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. 2018 Feb 2;8(5):1350–1360. doi: 10.7150/thno.22736

Figure 2.

Figure 2

GBM-derived conditioned medium (CM) cultured under hypoxia enhanced hADSCs migration, and CXCR4-overexpression in hADSCs showed further enhanced migration. (A) Schematic of a transwell-mediated chemotactic migration assay of hADSCs toward tumor-derived conditioned medium cultured under hypoxia or normoxia. Tumor growth medium alone was included as a control. (B) Compared with untransfected hADSCs, overexpression of CXCR4 in hADSCs increased cell migration toward tumor-derived CM under normoxia. CM derived under hypoxia (O2, 1%) further enhanced migration of both hADSCs and CXCR4-hADSCs. Pre-incubation of hADSCs with the CXCR4 antagonist AMD3100 abolished such migration of both hADSCs and CXCR4-overexpressing hADSCs to a minimal level as the control. hADSCs were stained red with the fluorescent dye PKH26; nuclei were labeled blue with Hoechst 33342. Scale bar = 200 μm. (C) Quantification of cell migration. CM, conditioned medium. αp<0.05 vs. hADSC migrated towards conditioned medium from normoxia (O2, 20%); βp<0.05 vs. hADSCs migrated towards CM-Hypoxia, γp<0.05 vs. CXCR4-hADSCs migrated towards CM-Normoxia. (D) Hypoxia significantly up-regulates SDF-1α secreted in U87MG glioma cells. The amount of SDF-1α in conditioned media from U87MG under hypoxia (O2, 1%) or normoxia (O2, 20%) was quantified using ELISA. **P<0.01.