MOSJ-Dkk1小鼠骨肉瘤细胞系MOS-J基因工程改造版细胞-BioVector NTCC典型培养物保藏中心 BioVector NTCC保藏中心
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- 货 号：BioVector®-MOSJ-Dkk1
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BioVector® NTCC® MOSJ-Dkk1小鼠骨肉瘤细胞系MOS-J基因工程改造版细胞-BioVector NTCC典型培养物保藏中心
The BioVector® MOSJ-Dkk1 cell line is a genetically modified version of the mouse osteosarcoma cell line, MOS-J. In this modified line, the cells have been engineered to constitutively overexpress the human protein Dickkopf-1 (Dkk-1). This was done to study the role of Dkk-1 in osteosarcoma progression and its effects on bone formation.
Key characteristics and findings
Origin: The cell line is derived from the MOS-J cell line, which originated from a spontaneously occurring chondroblastic osteosarcoma in a C57BL/6J mouse. The MOS-J cells were transfected with a plasmid to express the human Dkk-1 gene.
Increased proliferation: Contrary to the canonical function of Dkk-1 as a Wnt signaling inhibitor, researchers found that expressing Dkk-1 in MOS-J cells increased cell proliferation and resistance to metabolic stress in vitro.
Aggressive tumor phenotype: In animal models, MOSJ-Dkk1 cells formed tumors that were larger and more destructive than those from the original MOS-J line. This confirms a pro-tumorigenic role for Dkk-1 in this specific osteosarcoma context.
Osteolytic capacity: The tumors from MOSJ-Dkk1 cells caused significant bone destruction (osteolysis) in mouse models, as Dkk-1 inhibits osteogenic differentiation (bone repair).
Signaling pathway modulation: Dkk-1 in these cells is shown to activate a non-canonical Wnt signaling pathway involving JNK, which leads to the upregulation of aldehyde-dehydrogenase-1 (ALDH1), a marker associated with cancer stem cells and stress resistance.
Therapeutic target: Because Dkk-1 drives an aggressive phenotype in this model, it is considered a potential therapeutic target for osteosarcoma. Studies have used blocking agents, like a Dkk-1-targeting morpholino (DkkMo), to inhibit Dkk-1 in these cells, which reduced tumor expansion and bone damage.
BioVector® MOSJ-Dkk1细胞系是小鼠骨肉瘤细胞系MOS-J的基因工程改造版本。在这个改造后的细胞系中，细胞被工程化，使其能够组成型地高表达人**Dickkopf-1 (Dkk-1)**蛋白。该细胞系用于研究Dkk-1在骨肉瘤进展中的作用及其对骨形成的影响。
主要特点与研究发现
来源：该细胞系源自MOS-J细胞系，后者来自C57BL/6J小鼠自发性发生的软骨母细胞性骨肉瘤。研究人员通过转染含有表达人Dkk-1基因的质粒，获得了MOSJ-Dkk1细胞。
增殖能力增强：尽管Dkk-1通常作为Wnt信号通路的抑制剂，但研究人员发现，在MOS-J细胞中表达Dkk-1反而增强了细胞的增殖能力和对代谢应激的抵抗力（体外实验）。
肿瘤表型更具侵袭性：在动物模型中，MOSJ-Dkk1细胞形成的肿瘤比原始MOS-J细胞形成的肿瘤更大、破坏性更强。这证实了Dkk-1在该特定骨肉瘤环境中具有促肿瘤作用。
溶骨能力：MOSJ-Dkk1细胞形成的肿瘤在小鼠模型中导致了显著的骨破坏（溶骨），因为Dkk-1会抑制成骨分化（骨修复）。
信号通路调节：这些细胞中的Dkk-1被证明能够激活一个非经典的Wnt信号通路，其中涉及JNK，这导致醛脱氢酶-1（ALDH1）的上调，而ALDH1是与癌症干细胞和应激抵抗相关的标志物。
治疗靶点：由于Dkk-1在这种模型中驱动了侵袭性表型，它被认为是一个潜在的骨肉瘤治疗靶点。研究中使用了靶向Dkk-1的吗啉代（DkkMo）等阻断剂来抑制这些细胞中的Dkk-1，结果显示能够减少肿瘤的扩张和骨损伤
Supplier来源:BioVector NTCC Inc.
