<p>Water Extract of Sporoderm-Broken Spores of <em>Ganoderma lucidum</em> Induces Osteosarcoma Apoptosis and Restricts Autophagic Flux</p>
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Osteosarcoma (OS) is a malignant bone tumor with easy metastasis and poor prognosis. Ganoderma lucidum (G. lucidum), a traditional Chinese medicine, was reported playing a critical role in suppressing multiple tumor progress. So we wanted to investigate the effects and molecular mechanisms of water extract of sporoderm-broken spores of G. lucidum (BSGLWE) on osteosarcoma.In vitro, the effects on cell proliferation of BSGLWE in osteosarcoma cells were detected by CCK-8, colony formation assay and flow cytometry; migration ability of osteosarcoma cells was evaluated by cell scratch and transwell assays. Cell apoptosis and autophagy were tested by transmission electron microscopy (TEM). Potential signaling pathways were detected by Western blotting and immunofluorescence. In xenograft orthotopic model, the luminescence intensity measured by an in vivo bioluminescence imaging system, and the expression of related proteins in tumor cells were assessed by IHC analysis.BSGLWE suppressed the proliferation and migration of osteosarcoma cells in a dose-dependent manner, and osteosarcoma cell cycle progression at the G2/M phase was arrested by the BSGLWE. In addition, increased apoptosis-related protein expression meant BSFLWE induced caspase-dependent apoptosis of osteosarcoma cells. TEM results indicated that BSGLWE promoted the formation of apoptotic bodies and autophagosomes in HOS and U2 cells. Western blotting or immunofluorescence and rescue assay revealed that BSGLWE blocked autophagic flux by inducing initiation of autophagy and increasing autophagosome accumulation of osteosarcoma cells. BSGLWE not only repressed the angiogenesis in the mouse model, but also induced apoptosis and blocked autophagy in vivo.BSGLWE inhibits osteosarcoma progression.Inducer
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Autophagy is a crucial biological process of eukaryotes, which is involved in cell growth, survival and energy metabolism, while the premise of the autophagy function is activated autophagic flux. It has been confirmed that impaired autophagic flux promotes pathogenesis of many chronic inflammatory diseases, especially cancer, neurodegenerative disease and tissue fibrosis, therefore the analysis of autophagic flux state is important for revealing autophagy function and the mechanism of autophagy related diseases. Given that autophagy is a dynamic process with multiple steps, it is very hard to observe the real state of autophagic flux. Summarized here is the novel concept and current approach to detect autophagic flux. This knowledge is crucial for the researching of the biological function of autophagy, and may provide some strategies for developing autophagy-related drug.
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macroautophagy 的角色(此后 autophagy ) 在癌症，到临床的干预的生物学和反应是复杂的。autophagy 是在许多肿瘤背景的 dysregulated，是清楚的，在肿瘤开始和前进期间，并且响应治疗。然而，在控制房间行为的 autophagy 的多种的机械学的角色使在一个给定的肿瘤背景预言困难 autophagy 的角色，并且，由扩展，指向 autophagy 的治疗学的结果，力量。在这评论，我们在在癌症支持 pro-tumorigenic 和 anti-tumorigenic 和 autophagy 的治疗学的角色的文学总结证据。这概述在滋养的管理，房间死亡，房间老朽， proteotoxic 应力的规定和细胞的动态平衡包含 autophagy 的角色，在在新陈代谢的变化的肿瘤主人相互作用和参予的规定。在可能的地方，我们也试着理解，为 autophagy 的这些角色的机械学的底。我们明确地阐述在在 vivo.We 使这些问题清楚些的癌症的模型也考虑 autophagy 蛋白质的任何东西或上述所有函数怎么可能是可指向的由的遗传上设计的老鼠的新兴的角色现存或 pharmacologic 代理人的未来类。我们由简短在细胞的过程为关键 autophagy 蛋白质的子集探索不在经典中的角色得出结论，并且这些怎么可能在癌症之上影响。
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Introduction: Osteosarcoma usually originates in the metaphyseal region of long bone, but may also arise in the diaphyseal of long bone. Diaphyseal osteosarcoma is a rare cases account for <10% of all osteosarcoma. In some cases two or more osteosarcoma lesions are seen in the same patient, at the same time (Synchronous osteosarcoma). It’s unusual condition of osteosarcoma, they are found at a frequency of about 1–3% osteosarcoma cases.
