Studies of the mechanistic (mammalian) target of rapamycin inhibitors (mTOR) represent a step towards the targeted treatment of gynecological cancers. It has been shown that women with increased levels of mTOR signaling pathway targets have worse prognosis compared to women with normal mTOR levels. Yet, targeting mTOR alone has led to unsatisfactory outcomes in gynecological cancer. The aim of our review was therefore to provide an overview of the most recent clinical results and basic findings on the interplay of mTOR signaling and cold shock proteins in gynecological malignancies. Due to their oncogenic activity, there are promising data showing that mTOR and Y-box-protein 1 (YB-1) dual targeting improves the inhibition of carcinogenic activity. Although several components differentially expressed in patients with ovarian, endometrial, and cervical cancer of the mTOR were identified, there are only a few investigated downstream actors in gynecological cancer connecting them with YB-1. Our analysis shows that YB-1 is an important player impacting AKT as well as the downstream actors interacting with mTOR such as epidermal growth factor receptor (EGFR), Snail or E-cadherin.

译文

雷帕霉素抑制剂 (mTOR) 的机制 (哺乳动物) 靶标的研究代表了妇科癌症靶向治疗的一步。研究表明,与mTOR水平正常的女性相比,mTOR信号通路靶标水平升高的女性预后较差。然而,单独靶向mTOR导致妇科癌症的结果不令人满意。因此,我们审查的目的是概述妇科恶性肿瘤中mTOR信号传导和冷休克蛋白相互作用的最新临床结果和基本发现。由于其致癌活性,有前景的数据表明mTOR和Y-box蛋白1 (YB-1) 双重靶向改善了对致癌活性的抑制。尽管在mTOR的卵巢癌,子宫内膜和宫颈癌患者中发现了几种差异表达的成分,但在妇科癌症中只有少数研究的下游参与者将其与YB-1联系起来。我们的分析表明,YB-1是影响AKT以及与mTOR相互作用的下游参与者的重要参与者,例如表皮生长因子受体 (EGFR),蜗牛或E-cadherin。

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