LINC00460 promotes angiogenesis by enhancing NF-κB-mediated VEGFA expression in cervical cancer cells

Angiogenesis is a characteristic of tumor development and is key for tumor growth and metastasis. LINC00460 is a long non-coding RNA that plays important yet complex roles in cancer development and progression. Here, we explored the functional mechanism of action of LINC00460 in cervical cancer (CC) angiogenesis for the first time. We found that conditioned medium (CM) from LINC00460-knockdown CC cells attenuated human umbilical vein endothelial cell (HUVEC) migration, invasion, and tube formation, whereas LINC00460 upregulation had the opposite effects. Mechanistically, LINC00460 stimulated VEGFA transcription. Suppressing VEGF-A reversed the effects of CM from LINC00460-overexpressing CC cells on HUVEC angiogenesis. Recombinant VEGFA eliminated the suppressive effects of CM from LINC00460-knockdown CC cells. Furthermore, LINC00460 enhanced VEGFA expression and promoted angiogenesis by activating the NF-κB pathway. Our data illustrate that LINC00460 can promote angiogenesis by activating the NF-κB–VEGFA axis, suggesting that the axis is a promising target for blocking tumor angiogenesis. •LINC00460 promoted angiogenesis in vitro•LINC00460 promoted VEGFA expression in CC cells.•LINC00460 promoted VEGFA expression and angiogenesis via the NF-κB pathway in CC cells.