PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
27690301-0	2016	MiR-128 reverses the gefitinib resistance of the lung cancer stem cells by inhibiting the c-met/PI3K/AKT pathway.	mir-128	0-7	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	90-95	
27690301-7	2016	In addition, the gene of c-met was proved to be directly inhibited by miR-128.	mir-128	70-77	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	25-30	
27690301-8	2016	Enforced expression of c-met could "rescue" the miR-128 promoted apoptosis and cleavage of caspases in PC9-CSCs treated with gefitinib.	mir-128	48-55	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	23-28	
34553041-6	2021	In addition, BMI-1, ABCC-5, E2F3, and c-MET were identified as candidate targets of miR-128, and the overexpression of miR-128 significantly reduced mRNA/protein levels of BMI-1, ABCC-5, E2F3, and c-MET in A549 and H460 cells.	mir-128	84-91	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	38-43	
34553041-6	2021	In addition, BMI-1, ABCC-5, E2F3, and c-MET were identified as candidate targets of miR-128, and the overexpression of miR-128 significantly reduced mRNA/protein levels of BMI-1, ABCC-5, E2F3, and c-MET in A549 and H460 cells.	mir-128	84-91	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	197-202	
35252056-13	2022	Conclusion: The present results indicate that the miR-128-3p/c-Met axis may be potential therapeutic targets for circumventing lenvatinib resistance in HCC and warrant further investigation.	mir-128	50-57	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	61-66	
28928797-5	2017	A luciferase assay was applied to assess the binding of miR-128 to c-Met mRNA.	mir-128	56-63	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	67-72	
28928797-8	2017	Similarly, miR-128 expression in primary cardiomyocytes cultured under deprivation of oxygen and glucose increased with the culture time and reached a peak at 12 h. c-Met expression decreased significantly (P<0.05) and the ratio of apoptotic cells increased significantly (P<0.05), following transfection of miR-128 mimics.	mir-128	314-321	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	165-170	
28928797-10	2017	The dual luciferase assay indicated that fluorescence intensity decreased significantly in miR-128 mimics and wild type c-Met group (P<0.05), indicating that miR-128 can directly target c-Met.	mir-128	91-98	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	189-194	
28928797-10	2017	The dual luciferase assay indicated that fluorescence intensity decreased significantly in miR-128 mimics and wild type c-Met group (P<0.05), indicating that miR-128 can directly target c-Met.	mir-128	161-168	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	120-125	
28928797-10	2017	The dual luciferase assay indicated that fluorescence intensity decreased significantly in miR-128 mimics and wild type c-Met group (P<0.05), indicating that miR-128 can directly target c-Met.	mir-128	161-168	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	189-194	
28928797-11	2017	Therefore, the results of the current study suggest that miR-128 may promote myocardial cell injury by regulating c-Met expression.	mir-128	57-64	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	114-119