Cantharidin (CTD) is a traditional Chinese medicine that shows an anticancer effects in multiple types of cancer cells. However, the mechanism of CTD anti-cancer function in gastric cancer (GC) is still unclear. The aim of the present study was to investigate the underlying mechanism that CTD inhibits proliferation and migration through suppression of the PI3K/Akt signaling. CTD induced GC cell apoptosis and inhibited metastasis measured by CCK8 assays as well as wound healing assays and transwell assays. Mechanistic investigations suggested that CTD modulated the PI3K/Akt signaling via western-blot and quantitative q-PCR. In addition, we identified and confirmed CCAT1 as a novel direct target of CTD inhibited PI3K/AKt signaling expression. In conclusion, our results provide new point into the critical role of CTD in suppressing PI3K/Akt signaling via down-regulation of CCAT1, resulting in suppression GC cell growth and migration/invasion.

中文翻译：

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斑th素通过抑制经由CCAT1的PI3K / Akt信号通路来抑制胃癌细胞的迁移/侵袭。

斑th素（CTD）是一种中药，对多种类型的癌细胞均显示出抗癌作用。然而，CTD抗癌功能在胃癌（GC）中的机制仍不清楚。本研究的目的是研究CTD通过抑制PI3K / Akt信号传导来抑制增殖和迁移的潜在机制。CTD诱导了GC细胞凋亡，并通过CCK8测定以及伤口愈合测定和Transwell测定测定了抑制的转移。机理研究表明，CTD通过蛋白质印迹和定量q-PCR调节了PI3K / Akt信号传导。此外，我们确定并确认CCAT1为CTD抑制PI3K / AKt信号表达的新型直接靶标。结论，