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非编码 RNA 与结直肠癌中 PI3K/AKT/mTOR 通路的相互作用。

Cross-talk between non-coding RNAs and PI3K/AKT/mTOR pathway in colorectal cancer.

机构信息

Protein Chemistry Laboratory (PCL), Department of Biology, College of Sciences, Shiraz University of Medical Sciences, Shiraz, Iran.

Department of Medical Genetics, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran.

出版信息

Mol Biol Rep. 2021 May;48(5):4797-4811. doi: 10.1007/s11033-021-06458-y. Epub 2021 May 31.

DOI:10.1007/s11033-021-06458-y
PMID:34057685
Abstract

Colorectal cancer (CRC) is the third commonest cancer globally, with metastasis being the reason for cancer-associated mortality. Much is still unknown biochemically about CRC, and with current treatments that are not wholly effective over time, new therapeutics are urgently needed. Emerging evidence has shown the importance of non-coding RNAs such as lncRNAs and miRNAs functions in the development and progression of CRC. However, the exact underlying mechanism of these types of RNAs in CRC is still mostly unknown. PI3K/AKT/mTOR pathway contributes to many cellular processes, and dysregulation of this pathway frequently occurs in cancers. In this review, the authors have mostly focused on the significant non-coding RNAs regulators of the PI3K/AKT/mTOR pathway and their contribution to the development or inhibition of CRC and their potential as diagnostic or therapeutic targets in CRC treatment.

摘要

结直肠癌(CRC)是全球第三大常见癌症,转移是癌症相关死亡的原因。CRC 在生物化学方面仍有许多未知之处,而且随着当前治疗方法的效果并不完全持久,急需新的治疗方法。新出现的证据表明,非编码 RNA(如长链非编码 RNA 和 microRNA)在 CRC 的发展和进展中的作用非常重要。然而,这些类型的 RNA 在 CRC 中的确切潜在机制在很大程度上仍然未知。PI3K/AKT/mTOR 途径有助于许多细胞过程,该途径的失调经常发生在癌症中。在这篇综述中,作者主要关注 PI3K/AKT/mTOR 途径的重要非编码 RNA 调节剂及其对 CRC 的发展或抑制的贡献,以及它们作为 CRC 治疗中诊断或治疗靶点的潜力。

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FNDC3B, Targeted by miR-125a-5p and miR-217, Promotes the Proliferation and Invasion of Colorectal Cancer Cells via PI3K/mTOR Signaling.FNDC3B受miR-125a-5p和miR-217靶向调控,通过PI3K/mTOR信号通路促进结肠癌细胞的增殖和侵袭。
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KW2478 and Cisplatin Synergistically Anti-colorectal Cancer by Targeting PI3K/AKT/mTOR Pathway.KW2478和顺铂通过靶向PI3K/AKT/mTOR通路协同抗结直肠癌
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