PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
34643375-0	2021	LINC01915 Facilitates the Conversion of Normal Fibroblasts into Cancer-Associated Fibroblasts Induced by Colorectal Cancer-Derived Extracellular Vesicles through the miR-92a-3p/KLF4/CH25H Axis.	linc01915	0-9	cholesterol 25-hydroxylase	Homo sapiens	182-187	
34643375-3	2021	Identification of the interaction between LINC01915, miR-92a-3p, KLF4, and CH25H was done.	linc01915	42-51	cholesterol 25-hydroxylase	Homo sapiens	75-80	
34643375-9	2021	Mechanistically, LINC01915 could competitively bind to miR-92a-3p and caused upregulation of the miR-92a-3p target KLF4 which, in turn, promoted the transcription of CH25H, leading to the suppressed uptake of EVs by NFs.	linc01915	17-26	cholesterol 25-hydroxylase	Homo sapiens	166-171	
34643375-10	2021	The in vivo and in vitro experimental results showed that LINC01915 inhibited the uptake of CRC-derived EVs by NFs through the miR-92a-3p/KLF4/CH25H axis, thus arresting the angiogenesis and the conversion of NFs into CAFs and in turn prevent tumor growth.	linc01915	58-67	cholesterol 25-hydroxylase	Homo sapiens	143-148	
34643375-11	2021	These data together supported the inhibiting role of LINC01915 in the conversion of NFs into CAFs triggered by the CRC-derived EVs and the ensuing tumor growth, which may be related to its regulation on the miR-92a-3p/KLF4/CH25H axis.	linc01915	53-62	cholesterol 25-hydroxylase	Homo sapiens	223-228