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Cases of unusual osteosarcoma comprising parosteal osteosarcoma, intraosseous well differentiated osteosarcoma, postradiation osteosarcoma, epithelioid osteosarcoma, and MFH-like osteosarcoma were reported. They were apparently differed from conventional osteosarcoma in the point of biologic activity and prognosis. Osteosarcoma is, therefore, considered as a heterogeneic tumor. It is important to make an exact diagnosis and to make an appropriate treatment depending on the diagnosis.
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Autophagy 是导致长寿蛋白质和不正常的细胞器的降级的高度调整的细胞的机制。这个过程处于与神经病学的疾病相关的许多生理、病理学的条件被含有。最近的研究证明在服的局部缺血的 autophagy 的存在，而是没有一致还处于这个条件关于 autophagy 的功能被到达了。这篇文章在服的局部缺血或灌注期间加亮 autophagy 的激活，特别在神经原和星形细胞，以及在 neuronal 或 astrocytic 房间死亡和幸存的 autophagy 的角色。我们建议那 autophagy 的生理的层次，大概引起了由对谦虚组织缺氧或局部缺血温和，看起来保护。然而，严重组织缺氧或局部缺血或灌注引起的 autophagy 的高水平可以引起自我消化和最终的 neuronal 和 astrocytic 房间死亡。我们也讨论那氧化并且 endoplasmic 蜂窝胃(嗯) 在服的组织缺氧或局部缺血或灌注的压力是在神经原和星形细胞的 autophagy 的有势力刺激。另外，我们考察一方面建议在 autophagy 之间的可观的重叠的证据，和 apoptosis，坏死和 necroptosis 在另一方面，在决定结果和损坏神经原和星形细胞的最后的形态学。
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Autophagy is a highly conserved cell degradation process which can decompose the organelles and recycling the macromolecules by lysosomes. Autophagy is induced by multiple factors, such as starvation, ischemia, and oxidative stress, and plays a key role in development and differentiation of cells. It has been shown that autophagy is closely related to cardiovascular diseases. Moderate autophagy protects myocardial cells from injury, whereas insufficient or excessive autophagy triggers or aggravates diseases. The present article reviews the progress of autophagy in cardiovascular diseases.
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最近的研究揭示了那 autophagy，基本细胞内部的进程，在淋巴细胞开发和功能起许多不同作用。Autophagy 调整天真的 T 淋巴细胞动态平衡，明确地由调整 mitochondrial 质量和周转，并且为成熟 T 房间的增长是必要的。Autophagy 也在淋巴细胞充当一条细胞的死亡小径，在延长 cytokine 退却之上并且在尖锐抗原受体刺激期间如果不正确地调整了。在 HIV 感染期间，而且， autophagy 的 hyperinduction 在 uninfected CD4+ T 房间导致巨大的 T 房间死亡，并且被禁止 autophagic 救开始。在 thymic 的 autophagy 组成地高级上皮的房间为最佳的处理和内长的抗原的表示是必要的，并且为开发 thymocytes 的合适的积极、否定的选择要求。Autophagy 也支持早 B 房间祖先的 B 淋巴细胞，以及发展的幸存。在 B 房间， autophagy 是一条其他的死亡小径，当当 costimulation 不在时的抗原受体刺激导致有势力 autophagic 死亡。因此， autophagy 在淋巴细胞起一个复杂作用并且在他们的 lifespan 期间被调整保证一个健康免疫系统。
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Autophagy 是涉及长寿蛋白质的降级并且损坏了细胞器的一个 evolutionarily 保存的 lysosomal 自我消化过程。在最近的年里，增加证据显示 autophagy 与很多个病理学的过程被联系，包括癌症。在这评论，我们集中于在包含的 autophagosome 形成和小径被含有的 evolutionarily 保存的 autophagy 相关的基因(ATG ) 的最近的研究。我们讨论几个关键 autophagic 调停人(例如， Beclin-1， UVRAG， Bcl-2，类 III 并且我 PI3K， mTOR，和 p53 ) 在在癌症表明网络的 autophagic 起枢轴的作用。我们在癌症讨论 autophagy 的 Janus 角色并且加亮他们的关系到肿瘤抑制和肿瘤前进。我们也举作为 anticancer 策略指向 ATG 和几蛋白质 kinases 的一些例子，并且作为 antitumor 代理人讨论一些模块化 autophagy 代理人。在 autophagy 和癌症之间的关系的更好的理解将最终允许我们在癌症治疗学为药发现作为新目标利用 autophagic 小径。
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