AI Article Synopsis
- Long intergenic noncoding RNAs (lincRNAs), particularly linc-ROR, are found to be overexpressed in nasopharyngeal carcinoma (NPC) and are linked to tumor growth.
- The study reveals that linc-ROR increases cell proliferation, migration, and angiogenesis in experiments using human umbilical vein endothelial cells (HUVECs) and the zebrafish model.
- The effects of linc-ROR on angiogenesis are mediated through the p-AKT/p-VEGFR2 signaling pathway, suggesting it could be a potential therapeutic target in treating NPC.
Article Abstract
Long intergenic noncoding RNAs (lincRNAs) are expressed aberrantly in several malignancies, including nasopharyngeal carcinoma (NPC), where linc-ROR expression was found to be elevated. Being a hallmark of malignant tumors, angiogenesis has prompted us to investigate the impact of linc-ROR on NPC angiogenesis. This study demonstrates that linc-ROR is substantially expressed in serum exosomes from NPC and can be taken up by HUVECs. Using qRT-PCR, the CCK8 test, the transwell migration assay, the wound healing assay, and the tube formation assay, we demonstrated that linc-ROR increases proliferation, migration, and angiogenesis in vitro. Similar to prior research, our results have shown that linc-ROR can stimulate tumor angiogenesis in the zebrafish model. Thus, the p-AKT/p-VEGFR2 pathway is the mechanism by which linc-ROR affects the aforementioned biological activities. By stimulating angiogenesis, linc-ROR appears to play a significant role in the course of NPC and could account for a therapeutic target.
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| http://dx.doi.org/10.1016/j.mcp.2022.101868 | DOI Listing |
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