多叶皂苷B (PPB) 是一种具有抗肿瘤作用的化合物。核剪纸组装转录本1 (NEAT1) 是一种长链非编码RNA，能诱导肿瘤细胞的上皮间质转化 (EMT)，促进肿瘤生长和转移。然而，PPB在黑色素瘤中的作用和机制以及它们之间的相关性仍不清楚。本研究利用LncRNA转录组测序筛选了NEAT1，再使用OVER-NEAT1慢病毒转染B16F10细胞。接下来，通过MTT实验和建立小鼠皮下移植瘤模型，我们发现PPB能显著抑制黑色素瘤和B16F10细胞的增殖；此外，通过伤口愈合实验、Transwell实验和建立小鼠黑色素瘤肺转移模型，我们发现PPB显著抑制B16F10细胞在体外的侵袭和迁移，并且抑制黑色素瘤向肺、骨和肝转移。最后，通过免疫印迹和免疫组化检测EMT相关蛋白的表达水平，发现PPB显著下调了MMP-9、N-粘附素等蛋白的表达水平，并上调了E-粘附素的表达。而过表达的NEAT1显示出促进黑色素瘤增殖、迁移和侵袭的能力，除此之外，还部分逆转了PPB抑制黑色素瘤增殖、迁移和侵袭的作用。© 2023。作者(也就是我)已授予Springer-Verlag GmbH Germany独家许可，属于Springer Nature的一部分。

Polyphyllin B (PPB) is a compound with anti-tumor effects. Nuclear paraspeckle assembly transcript 1 (NEAT1) is a long-stranded noncoding RNA that induces epithelial-mesenchymal transition (EMT) of tumor cells and promotes tumor growth and metastasis. However, the role and mechanism of PPB on melanoma and the correlation between them remain unclear. In this study we screened NEAT1 by using LncRNA transcriptomic sequencing, and then transfected B16F10 cells using OVER-NEAT1 lentivirus. Next, we found that PPB had significant proliferation inhibition of melanoma and B16F10 cells through MTT assay and establishment of mouse subcutaneous transplantation tumor model; in addition, through wound healing assay, transwell assay and establishment of mouse melanoma lung metastasis model, we found that PPB significantly inhibited the invasion and migration of B16F10 cells in vitro, and inhibited the metastasis of melanoma to lung, bone and liver in vivo. Finally, changes in the expression levels of EMT-related proteins were assessed by western blot (WB) and immunohistochemistry, and PPB significantly downregulated the expression levels of MMP-9, N-cadherin, etc., and upregulated E-cadherin. While overexpressed NEAT1 showed the ability to promote melanoma proliferation, migration and invasion, in addition to partially reversed the inhibition of proliferation, migration and invasion of melanoma by PPB mentioned above.© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.