相关实验视频
Updated: Jun 12, 2025

11:42
Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
Published on: April 7, 2017
9.4K
METTL18作为HER2-阴性乳腺癌的Src-依赖性瘤反应中的表型调节剂
Han Gyung Kim1, Ji Hye Kim1, Kyung-Hee Kim2
1Department of Integrative Biotechnology, Sungkyunkwan University, Suwon 16419, Republic of Korea.
International journal of biological sciences
|September 23, 2024
概括
甲基转移酶类18 (METTL18) 通过调节actin聚合和Src酸化来驱动HER2阴性乳腺癌转移. 针对这种METTL18-HSP90-Actin-Src通路为侵袭性乳腺癌提供了潜在的治疗策略.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 生物化学 生物化学
背景情况:
- 类似甲基转移酶18 (METTL18) 涉及于核糖体生物发生和翻译.
- 动氨酸聚合和HSP90是已知的细胞运动的调节者.
- METTL18在乳腺癌转移中的作用仍然在很大程度上未被探索.
研究的目的:
- 研究METTL18在乳腺癌中的功能,特别是HER2阴性亚型.
- 阐明METTL18影响乳腺癌细胞转移的分子机制.
- 评估METTL18-HSP90-Actin-Src轴作为潜在的治疗标.
主要方法:
- 乳腺癌患者的基因表达分析.
- 使用乳腺瘤细胞系 (例如,MDA-MB-231) 的体外研究.
- 在体内瘤异种移植模型.
- 生物化学分析,分子生物学技术和免疫学方法.
- 同焦点显微镜和F/G-actin测定.
主要成果:
- 在HER2阴性乳腺癌中,METTL18高度放大,并与预后不佳有关.
- 失去METTL18显著抑制乳腺瘤细胞转移在体外和体内.
- METTL18通过HSP90促进了actin聚合,从而导致Src酸化和激活.
- 通过METTL18介导的RPL3甲基化对于HSP90的完整性和下游信号传输至关重要.
结论:
- METTL18-HSP90-Actin-Src轴是HER2-阴性乳腺癌转移的关键瘤原因驱动因素.
- METTL18在调节细胞迁移和入侵方面发挥着重要作用.
- 这一途径代表了治疗侵袭性乳腺癌的有希望的治疗标.
相关概念视频
mTOR Signaling and Cancer Progression
3.8K
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.
The mTOR pathway or the...
The mTOR pathway or the...
3.8K
Mitogens and the Cell Cycle
6.4K
Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
6.4K
Master Transcription Regulators
6.9K
Master transcription regulators are regulatory proteins that are predominantly responsible for regulating the expression of multiple genes. Often these genes work in concert to drive a complex process. Activation of a master transcription regulator can lead to a cascade of transcriptional activation necessary for that outcome. These regulators can directly bind to the regulatory sequences of the various genes involved, or they can indirectly regulate transcription by binding to regulatory...
6.9K
Abnormal Proliferation
4.5K
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...
4.5K
PI3K/mTOR/AKT Signaling Pathway
3.4K
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...
3.4K
Metastasis
5.5K
Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
5.5K

