Pericytes augment glioblastoma cell resistance to temozolomide through CCL5-CCR5 paracrine signaling - Zhang, Xiao-Ning; Yang, Kai-Di; Chen, Cong; He, Zhi-Cheng; Wang, Qiang-Hu; Feng, Hua; Lv, Sheng-Qing; Wang, Yan; Mao, Min; Liu, Qing; Tan, Yao-Yao; Wang, Wen-Ying; et al. (Cell research, 2021)
Keywords: 13; 13/21; 13/31; 13/51; 14; 14/19; 14/5; 38; 38/77; 42; 631/67/1059; 631/67/1922; 631/67/327; Animals; Antiretroviral drugs; Biomedical and Life Sciences; Brain cancer; CCR5 protein; Cell Biology; Cell Line, Tumor; Chemokine receptors; Chemokines; Chemoresistance; Chemotherapy; Combined treatment; Cytotoxicity; Deoxyribonucleic acid; Depletion; DNA; DNA damage; DNA repair; DNA-dependent protein kinase; Drug Resistance, Neoplasm; Glioblastoma; Glioblastoma - drug therapy; Glioma; Kinases; Life Sciences; Medical prognosis; Mice; Niches; Paracrine Communication; Paracrine signalling; Pericytes; Protein kinase C; Signaling; Stimulators; Temozolomide; Temozolomide - pharmacology; Temozolomide - therapeutic use; Toxicity; Tumors; Xenograft Model Antitumor Assays; Xenografts; Xenotransplantation