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炎症小体与自噬在癌症中的相互作用。

Crosstalks between inflammasome and autophagy in cancer.

机构信息

Division of Pulmonary and Critical Care, Department of Internal Medicine, Chungnam National University School of Medicine, Daejeon, 35015, Korea.

Infection Control Convergence Research Center, Chungnam National University School of Medicine, Daejeon, 35015, Korea.

出版信息

J Hematol Oncol. 2020 Jul 23;13(1):100. doi: 10.1186/s13045-020-00936-9.

DOI:10.1186/s13045-020-00936-9
PMID:32703253
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7376907/
Abstract

Both inflammasomes and autophagy have important roles in the intracellular homeostasis, inflammation, and pathology; the dysregulation of these processes is often associated with the pathogenesis of numerous cancers. In addition, they can crosstalk with each other in multifaceted ways to influence various physiological and pathological responses, including cancer. Multiple molecular mechanisms connect the autophagy pathway to inflammasome activation and, through this, may influence the outcome of pro-tumor or anti-tumor responses depending on the cancer types, microenvironment, and the disease stage. In this review, we highlight the rapidly growing literature on the various mechanisms by which autophagy interacts with the inflammasome pathway, to encourage additional applications in the context of tumors. In addition, we provide insight into the mechanisms by which pathogen modulates the autophagy-inflammasome pathway to favor the infection-induced carcinogenesis. We also explore the challenges and opportunities of using multiple small molecules/agents to target the autophagy/inflammasome axis and their effects upon cancer treatment. Finally, we discuss the emerging clinical efforts assessing the potential usefulness of targeting approaches for either autophagy or inflammasome as anti-cancer strategies, although it remains underexplored in terms of their crosstalks.

摘要

炎症小体和自噬在细胞内稳态、炎症和病理学中都具有重要作用;这些过程的失调通常与许多癌症的发病机制有关。此外,它们可以通过多种方式相互交流,影响包括癌症在内的各种生理和病理反应。多种分子机制将自噬途径与炎症小体激活联系起来,并通过这种方式,根据癌症类型、微环境和疾病阶段,可能影响促肿瘤或抗肿瘤反应的结果。在这篇综述中,我们强调了自噬与炎症小体途径相互作用的各种机制的快速发展的文献,以鼓励在肿瘤背景下的更多应用。此外,我们还深入探讨了病原体调节自噬-炎症小体途径以促进感染诱导的致癌作用的机制。我们还探讨了使用多种小分子/药物靶向自噬/炎症小体轴及其对癌症治疗的影响的挑战和机遇。最后,我们讨论了评估靶向自噬或炎症小体作为抗癌策略的潜在有用性的新兴临床努力,尽管在它们的相互作用方面仍未得到充分探索。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9a6/7376907/31b30d61321a/13045_2020_936_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9a6/7376907/439adf33c4dd/13045_2020_936_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9a6/7376907/a478a042d1df/13045_2020_936_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9a6/7376907/3c21022c764a/13045_2020_936_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9a6/7376907/31b30d61321a/13045_2020_936_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9a6/7376907/439adf33c4dd/13045_2020_936_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9a6/7376907/a478a042d1df/13045_2020_936_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9a6/7376907/3c21022c764a/13045_2020_936_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9a6/7376907/31b30d61321a/13045_2020_936_Fig4_HTML.jpg

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