AXL 氨酸激酶:一个不断增长的异形家族,促进癌症发病的致病性
May Eriksen Gjerstad1, Pia Aehnlich1, Pascal Gelebart1
1University of Bergen, Bergen, Norway.
Cancer research
|April 17, 2025
概括
AXL受体氨酸激酶 (RTK) 参与癌症进展和治疗耐药性. 了解其独特的异构体,包括新型AXL3,对于开发向癌症治疗至关重要.
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:
- AXL受体氨酸激酶 (RTK) 是各种癌症的关键参与者,与预后不佳和治疗耐药性相关.
- 包括PI3K/AKT,MAPK/ERK,JAK/STAT和NF-κB在内的AXL信号通路驱动癌细胞生存,增殖,迁移和免疫逃避.
研究的目的:
- 审查AXL受体氨酸激酶 (RTK) 的复杂信号机制.
- 突出AXL异型之间的区别,特别是新发现的AXL3.3.
- 强调了解AXL异形功能的重要性,以开发有效的癌症疗法.
主要方法:
- 关于AXL受体氨酸激酶 (RTK) 信号传导的最近研究的文献综述.
- 分析AXL异形结构及其对激活和信号的影响.
- 检查AXL促进器区域的潜在转录因子结合位点.
主要成果:
- 已经确定了第三种AXL异型,AXL3,它缺乏AXL1和AXL2中存在的GAS6结合域,这表明了独特的激活途径.
- 癌症中的AXL上调通常由非遗传机制调节,与其他瘤性激酶不同.
- 转录因子KLF16和MEIS3显示了与AXL3促进体的潜在结合,将其与瘤性途径联系起来.
结论:
- 区分AXL异型对于理解它们在癌症中的作用至关重要.
- 向抑制AXL是有前途的,但需要根据异型特异性功能进一步改进.
- 对AXL异形调节和信号的进一步研究对于推进向癌症治疗至关重要.
相关概念视频
mTOR Signaling and Cancer Progression
3.6K
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...
3.6K
Mitogens and the Cell Cycle
6.3K
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...
6.3K
Abnormal Proliferation
4.3K
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...
4.3K
Adaptive Mechanisms in Cancer Cells
5.5K
Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
5.5K
The Ras Gene
6.1K
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...
Ras is a...
6.1K
The Intrinsic Apoptotic Pathway
5.6K
Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
5.6K


