The antitumor activity of Momordica anti-human immunodeficiency virus protein of 30 kDa (MAP30) has been proved. However, the role of MAP30 on tumor metastasis has not yet been identified. For this purpose, we investigated this effect and underlying mechanism of MAP30 in bladder cancer (BC). Here, we reported that MAP30 significantly inhibited the cell proliferation and clone formation of 5637 and T24 cells in vitro by promoting apoptosis and cell cycle arrest. We also found MAP30 inhibited cell migration and invasion by suppressing the epithelial/mesenchymal transition (EMT) process. Moreover, the Affymetrix GeneChip assay revealed that MAP30 significantly changed gene expression profile in T24 cells, especially the genes in cell cycle regulation pathways. After the Ingenuity Pathway Analysis, we predicted that NUPR1 was the most important upstream regulator. Subsequently, we verified that the AKT and EMT signaling pathways were inhibited by MAP30 treatment in T24 cells. In conclusion, MAP30 treatment inhibited the progression of human BC, especially cell migration and invasion through suppressing AKT pathways.

中文翻译：

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MAP30通过抑制Akt途径和上皮/间充质转化过程抑制膀胱癌细胞的体外迁移和侵袭。

已经证明了30kDa的苦瓜抗人免疫缺陷病毒蛋白（MAP30）的抗肿瘤活性。然而，尚未确定MAP30在肿瘤转移中的作用。为此，我们调查了MAP30在膀胱癌（BC）中的作用及其潜在机制。在这里，我们报道MAP30在体外显着抑制5637和T24细胞的细胞增殖和克隆形成通过促进细胞凋亡和细胞周期阻滞。我们还发现MAP30通过抑制上皮/间质转化（EMT）过程来抑制细胞迁移和侵袭。此外，Affymetrix基因芯片检测表明，MAP30显着改变了T24细胞中的基因表达谱，尤其是细胞周期调控途径中的基因。经过独创性路径分析后，我们预测NUPR1是最重要的上游调节器。随后，我们证实MAP30处理可在T24细胞中抑制AKT和EMT信号通路。总之，MAP30处理通过抑制AKT途径抑制了人类BC的进展，特别是细胞迁移和侵袭。