Fig. 1: c-SRC promotes glioblastoma progression.
a Western blot analysis of clinical glioma samples to determine c-SRC expression and activation (p-c-SRC). IDH1 R132 mutation occurs in two cases of low-grade gliomas (#23 and #32). IDH1 mutations were not found in high-grade gliomas. The protein marker kilodalton (kDa) in Western Blot is abbreviated as Mr (K). The same applies to the WB figure below. The samples derive from the same experiment but different gels for p-c-SRC and c-SRC. N: normal tissue; WHO glioma grade: I–IV, n = 35. b The correlation between c-SRC activation and glioma malignancy (WHO glioma grade: I–IV) was analyzed based on optical density integrity (ODI) with ImageJ in clinical tissue (patient 3–35, n = 33 clinical samples). c–e, c-SRC in U87 and CHG-5 was knocked down by two independent short hairpin RNA (shSRC #1 and shSRC #2; shCtrl: pLL3.7-based scramble shRNA as control) (e). 1 × 104 U87 and 1 × 104 CHG-5 cells were seeded in 6-well plates, and the cell numbers were quantified at the indicated time. Growth curves illustrating cell proliferation of U87 (c) and CHG-5 (d) are depicted, based on cell numbers (n = 3 independent experiments). f, g MRI images of brain sections were captured 30 days after intracranial infusion of 1 × 105 U87 cells (f). Tumor volume was calculated based on the sphere radius of brain tumors (g) (n = 6 independent mice). Statistical data in (b, c, d, and g) are presented as the mean ± SD. p-values were calculated based on unpaired and two-sided Student’s t-test.
