Smad4 通过 PI3K-mTOR 的参与诱导 HO-8910 和 SKOV3 卵巢癌细胞系的细胞死亡。
Smad4 induces cell death in HO-8910 and SKOV3 ovarian carcinoma cell lines via PI3K-mTOR involvement.
机构信息
Department of Gynecology, the Affiliated Hospital of Qingdao University, Qingdao 266000, People's Republic of China.
Cell Biology & Genetics Department, Medical College, Qingdao University, Qingdao 266021, People's Republic of China.
出版信息
Exp Biol Med (Maywood). 2020 May;245(9):777-784. doi: 10.1177/1535370220916709. Epub 2020 Apr 10.
This study investigated the effect and mechanism of Smad4 in ovarian carcinoma (OC) cell viability and demonstrated that Smad4 acted as a tumor suppressor in OC, which may contribute to the understanding of molecular mechanisms underlying OC occurrence and progression. Smad4 expression was decreased in the OC specimens, but Smad4 recovery in the OC cell lines impaired the survival and viability of OC cells by increasing autophagy and apoptosis. Further investigation showed that Smad4 interacted with the P85 subunit of PI3K and caused deactivation of the PI3K/mTOR pathway. Therefore, Smad4 could be considered as a target in cancer therapy due to its regulatory effect in OC carcinogenesis.
本研究探讨了 Smad4 在卵巢癌 (OC) 细胞活力中的作用和机制，并证实 Smad4 在 OC 中起肿瘤抑制作用，这可能有助于理解 OC 发生和发展的分子机制。Smad4 在 OC 标本中的表达降低，但 OC 细胞系中 Smad4 的恢复通过增加自噬和凋亡来损害 OC 细胞的存活和活力。进一步的研究表明，Smad4 与 PI3K 的 P85 亚基相互作用，导致 PI3K/mTOR 通路失活。因此，Smad4 可以因其在 OC 癌变中的调节作用而被视为癌症治疗的靶点。
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