PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
26384345-0	2015	Crizotinib induces autophagy through inhibition of the STAT3 pathway in multiple lung cancer cell lines.	Crizotinib	0-10	signal transducer and activator of transcription 3	Homo sapiens	55-60	
34657149-8	2022	Downstream signaling analysis showed that deletion of PTPN1 or PTPN2 induces resistance to crizotinib by hyperactivating SHP2, the MAPK and JAK/STAT pathways.	Crizotinib	91-101	signal transducer and activator of transcription 3	Homo sapiens	144-148	
29755689-11	2018	Rapamycin/crizotinib simultaneously inhibited mTORC1 (evidenced by S6 kinase and RPS6 dephosphorylation) and ALK signaling (ALK, AKT, STAT3 dephosphorylation), and crizotinib suppressed the adverse AKT activation induced by rapamycin.	Crizotinib	10-20	signal transducer and activator of transcription 3	Homo sapiens	134-139	
33887553-6	2021	Crizotinib effectively decreased viability, proliferation, growth, and the metastatic properties of the PDX tumor through downregulation of STAT3 signaling, but expression of PDGFRss was increased.	Crizotinib	0-10	signal transducer and activator of transcription 3	Homo sapiens	140-145	
32484926-7	2020	Signaling pathways required for crizotinib-induced apoptosis of autophagic cells were explored with flow cytometric analysis, Western blot analysis, short-hairpin RNA knockdown of autophagic proteins, and small-molecule inhibitors of STAT3 and BCL-2.	Crizotinib	32-42	signal transducer and activator of transcription 3	Homo sapiens	234-239	
32484926-10	2020	Crizotinib treatment of autophagic cancer cells further enhanced autophagy and induced autophagy-mediated apoptosis by decreasing phosphorylated STAT3 and BCL-2 signaling.	Crizotinib	0-10	signal transducer and activator of transcription 3	Homo sapiens	145-150	
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	signal transducer and activator of transcription 3	Homo sapiens	58-63	
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	signal transducer and activator of transcription 3	Homo sapiens	126-131	
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	signal transducer and activator of transcription 3	Homo sapiens	97-102	
29444468-4	2018	It also effectively attenuated the crizotinib-induced inhibition of EML4-ALK and its downstream molecules, STAT3 and ERK, and suppressed the inhibitory effects of crizotinib on EML4-ALK-mediated transformation in the focus formation assay.	Crizotinib	35-45	signal transducer and activator of transcription 3	Homo sapiens	107-112	
27753543-0	2016	STAT3-targeted treatment with silibinin overcomes the acquired resistance to crizotinib in ALK-rearranged lung cancer.	Crizotinib	77-87	signal transducer and activator of transcription 3	Homo sapiens	0-5	
27753543-3	2016	Taking advantage of the flavonolignan silibinin as a naturally occurring STAT3-targeted pharmacological inhibitor, we confirmed that STAT3 activation protects ALK-translocated NSCLC from crizotinib.	Crizotinib	187-197	signal transducer and activator of transcription 3	Homo sapiens	133-138	
27753543-4	2016	Accordingly, silibinin-induced inhibition of STAT3 worked synergistically with crizotinib to reverse acquired resistance and restore sensitivity in crizotinib-resistant cells.	Crizotinib	148-158	signal transducer and activator of transcription 3	Homo sapiens	45-50	
26384345-3	2015	In this study, we found that crizotinib induced a high level of autophagy in lung cancer cells through inhibition of STAT3.	Crizotinib	29-39	signal transducer and activator of transcription 3	Homo sapiens	117-122	
26384345-4	2015	Ectopic expression of wild-type or constitutive activated STAT3 significantly suppressed the effect of crizotinib on autophagy.	Crizotinib	103-113	signal transducer and activator of transcription 3	Homo sapiens	58-63	
26384345-5	2015	Interestingly, crizotinib-mediated inhibition of STAT3 is in a step-wise manner.	Crizotinib	15-25	signal transducer and activator of transcription 3	Homo sapiens	49-54	
26384345-9	2015	In conclusion, crizotinib can induce cytoprotective autophagy by suppression of STAT3 in lung cancer cells.	Crizotinib	15-25	signal transducer and activator of transcription 3	Homo sapiens	80-85	
24486291-7	2014	Crizotinib induced marked downregulation of STAT3 phosphorylation, which was associated with significant apoptotic cell death.	Crizotinib	0-10	signal transducer and activator of transcription 3	Homo sapiens	44-49