PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
33378036-9	2020	Under the induction of increased doses of glucose, UCA1 stimulated proliferative and invasive abilities in VSMCs.	Glucose	42-49	urothelial cancer associated 1	Homo sapiens	51-55	
24890811-6	2014	Taken together, these findings provide the first evidence that UCA1 plays a positive role in cancer cell glucose metabolism through the cascade of mTOR-STAT3/microRNA143-HK2, and reveal a novel link between lncRNA and the altered glucose metabolism in cancer cells.	Glucose	105-112	urothelial cancer associated 1	Homo sapiens	63-67	
33204264-10	2020	Further research showed that upregulated UCA1 effectively increased the rate of glucose uptake, lactate output, and ECAR value, all of which can be attenuate by HK2 interference and 2-DG, whereas knockdown of UCA1 had the opposite effect.	Glucose	80-87	urothelial cancer associated 1	Homo sapiens	41-45	
34137197-0	2021	Long noncoding RNA UCA1 promotes high glucose-induced human retinal endothelial cells angiogenesis via regulating miR-624-3p/VEGF-C.	Glucose	38-45	urothelial cancer associated 1	Homo sapiens	19-23	
34137197-6	2021	RESULTS: UCA1 and VEGF-C was elevated in DR patients and high glucose-induced HRECs cell lines, while miR-624-3p was decreased.	Glucose	62-69	urothelial cancer associated 1	Homo sapiens	9-13	
34137197-7	2021	UCA1 inhibition inhibited proliferation, angiogenesis and migration of HRECs cells under high glucose condition.	Glucose	94-101	urothelial cancer associated 1	Homo sapiens	0-4	
34137197-9	2021	Finally, we proved a pathway that UCA1 promoted cell proliferation, migration and angiogenesis through sponging with miR-624-3p thereby upregulating VEGF-C in high glucose-induced HRECs.	Glucose	164-171	urothelial cancer associated 1	Homo sapiens	34-38