相关实验视频
Updated: Jun 11, 2025

08:41
Modeling Chemotherapy Resistant Leukemia In Vitro
Published on: February 9, 2016
9.0K
急性髓性白血病细胞粘附于骨髓,并通过降低UNC5B表达的调节来获得化学抵抗
Teng Teng1, Liping Ren2, Jilong Xiao3
1Shandong Key Laboratory of Traditional Chinese Medicine and Stress Injury, Department of Laboratory Animal Center, Central Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
Frontiers in oncology
|October 9, 2024
概括
发现一种蛋白质UNC5B可以抑制急性髓性白血病 (AML) 细胞粘附和增殖,增强化疗敏感性. 这表明UNC5B是AML治疗的潜在治疗标.
科学领域:
- 血液学 血液学 血液学
- 在瘤学瘤学.
- 分子生物学分子生物学
背景情况:
- 急性髓性白血病 (AML) 是一种由复发,折射性和化学抵抗性特征的血液性恶性瘤.
- AML细胞粘附和扩散是导致化疗耐药性的关键因素.
- 识别新的治疗点对于改善AML治疗结果至关重要.
研究的目的:
- 研究UNC5B在急性髓性白血病 (AML) 中的作用.
- 确定UNC5B是否可以克服AML中的化疗抵抗.
- 阐明UNC5B影响AML细胞行为的分子机制.
主要方法:
- 在AML细胞中过度表达UNC5B.
- 用于全球基因表达分析的RNA测序 (RNA-seq).
- 信号通路和基因表达的实验验证.
主要成果:
- 过度表达UNC5B显著抑制了AML细胞骨髓粘附.
- UNC5B抑制了AML细胞的增殖.
- UNC5B增强了AML细胞对化疗的敏感性.
- 机制研究显示,UNC5B抑制关键的粘附和扩散通路,降低MPZL1,CLDN23,IGF2和WNT7B的表达.
结论:
- UNC5B作为AML细胞粘附和扩散的抑制剂.
- UNC5B可以提高AML患者对化疗的敏感性.
- UNC5B代表了AML潜在的预后指标和治疗目标.
相关概念视频
Cancer Stem Cells and Tumor Maintenance
4.9K
Early diagnosis and treatment can often cure cancer. However, even with treatment, residual cells called cancer stem cells (CSC) might remain, often causing tumor recurrence. These cancer stem cells possess the potential for self-renewal and multi-lineage differentiation and are often responsible for the therapeutic resistance displayed in most cancers.
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...
4.9K
Treatment Resistant Cancers
3.3K
Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
3.3K
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
Differentiation of Common Myeloid Progenitor Cells
3.2K
Common myeloid progenitors (CMPs) are oligopotent cells that can differentiate into granulocytes and macrophages. Granulocytes and macrophages are essential for protecting the body against bacterial, viral, or fungal infections. They migrate from the bone marrow into the circulating blood to reach specific tissue sites where they differentiate and help in immune surveillance. However, they survive only for a few days and must be continuously made available to the organism to maintain a robust...
3.2K
Adaptive Mechanisms in Cancer Cells
5.7K
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,...
5.7K
Receptor Downregulation in MVBs
2.0K
Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR...
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR...
2.0K

