
LINC01503, which is transcriptionally regulated by histone acetylation, promotes angiogenesis in colorectal cancer (CRC) by inducing the expression of VEGFA through both the miR-342-3p/VEGFA and hsp60/VEGFA signaling pathways.
Figures of the Article
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LINC01503 was specifically overexpressed in colorectal cancer (CRC) tissues and was associated with a poor prognosis.
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LINC01503 promoted cell proliferation and invasion in vitro.
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LINC01503 promoted cell proliferation and invasion in vivo.
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LINC01503 promoted the proliferation and migration of vascular endothelial cells.
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LINC01503 induced vascular endothelial growth factor A (VEGFA) expression and secretion.
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LINC01503 promoted VEGFA expression by binding to miR-342-3p.
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LINC01503 enhanced the protein stability of VEGFA by binding to HSP60.
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LINC01503 was transcriptionally activated by histone H3 lysine 27 (H3K27) acetylation.
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LINC01503, which is transcriptionally regulated by histone acetylation, promotes angiogenesis in colorectal cancer (CRC) by inducing the expression of VEGFA through both the miR-342-3p/VEGFA and hsp60/VEGFA signaling pathways.
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