相关实验视频
Updated: Jun 27, 2025

06:53
Cell Population Analyses During Skin Carcinogenesis
Published on: August 21, 2013
12.4K
一个质细胞-脂肪细胞信号循环通过BTG3的损失被重新编程,以增加皮肤致癌的发生
Yu-Che Cheng1, Jack Dalit Acedera1,2, Yi-Ju Li1
1Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
Cell death and differentiation
|May 7, 2024
概括
瘤抑制剂BTG3通常通过调节皮肤细胞和脂肪细胞之间的通信来预防皮肤癌. 失去BTG3通过改变这种交叉语音来促进皮肤癌,从而提供潜在的治疗点.
科学领域:
- 在瘤学瘤学.
- 皮肤病学 皮肤病学
- 细胞生物学 细胞生物学
背景情况:
- 肥胖会增加癌症的风险,功能障碍的脂肪组织会影响癌细胞的行为.
- 瘤上皮细胞和脂肪组织之间的通信机制仍然不太清楚.
- BTG3是一种瘤抑制剂,与细胞增殖有关,在某些皮肤癌中被降低调节.
研究的目的:
- 为了研究BTG3在皮肤癌症发生中的作用.
- 阐明瘤角质细胞与脂肪细胞相互作用的分子机制.
- 为了确定皮肤癌治疗的潜在治疗点.
主要方法:
- 在正常皮肤中比较BTG3表达与基底细胞癌和状细胞癌.
- 使用DMBA/TPA诱导的皮肤致癌与Btg3淘汰的小鼠模型.
- 对脂肪细胞分化和细胞因子/化学因子从角质细胞释放的分析.
- 研究NF-κB通路激活和涉及脂肪细胞衍生因子的反循环.
主要成果:
- 在基底细胞癌和状细胞癌中,BTG3水平降低.
- Btg3淘汰赛小鼠对化学诱导的皮肤瘤的敏感性增加.
- 缺乏BTG3的角质细胞通过IL1α,IL10和CCL4释放促进了脂肪细胞的分化,这与NF-κB活性升高有关.
- 诱导脂肪细胞释放了CCL20和FGF7,增强了角质细胞迁移.
结论:
- BTG3在维持角质细胞和脂肪细胞之间的正常相互作用方面发挥着至关重要的作用.
- 对BTG3的失调会破坏这种交叉声,促进皮肤致癌.
- 已确定的分子媒介 (IL1α,IL10,CCL4,CCL20,FGF7,NF-κB) 是皮肤癌的潜在治疗点.
相关概念视频
Renewal of Skin Epidermal Stem Cells
2.5K
The skin is divided into epidermis, dermis, and hypodermis, the skin's outermost, middle, and inner layers. The human epidermal layer regularly undergoes renewal, where old, dead cells are replaced by new cells. Epidermal stem cells or EpiSCs divide and differentiate to restore the lost cells. For the renewal process, some EpiSCs continuously self-renew. In contrast, few others differentiate into transit-amplifying cells, which later form prickle or spinous cells, followed by granular...
2.5K
TGF - β Signaling Pathway
7.3K
The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
7.3K
PI3K/mTOR/AKT Signaling Pathway
3.5K
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...
3.5K
Hedgehog Signaling Pathway
7.3K
The Hedgehog gene (Hh) was first discovered due to its control of the growth of disorganized, hair-like bristles phenotype in Drosophila, much like hedgehog spines. Hh plays a crucial role in the development of organs and the maintenance of homeostasis in both invertebrates and vertebrates. However, while Drosophila has only one Hh protein, mammals have multiple functional Hedgehog proteins - Sonic (Shh), Desert (Dhh), and Indian Hedgehog (Ihh). All of these homologous proteins have adapted to...
7.3K
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
Role Of Notch Signalling In Intestinal Stem Cell Renewal
2.1K
Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
2.1K

