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Noncoding RNAs:the shot callers in tumor immune escape

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摘要 Immunotherapy,designed to exploit the functions of the host immune system against tumors,has shown considerable potential against several malignancies.However,the utility of immunotherapy is heavily limited due to the low response rate and various side effects in the clinical setting.Immune escape of tumor cells may be a critical reason for such low response rates.Noncoding RNAs(ncRNAs)have been identified as key regulatory factors in tumors and the immune system.Consequently,ncRNAs show promise as targets to improve the efficacy of immunotherapy in tumors.However,the relationship between ncRNAs and tumor immune escape(TIE)has not yet been comprehensively summarized.In this review,we provide a detailed account of the current knowledge on ncRNAs associated with TIE and their potential roles in tumor growth and survival mechanisms.This review bridges the gap between ncRNAs and TIE and broadens our understanding of their relationship,providing new insights and strategies to improve immunotherapy response rates by specifically targeting the ncRNAs involved in TIE.
出处 《Signal Transduction and Targeted Therapy》 SCIE CSCD 2020年第1期1557-1580,共24页 信号转导与靶向治疗(英文)
基金 supported by funding from the Project Nn10 of Harbin Medical University Cancer Hospital(Grant Number Nn102017-02) National Natural Science Foundation of China(Grant Number 81602323,81872149) Outstanding Youth Project of Heilongjiang Provincial Natural Science Foundation(Grant Number YQ2019H027) Distinguished Young Scholars of Harbin Medical University Cancer Hospital(Grant Number JCQN2018-03) Yong Elite Training Foundation Grant of Harbin Medical University Cancer Hospital(Grant Number JY2016-02) Haiyan Fund Project of Harbin Medical University Cancer Hospital(Grant Number JJQN 2018-10).
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  • 1Hong-Wei Shen Shun-Liang Gao Yu-Lian Wu Shu-You Peng.Overexpression of decoy receptor 3 in hepatocellular carcinoma and its association with resistance to Fas ligand-mediated apoptosis[J].World Journal of Gastroenterology,2005,11(38):5926-5930. 被引量:29
  • 2Oft M, Akhurst RJ, Balmain A. Metastasis is driven by sequential elevation of H-ras and Smad2 levels. Nat Cell Biol 2002; 4:487-494.
  • 3Takano S, Kanai F, Jazag A, et al. Smad4 is essential for down-regulation of E-cadherin induced by TGF-β in pancreatic cancer cell line PANC-1. JBiochem 2007; 141:345-351.
  • 4Kaimori A, Potter J, Kaimori JY, et al. Transforming growth factor-β1 induces an epithelial-to-mesenchymal transition state in mouse hepatocytes in vitro. J Biol Chem 2007; 282:22089-22101.
  • 5Bardeesy N, Cheng KH, Berger JH, et al. Smad4 is dispensable for normal pancreas development yet critical in progres- sion and tumor biology of pancreas cancer. Genes Dev 2006; 20:3130-3146.
  • 6Desgrosellier JS, Mundell NA, McDonnell MA, Moses HL, Barnett JV. Activin receptor-like kinase 2 and Smad6 regulate epithelial-mesenchymal transformation during cardiac valve formation. Dev Biol 2005; 280:201-210.
  • 7Armstrong E J, Bischoff J. Heart valve development: endothelial cell signaling and differentiation. Circ Res 2004; 95:459- 470.
  • 8Saika S, Ikeda K, Yamanaka O, et al. Transient adenoviral gene transfer of Smad7 prevents injury-induced epithelialmesenchymal transition of lens epithelium in mice. Lab Invest 2004; 84:1259-1270.
  • 9Xu GP, Li QQ, Cao XX, et al. The fffect of TGF-β1 and SMAD7 gene transfer on the phenotypic changes of rat al- veolar epithelial cells. Cell Mol Biol Lett 2007; 12:457-472.
  • 10Dooley S, Hamzavi J, Ciuclan L, et al. Hepatocyte-specific Smad7 expression attenuates TGF-β-mediated fibrogenesis and protects against liver damage. Gastroenterology 2008; 135:642-659.

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