PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
33167678-11	2020	We identified that copy number amplification significantly contributes to the high level of PVT1 transcripts in lung cancer, which promotes cell proliferation and metastatic behavior via modulating VEGFC expression by endogenous competition with miR-128.	mir-128	246-253	Pvt1 oncogene	Homo sapiens	92-96	
33848670-13	2021	Knockdown of miR-128 restored the altered proliferation, migration and invasion and the expression of ZEB1 and E-cadherin caused by knockdown of PVT1.	mir-128	13-20	Pvt1 oncogene	Homo sapiens	145-149	
31173288-9	2019	Spearman"s correlation coefficient was adopted to evaluate the correlation between miR-128 and PVT1-214 levels.	mir-128	83-90	Pvt1 oncogene	Homo sapiens	95-99	
31173288-13	2019	Additionally, PVT1-214 functions as a competing endogenous RNA (ceRNA) by binding to miR-128.	mir-128	85-92	Pvt1 oncogene	Homo sapiens	14-18	
31173288-15	2019	CONCLUSIONS: PVT1-214-induced miR-128 repression regulates TrkC to further the progression of GC, indicating that this process will provide a promising therapeutic target in GC.	mir-128	30-37	Pvt1 oncogene	Homo sapiens	13-17	
30076714-0	2019	LncRNA PVT1 regulates VEGFC through inhibiting miR-128 in bladder cancer cells.	mir-128	47-54	Pvt1 oncogene	Homo sapiens	7-11	
30076414-0	2019	Long noncoding RNA PVT1-214 promotes proliferation and invasion of colorectal cancer by stabilizing Lin28 and interacting with miR-128.	mir-128	127-134	Pvt1 oncogene	Homo sapiens	19-23