PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
30946555-4	2019	METHODS: NEAT1 expression was determined in either sensitive, or sorafenib, or doxorubicin resistant HepG2, PLC/PRF/5, and Huh7 cells by qPCR.	Sorafenib	65-74	nuclear paraspeckle assembly transcript 1	Homo sapiens	9-14	
32461380-0	2020	LncRNA NEAT1 modulates sorafenib resistance in hepatocellular carcinoma through regulating the miR-149-5p/AKT1 axis.	Sorafenib	23-32	nuclear paraspeckle assembly transcript 1	Homo sapiens	7-12	
32461380-1	2020	Background/Aims: The purpose of this study is to explore the expression characteristics of lncRNA NEAT1 in hepatocellular carcinoma (HCC) and the molecular mechanism of its regulation on sorafenib resistance.	Sorafenib	187-196	nuclear paraspeckle assembly transcript 1	Homo sapiens	98-103	
32461380-9	2020	Furthermore, NEAT1 expressions were significantly associated with HCC prognosis and chemoresistance patterns against sorafenib.	Sorafenib	117-126	nuclear paraspeckle assembly transcript 1	Homo sapiens	13-18	
32461380-11	2020	NEAT1 targets the miR-149-5p, and therefore, decrease the activity of sorafenib against HCC cells.	Sorafenib	70-79	nuclear paraspeckle assembly transcript 1	Homo sapiens	0-5	
30946555-8	2019	RESULTS: NEAT1 was overexpressed in all three sorafenib and doxorubicin resistant cell lines.	Sorafenib	46-55	nuclear paraspeckle assembly transcript 1	Homo sapiens	9-14	
28968960-6	2017	Down-regulation of NEAT1 increased the sensitivity of RCC cells to sorafenib in vitro.	Sorafenib	67-76	nuclear paraspeckle assembly transcript 1	Homo sapiens	19-24	
34076978-0	2021	Long noncoding RNA NEAT1 aggravates sorafenib-resistance in non-small cell lung cancer via regulating miRNA-335/c-Met.	Sorafenib	36-45	nuclear paraspeckle assembly transcript 1	Homo sapiens	19-24	
34076978-1	2021	PURPOSE: The purpose of this study was to illustrate the role of long non-coding RNA (lncRNA) NEAT1 in inhibiting sorafenib sensitivity in non-small cell lung cancer (NSCLC) through targeting microRNA-335 (miR-335)/c-Met axis.	Sorafenib	114-123	nuclear paraspeckle assembly transcript 1	Homo sapiens	94-99	
34076978-2	2021	METHODS: Regulatory effects of NEAT1/miR-335/c-Met axis on proliferative ability of sorafenib-induced A549 and PC9 cells were assessed by cell counting kit-8 (CCK-8) and colony formation assay.	Sorafenib	84-93	nuclear paraspeckle assembly transcript 1	Homo sapiens	31-36	
34076978-3	2021	Apoptosis changes influenced by nuclear paraspeckle assembly transcript 1 (NEAT1)/miR-335/c-Met axis after sorafenib treatment in lung cancer cells were examined by detecting apoptotic rate, as well as relative levels of Bcl-2 and Bax.	Sorafenib	107-116	nuclear paraspeckle assembly transcript 1	Homo sapiens	75-80	
34076978-5	2021	RESULTS: Sorafenib treatment in A549 cells and PC9 cells attenuated the proliferation and induced apoptosis, which were more pronounced after silencing of NEAT1.	Sorafenib	9-18	nuclear paraspeckle assembly transcript 1	Homo sapiens	155-160	
34076978-8	2021	Rescue experiments verified the role of NEAT1/ MiR-335/c-Met regulatory loop in reducing the proliferative ability and inducing apoptosis of sorafenib-treated lung cancer cells.	Sorafenib	141-150	nuclear paraspeckle assembly transcript 1	Homo sapiens	40-45	
34076978-9	2021	CONCLUSIONS: LncRNA NEAT1 aggravates sorafenib resistance in NSCLC through inhibiting MiR-335 to upregulate c-Met level, manifesting as attenuated proliferation and accelerated apoptosis.	Sorafenib	37-46	nuclear paraspeckle assembly transcript 1	Homo sapiens	20-25