGF-producing fibroblasts (MRC-5 cells) subcutaneously into severe combined immunodeficient mice. Crizotinib 38-48 hepatocyte growth factor Homo sapiens 188-191 23962905-8 2013 In conclusion, these findings provided preclinical evidence that crizotinib can be used in the treatment of HGF-induced resistance to gefitinib in EGFR mutant lung cancer. Crizotinib 65-75 hepatocyte growth factor Homo sapiens 108-111 24118504-9 2013 MET tyrosine kinase inhibitors, crizotinib and TAS-115, inhibited HGF-stimulated proliferation of NUGC4 and GCIY as well as constitutive proliferation of MKN45. Crizotinib 32-42 hepatocyte growth factor Homo sapiens 66-69 23962905-0 2013 Crizotinib overcomes hepatocyte growth factor-mediated resistance to gefitinib in EGFR-mutant non-small-cell lung cancer cells. Crizotinib 0-10 hepatocyte growth factor Homo sapiens 21-45 23962905-4 2013 Here, we tested whether crizotinib (PF02341066), a MET kinase inhibitor, can overcome two different HGF-triggered mechanisms of resistance to gefitinib in human EGFR mutant lung cancer cell lines HCC827 and PC-9. Crizotinib 24-34 hepatocyte growth factor Homo sapiens 100-103 23962905-5 2013 Compared with the monotherapy, the combined treatment of crizotinib and gefitinib induced apoptosis and significantly inhibited the growth of cells in the presence of HGF by blocking the MET/PI3K/Akt pathway. Crizotinib 57-67 hepatocyte growth factor Homo sapiens 167-170 23962905-6 2013 Further, we demonstrated that crizotinib plus gefitinib successfully prevented the emergence of gefitinib-resistant HCC827 cells induced by transient exposure to HGF. Crizotinib 30-40 hepatocyte growth factor Homo sapiens 162-165 22683780-6 2012 However, leukemic cells treated with the specific MET kinase inhibitor crizotinib developed resistance resulting from compensatory upregulation of HGF expression, leading to the restoration of MET signaling. Crizotinib 71-81 hepatocyte growth factor Homo sapiens 147-150