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相关概念视频

Regulation of the Unfolded Protein Response01:31

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Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...
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The Unfolded Protein Response01:37

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The ER is the hub of protein synthesis in a cell. It has robust systems to quality control protein folding and also for degradation of terminally misfolded proteins. Under normal conditions, a small proportion of misfolded proteins that cannot be salvaged need to be transported to the cytoplasm by the ER-associated degradation or ERAD pathways. However, if the ERAD cannot handle the misfolded proteins, the cell activates the unfolded protein response or UPR to adjust the protein folding...
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Abnormal Proliferation02:23

Abnormal Proliferation

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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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mTOR Signaling and Cancer Progression

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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
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The Ras Gene02:38

The Ras Gene

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The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
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PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

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The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
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Sequencing Small Non-coding RNA from Formalin-fixed Tissues and Serum-derived Exosomes from Castration-resistant Prostate Cancer Patients
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NXP800激活了未折叠的蛋白质反应,改变了AR和E2F功能,以影响抗割的前列腺癌生长.

Jonathan Welti1, Denisa Bogdan1, Ines Figueiredo1

  • 1The Institute of Cancer Research, London, United Kingdom.

Clinical cancer research : an official journal of the American Association for Cancer Research
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概括

这项研究表明,使用NXP800准热冲击因子1 (HSF1) 途径,可以抑制晚期前列腺癌模型的生长. 这种方法为治疗耐药前列腺癌提供了一个新的策略.

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科学领域:

  • 在瘤学瘤学.
  • 分子生物学分子生物学
  • 遗传学 是一个遗传学.

背景情况:

  • 晚期前列腺癌仍然是一个致命的疾病,雄激素受体 (AR) 信号作为关键的治疗点.
  • 对当前AR抑制剂的耐药性是不可避免的,需要新的治疗策略.
  • 热冲击蛋白 (HSP) 在AR活性中起着关键作用,是潜在的治疗点.

研究的目的:

  • 研究基因本体学细胞对热基因表达特征的反应与割耐性前列腺癌 (CRPC) 的临床结果之间的关联.
  • 在治疗耐药前列腺癌的临床前模型中评估NXP800针对热冲击因子1 (HSF1) 途径的有效性.

主要方法:

  • 对CRPC队列的转录组分析,以将热反应特征与生存率相关联.
  • 在体外和体内研究使用NXP800以准前列腺癌模型中的HSF1途径.
  • 评估NXP800对HSP72表达,未折叠蛋白质反应和AR/E2F活性的影响.

主要成果:

  • 细胞对热基因表达特征的反应与AR信号传递和CRPC的较差结果有关.
  • 使用NXP800抑制HSF1通路会降低HSP72水平,并激活未折叠的蛋白质反应.
  • NXP800有效地抑制AR和E2F介导的活动,导致抗性前列腺癌模型中瘤生长的抑制.

结论:

  • NXP800在治疗耐药前列腺癌模型中显示出显著的抗瘤活性.
  • 这种针对HSF1的策略对治疗选择有限的前列腺癌亚型有效.
  • NXP800为晚期和耐治疗的前列腺癌提供了进一步的临床开发.