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. 2022 Mar 17;29(9):1834–1849. doi: 10.1038/s41418-022-00969-2

Fig. 2. GLT8D1 promotes tumor growth.

Fig. 2

a Individual GLT8D1 shRNA knockdown efficiency was verified by qRT-PCR (top) and IB (bottom) in indicated cells, scrambled shRNA was used as a control. Indicated cell lysates were probed with GLT8D1 and β-actin antibodies, representative images are shown. Green arrow: endogenous GLT8D1 proteins; Red arrow: exogenous GLT8D1 proteins. b Knockdown of GLT8D1 inhibited GSC11, GBM1, U251GSC and A172GSC cell growth. A172GSC = CD133+/CD44+ enriched A172 GSC cells; G8D sh#1 = GLT8D1 shRNA#1, G8D sh#2 = GLT8D1 shRNA#2, ove=overexpression. c, d GLT8D1 knockdown dramatically inhibits the colony formation ability of U251GSC and A172GSC in vitro. d Quantification data for c. Scale bar: 5 mm. e, f GLT8D1 knockdown inhibited the DNA synthesis in GSC11 cells by BrdU incorporation assay (e),(f) Quantification data for BrdU staining in GSC11 (top) and GBM1 (bottom) cells. DAPI: 4,6-diamidino-2-phenylindole (n ≥ 5). Scale bar: 100 μm. g, h GLT8D1 knockdown leads to accumulation of G2/M cells by FACS analysis in U251GSC (left) and A172GSC (right). Indicated cells were stained with PI for analyzing cell cycle distribution. h Depletion of GLT8D1 increased p21 and p-CDK1(Y15) expressions in U251GSC (left) and A172GSC (right) cells. Means ± SEM, *P < 0.05,**P < 0.01, ***P < 0.001; t-test.