Ba Xiaoyan,Li Shuyan,Zheng Ke,et al.Mechanistic research of B7 homolog 3-mediated radioresistance in glioblastoma[J].Chinese Journal of Radiological Medicine and Protection,2026,46(5):497-503
Mechanistic research of B7 homolog 3-mediated radioresistance in glioblastoma
Received:October 18, 2025  
DOI:10.3760/cma.j.cn112271-20251018-00363
KeyWords:B7-H3  Glioblastoma  Radiosensitivity  STAT3
FundProject: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)
Author NameAffiliationE-mail
Ba Xiaoyan Department of Radiation Oncology, Affiliated Cancer Hospital of Zhengzhou University, Henan Cancer Hospital, Zhengzhou 450008, China  
Li Shuyan Department of Radiation Oncology, Affiliated Cancer Hospital of Zhengzhou University, Henan Cancer Hospital, Zhengzhou 450008, China  
Zheng Ke Department of Radiation Oncology, Affiliated Cancer Hospital of Zhengzhou University, Henan Cancer Hospital, Zhengzhou 450008, China  
Huang Rong Department of Radiation Oncology, Affiliated Cancer Hospital of Zhengzhou University, Henan Cancer Hospital, Zhengzhou 450008, China  
Sun Xueming Department of Radiation Oncology, Affiliated Cancer Hospital of Zhengzhou University, Henan Cancer Hospital, Zhengzhou 450008, China  
Wu Hui Department of Radiation Oncology, Affiliated Cancer Hospital of Zhengzhou University, Henan Cancer Hospital, Zhengzhou 450008, China wuhui7008@126.com 
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Abstract::
      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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