BioVector? NTCC? MOSJ-Dkk1小鼠骨肉瘤細胞系MOS-J基因工程改造版細胞-BioVector NTCC典型培養(yǎng)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細胞系是小鼠骨肉瘤細胞系MOS-J的基因工程改造版本。在這個改造后的細胞系中，細胞被工程化，使其能夠組成型地高表達人**Dickkopf-1 (Dkk-1)**蛋白。該細胞系用于研究Dkk-1在骨肉瘤進展中的作用及其對骨形成的影響。
主要特點與研究發(fā)現(xiàn)
來源：該細胞系源自MOS-J細胞系，后者來自C57BL/6J小鼠自發(fā)性發(fā)生的軟骨母細胞性骨肉瘤。研究人員通過轉(zhuǎn)染含有表達人Dkk-1基因的質(zhì)粒，獲得了MOSJ-Dkk1細胞。
增殖能力增強：盡管Dkk-1通常作為Wnt信號通路的抑制劑，但研究人員發(fā)現(xiàn)，在MOS-J細胞中表達Dkk-1反而增強了細胞的增殖能力和對代謝應(yīng)激的抵抗力（體外實驗）。
腫瘤表型更具侵襲性：在動物模型中，MOSJ-Dkk1細胞形成的腫瘤比原始MOS-J細胞形成的腫瘤更大、破壞性更強。這證實了Dkk-1在該特定骨肉瘤環(huán)境中具有促腫瘤作用。
溶骨能力：MOSJ-Dkk1細胞形成的腫瘤在小鼠模型中導(dǎo)致了顯著的骨破壞（溶骨），因為Dkk-1會抑制成骨分化（骨修復(fù)）。
信號通路調(diào)節(jié)：這些細胞中的Dkk-1被證明能夠激活一個非經(jīng)典的Wnt信號通路，其中涉及JNK，這導(dǎo)致醛脫氫酶-1（ALDH1）的上調(diào)，而ALDH1是與癌癥干細胞和應(yīng)激抵抗相關(guān)的標志物。
治療靶點：由于Dkk-1在這種模型中驅(qū)動了侵襲性表型，它被認為是一個潛在的骨肉瘤治療靶點。研究中使用了靶向Dkk-1的嗎啉代（DkkMo）等阻斷劑來抑制這些細胞中的Dkk-1，結(jié)果顯示能夠減少腫瘤的擴張和骨損傷

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