Fig 2: XPA stimulates the repair of temozolomide-induced DNA double-strand breaks. (A) Representative western blot analysis of ?-H2AX and GAPDH in U87 cells and U87-R cells stably transfected with shCon or shXPA treated with TMZ. (B) Representative immunofluorescence assay of ?-H2AX in U87 cells and U87-R cells stably transfected wih shCon or shXPA treated with TMZ.TMZ: temozolomide; DMSO: dimethyl sulfoxide; DAPI: 4',6-diamidino-2-phenylindole.

Fig 3: XPA silencing increases temozolomide sensitivity in vivo. (A) U87 and U87-R cells stably transfected with shCon or shXPA, and subsequently injected into nude mice. Tumors were excised and volume was calculated every week. Representative images of isolated tumors were displayed. (B) The tumor inhibition rates according to the weight of explanted tumors in each experimental group. ***P = 0.001, compared with shCon group. ###P = 0.001, compared with U87 group. (C) Analysis of tumor growth in each experimental group. (D) Representative immunoblot analysis of XPA, ?-H2AX and GAPDH of xenografted tumors. (E) Representative immunohistochemical analysis of Ki67 and ?-H2AX protein levels (brown) in each experimental group.TMZ: temozolomide.

Fig 4: Temozolomide-resistant GBM cells exhibits a high expression level of XPA. (A) Representative western blot analysis of NER-related proteins and GAPDH in U87 cells, U87-R cells, U251 cells and U251-R cells. (B) qRT-PCR analysis of NER-related genes and GAPDH in U87 cells, U87-R cells, U251 cells and U251-R cells. ***P = 0.001, compared with U87 group. (C) Representative western blot analysis of XPA and GAPDH in HUVEC, HUASMC, U87 cells and U251 cells. *P = 0.05, compared with U251 group. (D) qRT-PCR analysis of XPA and GAPDH in HUVEC, HUASMC, U87 cells and U251 cells. **P = 0.01, ***P = 0.001, compared with HUVEC group. (E) Expression pattern of XPA in glioblastoma tumor tissue and brain tissue based on datasets in TCGA. ***P = 0.001, compared with Tumor group.