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相关概念视频

mTOR Signaling and Cancer Progression03:03

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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Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
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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.
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The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
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Biochemical reactions are occurring constantly in cells, converting starting substances to different products, usually with the help of enzymes that speed the reactions. Without enzymes, it would take far too long for most reactions to occur to be useful to the cell!
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相关实验视频

Updated: Jan 24, 2026

Molecular Profiling of the Invasive Tumor Microenvironment in a 3-Dimensional Model of Colorectal Cancer Cells and Ex vivo Fibroblasts
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针对衰老:天马颗粒通过调节瘤微环境中的miR-29a-5p/P53信号来抑制结肠直肠癌的进展.

Xiaojuan Tang1, Yuan Ren2, Yongmin Li1

  • 1Central Laboratory, Hunan Province Integrated Traditional Chinese and Western Medicine Hospital (Affiliated Hospital of Hunan Academy of Traditional Chinese Medicine), Changsha, China.

Molecular nutrition & food research
|January 23, 2026
PubMed
概括

天马颗粒 (TMG) 通过向miR-29a-5p/P53轴,重塑瘤微环境并抑制结肠直肠癌 (CRC). 这种传统中医药增强了细胞亡,减少了瘤生长和转移.

关键词:
天马颗粒 miR-29a-5p/P53 轴细胞衰老 结直肠癌 结直肠癌与衰老相关的瘤微环境

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科学领域:

  • 在瘤学瘤学.
  • 药理学 药理学是指药理学的学科.
  • 分子生物学分子生物学

背景情况:

  • 化疗诱导与衰老相关的瘤微环境 (S-TME),促进结直肠癌 (CRC) 的进展.
  • 传统中医 (TCM) 配方为癌症治疗提供了潜在的治疗策略.

研究的目的:

  • 阐明天马颗粒 (TMG) 重塑S-TME并抑制CRC的机制.
  • 研究miR-29a-5p/P53轴在TMG抗CRC作用中的作用.

主要方法:

  • LC-MS/MS确定了TMG的组成部分;网络药理学确定了P53作为核心目标.
  • 在体外测试中使用多克索鲁比诱导的衰老细胞和CRC线来评估TMG效应.
  • 在体内研究中使用了氧甲/德克斯硫酸盐 (AOM/DSS) 诱导的CRC小鼠模型.

主要成果:

  • TMG抑制了CRC细胞的增殖,迁移和入侵,同时促进了细胞亡.
  • TMG降低了P53/P21表达和与衰老相关的分泌表现型 (SASP) 因素,在衰老细胞中上调 miR-29a-5p.
  • 在小鼠中,TMG治疗降低了瘤负担,改善了生存率,并在瘤组织中调节了miR-29a-5p/P53轴.

结论:

  • TMG重塑化疗诱导的S-TME,并抑制CRC的进展.
  • TMG通过调节miR-29a-5p/P53轴来发挥其作用,增强衰老细胞中的亡.
  • TMG通过抵消S-TME介导的瘤生长和转移来证明CRC的治疗潜力.