| 巴晓琰,李书艳,郑珂,等.B7同源物3介导胶质母细胞瘤放射抗拒的机制研究[J].中华放射医学与防护杂志,2026,46(5):497-503.Ba Xiaoyan,Li Shuyan,Zheng Ke,et al.Mechanistic research of B7 homolog 3-mediated radioresistance in glioblastoma[J].Chin J Radiol Med Prot,2026,46(5):497-503 |
| B7同源物3介导胶质母细胞瘤放射抗拒的机制研究 |
| Mechanistic research of B7 homolog 3-mediated radioresistance in glioblastoma |
| 投稿时间：2025-10-18 |
| DOI：10.3760/cma.j.cn112271-20251018-00363 |
| 中文关键词: B7-H3 胶质母细胞瘤 放射敏感性 STAT3 |
| 英文关键词:B7-H3 Glioblastoma Radiosensitivity STAT3 |
| 基金项目:河南省科技攻关计划项目(212102310663);河南省医学科技攻关(SBGJ202503016);国家自然科学基金(82302937) |
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| 中文摘要: |
| 目的 探讨B7同源物3(B7-H3)对胶质母细胞瘤放射敏感性的调控作用及潜在机制。方法 选取人胶质母细胞瘤细胞系U251,通过慢病毒转染构建B7-H3过表达组、敲低组和空载对照组,经q-PCR和Western blot验证感染效率。采用0、2、4、6、8 Gy X射线照射,进行克隆形成实验,计算存活分数(SF)与增敏比(SER);另设10 Gy照射组,于照射后24、48、72、96 h利用CCK-8法检测细胞增殖活力,于照射后48 h通过Transwell实验评估侵袭能力、流式细胞术检测细胞凋亡,并采用Western blot检测B7-H3、Cleaved-Caspase-3、STAT3及磷酸化STAT3(p-STAT3)蛋白表达。结果 成功构建B7-H3表达调控的稳定转染细胞株。与空载对照组相比,过表达B7-H3诱导放射抵抗(SF2=0.70、0.60,P<0.01)。过表达B7-H3可降低射线对细胞增殖的抑制作用(48 h:t=4.40,P<0.01),促进细胞侵袭(t=4.87,P<0.01),并降低凋亡率(t=5.75,P<0.01),敲低组Cleaved-Caspase-3蛋白表达显著上调(t=7.49,P<0.01)。辐射可上调B7-H3表达(t=5.57,P<0.01);B7-H3过表达能激活STAT3磷酸化(t=9.97,P<0.01)。结论 B7-H3可能通过调控STAT3磷酸化影响胶质母细胞瘤细胞放射敏感性,有望成为改善胶质母细胞瘤放疗疗效的新靶点。 |
| 英文摘要: |
| Objective To investigate the regulatory effect of B7 homolog 3 (B7-H3) on the radiosensitivity of glioblastoma and its potential mechanisms. Methods Human glioblastoma U251 cells were selected. B7-H3 overexpression, knockdown, and empty vector control groups were established via lentiviral transfection, and the infection efficiency was verified by q-PCR and Western blot. Colony formation assay was performed with 0, 2, 4, 6, and 8 Gy X-ray irradiation to calculate the survival fraction (SF) and sensitization enhancement ratio (SER) Cells were irradiated with 10 Gy X-rays for functional assays. Cell proliferation was assessed by CCK-8 assay at 24, 48, 72, and 96 h post-irradiation. Invasion ability was evaluated by Transwell assay, and apoptosis was detected by flow cytometry and Western blot at 48 h post-irradiation. The protein expression levels of B7-H3, Cleaved-Caspase-3, STAT3, and phosphorylated STAT3 (p-STAT3) were determined by Western blot. Results Stable cell lines with regulated B7-H3 expression were successfully established. Compared with the empty vector control group, cells in the overexpression group exhibited radioresistance (SF2=0.70, 0.60, P<0.01). Overexpression of B7-H3 attenuated the inhibitory effect of radiation on cell proliferation (48 h: t=4.40, P<0.01), promoted cell invasion (t=4.87, P<0.01), and decreased the apoptosis rate (t=5.75, P< 0.01). Western blot showed that Cleaved-Caspase-3 expression was significantly upregulated in the knockdown group (t=7.49, P<0.01). Radiation upregulated B7-H3 expression (t=5.57, P<0.01). B7-H3 overexpression could activate STAT3 phosphorylation (t=9.97, P< 0.01). Conclusions B7-H3 influences the radiosensitivity of GBM cells by regulating STAT3 phosphorylation, suggesting its potential as a novel target for improving the efficacy of radiotherapy in GBM. |
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