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相关概念视频

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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The Ras Gene02:38

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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.
Ras is a...
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Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
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Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
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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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Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
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相关实验视频

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RhoC GTPase Activation Assay
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YTHDF1/RNF7/p27轴促进前列腺癌的进展.

Yulin Shi1,2,3, Baiyang Liu1,2, Yong Zhang4

  • 1The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.

Cell death & disease
|April 18, 2025
PubMed
概括

YTHDF1蛋白通过通过RNF7.7降解p27细胞循环抑制剂来促进前列腺癌 (PCa) 的生长. 准这种YTHDF1/RNF7/p27通路可能为前列腺癌提供新的治疗方法.

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科学领域:

  • 在瘤学瘤学.
  • 分子生物学分子生物学
  • 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.

背景情况:

  • 前列腺癌 (PCa) 是主要的男性癌症.
  • 在癌症中,N6-甲基氨酸 (m6A) 修饰至关重要.
  • YTHDF1是一种m6A读者蛋白,涉及到癌症.

研究的目的:

  • 调查YTHDF1在PCa中的作用.
  • 在PCa中阐明YTHDF1/RNF7/p27信号轴.
  • 探索PCa的治疗潜力.

主要方法:

  • 在PCa组织中分析YTHDF1表达.
  • 在PCa细胞和有机体中YTHDF1的敲除.
  • 蛋白质酶降解和E3结合酶查.
  • 对亡和药物敏感性的评估.
  • 用MLN4924进行体外和体外研究.

主要成果:

  • YTHDF1在PCa中表达很高,与糟糕的结果相关.
  • 抑制YTHDF1抑制PCa细胞的增殖,迁移和瘤的生长.
  • YTHDF1针对RNF7,导致p27降解并促进PCa.
  • YTHDF1或RNF7的枯竭使PCa细胞对西斯素敏感.
  • MLN4924可以抑制PCa的进展.

结论:

  • YTHDF1/RNF7/p27轴对PCa进展至关重要.
  • 这个轴代表了前列腺癌的潜在治疗目标.
  • 向YTHDF1或RNF7可能会提高化疗的疗效.