Title : 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.

Pub. Date : 2021 Nov 8

PMID : 34643375






5 Functional Relationships(s)
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1 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 cholesterol 25-hydroxylase Homo sapiens
2 Identification of the interaction between LINC01915, miR-92a-3p, KLF4, and CH25H was done. linc01915 cholesterol 25-hydroxylase Homo sapiens
3 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 cholesterol 25-hydroxylase Homo sapiens
4 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 cholesterol 25-hydroxylase Homo sapiens
5 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 cholesterol 25-hydroxylase Homo sapiens