Email: biovector@163.com
Website网址: http://www.biovector.net
The BioVector® MOSJ-Dkk1 cell line is a genetically modified version of the mouse osteosarcoma cell line, MOS-J. In this modified line, the cells have been engineered to constitutively overexpress the human protein Dickkopf-1 (Dkk-1). This was done to study the role of Dkk-1 in osteosarcoma progression and its effects on bone formation.
Key characteristics and findings
Origin: The cell line is derived from the MOS-J cell line, which originated from a spontaneously occurring chondroblastic osteosarcoma in a C57BL/6J mouse. The MOS-J cells were transfected with a plasmid to express the human Dkk-1 gene.
Increased proliferation: Contrary to the canonical function of Dkk-1 as a Wnt signaling inhibitor, researchers found that expressing Dkk-1 in MOS-J cells increased cell proliferation and resistance to metabolic stress in vitro.
Aggressive tumor phenotype: In animal models, MOSJ-Dkk1 cells formed tumors that were larger and more destructive than those from the original MOS-J line. This confirms a pro-tumorigenic role for Dkk-1 in this specific osteosarcoma context.
Osteolytic capacity: The tumors from MOSJ-Dkk1 cells caused significant bone destruction (osteolysis) in mouse models, as Dkk-1 inhibits osteogenic differentiation (bone repair).
Signaling pathway modulation: Dkk-1 in these cells is shown to activate a non-canonical Wnt signaling pathway involving JNK, which leads to the upregulation of aldehyde-dehydrogenase-1 (ALDH1), a marker associated with cancer stem cells and stress resistance.
Therapeutic target: Because Dkk-1 drives an aggressive phenotype in this model, it is considered a potential therapeutic target for osteosarcoma. Studies have used blocking agents, like a Dkk-1-targeting morpholino (DkkMo), to inhibit Dkk-1 in these cells, which reduced tumor expansion and bone damage.
BioVector® MOSJ-Dkk1细胞系是小鼠骨肉瘤细胞系MOS-J的基因工程改造版本。在这个改造后的细胞系中，细胞被工程化，使其能够组成型地高表达人**Dickkopf-1 (Dkk-1)**蛋白。该细胞系用于研究Dkk-1在骨肉瘤进展中的作用及其对骨形成的影响。
主要特点与研究发现
来源：该细胞系源自MOS-J细胞系，后者来自C57BL/6J小鼠自发性发生的软骨母细胞性骨肉瘤。研究人员通过转染含有表达人Dkk-1基因的质粒，获得了MOSJ-Dkk1细胞。
增殖能力增强：尽管Dkk-1通常作为Wnt信号通路的抑制剂，但研究人员发现，在MOS-J细胞中表达Dkk-1反而增强了细胞的增殖能力和对代谢应激的抵抗力（体外实验）。
肿瘤表型更具侵袭性：在动物模型中，MOSJ-Dkk1细胞形成的肿瘤比原始MOS-J细胞形成的肿瘤更大、破坏性更强。这证实了Dkk-1在该特定骨肉瘤环境中具有促肿瘤作用。
溶骨能力：MOSJ-Dkk1细胞形成的肿瘤在小鼠模型中导致了显著的骨破坏（溶骨），因为Dkk-1会抑制成骨分化（骨修复）。
信号通路调节：这些细胞中的Dkk-1被证明能够激活一个非经典的Wnt信号通路，其中涉及JNK，这导致醛脱氢酶-1（ALDH1）的上调，而ALDH1是与癌症干细胞和应激抵抗相关的标志物。
治疗靶点：由于Dkk-1在这种模型中驱动了侵袭性表型，它被认为是一个潜在的骨肉瘤治疗靶点。研究中使用了靶向Dkk-1的吗啉代（DkkMo）等阻断剂来抑制这些细胞中的Dkk-1，结果显示能够减少肿瘤的扩张和骨损伤
Supplier来源:BioVector NTCC Inc.
Email: biovector@163.com
Website网址: http://www.biovector.net
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