陕西省第二人民医院神经内科,陕西 西安 710000
Received:11 October 2024,
Published:25 June 2025
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赵凯涛,梁军丽,杨荣军等.盘状蛋白结构域受体1调控胶质瘤细胞增殖和凋亡的机制研究[J].局解手术学杂志,2025,34(06):484-488.
ZHAO Kai-tao,LIANG Jun-li,YANG Rong-jun,et al.Mechanism of disidin domain receptor 1 regulating the proliferation and apoptosis of glioma cells[J].JOURNAL OF REGIONAL ANATOMY AND OPERATIVE SURGERY,2025,34(06):484-488.
赵凯涛,梁军丽,杨荣军等.盘状蛋白结构域受体1调控胶质瘤细胞增殖和凋亡的机制研究[J].局解手术学杂志,2025,34(06):484-488. DOI: 10.11659/jjssx.10E024029.
ZHAO Kai-tao,LIANG Jun-li,YANG Rong-jun,et al.Mechanism of disidin domain receptor 1 regulating the proliferation and apoptosis of glioma cells[J].JOURNAL OF REGIONAL ANATOMY AND OPERATIVE SURGERY,2025,34(06):484-488. DOI: 10.11659/jjssx.10E024029.
目的
2
探究盘状蛋白结构域受体1(DDR1)对胶质瘤细胞增殖和凋亡的调控作用和机制。
方法
2
通过qRT-PCR和Western blot检测人胶质瘤细胞和正常胶质细胞中DDR1的表达量。用慢病毒感染法构建稳定过表达和敲降DDR1的胶质瘤细胞U251,利用CCK-8法检测稳定细胞系的增殖能力,并用流式细胞仪检测细胞凋亡能力。利用Western blot检测稳定细胞系中相关通路的激活情况,探究DDR1的调控机制。
结果
2
qRT-PCR和Western blot结果显示,人胶质瘤细胞U251中DDR1的表达量高于人胶质瘤细胞U87细胞和正常胶质细胞HEB,因此,选择U251细胞系进行后续实验。CCK-8实验显示,过表达DDR1能够促进胶质瘤细胞的增殖,敲降DDR1则抑制了胶质瘤细胞的增殖。流式细胞结果显示,过表达DDR1能够抑制胶质瘤细胞的凋亡,敲降DDR1则促进胶质瘤细胞凋亡。Western blot结果显示,过表达DDR1激活了PI3K/AKT通路,敲降DDR1抑制了PI3K/AKT通路的激活。
结论
2
DDR1能够通过激活PI3K/AKT通路增强胶质瘤细胞的增殖能力并抑制其凋亡,促进了胶质瘤细胞的发展。因此,DDR1可能成为治疗胶质瘤的一个潜在靶点。
Objective
2
To explore the regulatory effect and mechanism of disidin domain receptor 1 (DDR1) on the proliferation and apoptosis of glioma cells.
Methods
2
The expression levels of DDR1 in human glioma cells and normal glial cells were detected by qRT-PCR and Western blot. Glioma cells U251 with stable overexpression and knockdown of DDR1 were constructed by lentivirus infection, the proliferation ability of the stable cell line was detected by CCK-8 assay, and the apoptosis ability was detected by flow cytometry. Western blot was used to detect the activation of related pathways in stable cell lines and explore the regulatory mechanism of DDR1.
Results
2
The results of qRT-PCR and Western blot showed that the expression level of DDR1 in human glioma cell U251 was higher than those in human glioma cell U87 and normal glial cell HEB. Therefore, the U251 cell line was selected for subsequent experiments. CCK-8 assay showed that overexpression of DDR1 promote the proliferation of glioma cells, while knockdown of DDR1 inhibit the proliferation of glioma cells. The results of flow cytometry showed that overexpression of DDR1 inhibit the apoptosis of glioma cells, while knockdown of DDR1 induce the apoptosis of glioma cells. Western blot results showed that overexpression of DDR1 activate the PI3K/AKT pathway, while knockdown of DDR1 inhibit the activation of the PI3K/AKT pathway.
Conclusion
2
DDR1 can enhance the proliferation ability of glioma cells and inhibit their apoptosis by activating the PI3K/AKT pathway, promoting the development of glioma cells. Therefore, DDR1 may become a potential target for the treatment of glioma.
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