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miR-335 Acts as a Tumor Suppressor and Enhances Ionizing Radiation-Induced Tumor Regression by Targeting ROCK1

机译:miR-335用作肿瘤抑制剂,并通过靶向ROCK1增强电离辐射诱导的肿瘤回归

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摘要

Recent development of integrative therapy against melanoma combines surgery, radiotherapy, targeted therapy, and immunotherapy; however, the clinical outcomes of advanced stage and recurrent melanoma are poor. As a skin cancer, melanoma is generally resistant to radiotherapy. Hence, there is an urgent need for evaluation of the mechanisms of radioresistance. The present study identified miR-335 as one of the differential expression of miRNAs in recurrent melanoma biopsies post-radiotherapy. The expression of miR-335 declined in melanoma tissues compared to the adjacent tissues. Moreover, miR-335 expression correlated with advanced stages of melanoma negatively. Consistent with the prediction of STARBASE and miRDB database, miR-335 targeted ROCK1 via binding with 3′-UTR of ROCK1 directly, resulting in attenuation of proliferation, migration, and radioresistance of melanoma cells. The authors validated that overexpression of miR-335 enhanced X-ray-induced tumor regression by B16 mouse models. Briefly, the present findings gained insights into miR-335/ROCK1-mediated radiosensitivity and provided a promising therapeutic strategy for improving radiotherapy against melanoma.
机译:最近综合治疗对黑色素瘤的发展结合了手术,放疗,靶向治疗和免疫治疗;然而,晚期和复发黑素瘤的临床结果差。作为皮肤癌,黑色素瘤通常耐放射疗法。因此,迫切需要评估放射群体的机制。本研究将MIR-335鉴定为MIRNA在放射后复发性黑素瘤活组织检查中miRNA的差异表达之一。与相邻的组织相比,黑色素组织中miR-335的表达下降。此外,miR-335表达与黑素瘤的高级阶段负相关。通过直接与Rock1的3'-UTR的3'-UTR的结合来一致地通过Starbase和MiRDB数据库,MiR-335靶向Rock1,导致黑素瘤细胞的增殖,迁移和辐射衰退率衰减。作者验证了MIR-335的过表达通过B16小鼠模型增强了X射线诱导的肿瘤回归。简而言之,目前的研究结果对MiR-335 / Rock1介导的放射敏感性进行了见解,并提供了提高对黑色素瘤的放射治疗的有希望的治疗策略。

著录项

  • 作者

    Yanfeng Cheng; Peng Shen;

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  • 年度 2020
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  • 原文格式 PDF
  • 正文语种 eng
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