Pancreatic carcinoma (PC) is one of the most common and deadly human malignancies worldwide. LncRNAs play significant roles in the occurrence and development of various cancers. LncRNA SNHG11 (SNHG11) has been found to display high expression in serum of PC patients, which implies that dysregulated SNHG11 may be related to the development of PC. However, there is still a knowledge gap concerning the specific function and molecular mechanism of SNHG11 in PC. After conducting experiments with constructed models in vitro or in vivo, we found that exosomal SNHG11 promoted cell proliferation, migration, and angiogenesis but impeded cell apoptosis in PC in vitro, and additionally, it facilitated tumor growth in vivo. Exosome-mediated SNHG11 regulated the expression of VEGFA through sponging miR-324-3p. Rescue assays validated that the inhibitory effect of SNHG11 depletion on cell proliferation, migration, and angiogenesis could be reversed by miR-324-3p downregulation or VEGFA upregulation, and the promoting effect of SNHG11 silence on cell apoptosis could be rescued by transfection of miR-324-3p inhibitor or pcDNA3.1-VEGFA. To conclude, exosomal-mediated SNHG11 could regulate PC progression via miR-324-3p/VEGFA axis. Our findings may provide a novel insight for understanding PC, which might contribute to the development of potential PC biomarker.

中文翻译：

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外泌体介导的lncRNA SNHG11通过miR-324-3p/VEGFA轴调节胰腺癌的血管生成


胰腺癌（PC）是全世界最常见、最致命的人类恶性肿瘤之一。 LncRNA在多种癌症的发生和发展中发挥着重要作用。 LncRNA SNHG11 (SNHG11)被发现在PC患者血清中高表达，这表明SNHG11失调可能与PC的发生有关。然而，对于SNHG11在PC中的具体功能和分子机制仍存在知识空白。在对构建的模型进行体外或体内实验后，我们发现外泌体SNHG11在体外促进PC细胞增殖、迁移和血管生成，但阻碍细胞凋亡，此外，它在体内促进肿瘤生长。外泌体介导的 SNHG11 通过海绵 miR-324-3p 调节 VEGFA 的表达。救援实验证实，SNHG11 缺失对细胞增殖、迁移和血管生成的抑制作用可以通过 miR-324-3p 下调或 VEGFA 上调来逆转，而 SNHG11 沉默对细胞凋亡的促进作用可以通过转染 miR-324-3p 来逆转。 324-3p抑制剂或pcDNA3.1-VEGFA。总之，外泌体介导的 SNHG11 可以通过 miR-324-3p/VEGFA 轴调节 PC 进展。我们的研究结果可能为理解 PC 提供新的见解，这可能有助于潜在 PC 生物标志物的开发。