Fig. 2: PTGDS regulated the viability, proliferation, cell cycle, apoptosis, and invasion of DLBCL cells. | Cell Death & Differentiation

Fig. 2: PTGDS regulated the viability, proliferation, cell cycle, apoptosis, and invasion of DLBCL cells.

From: Glycoprotein PTGDS promotes tumorigenesis of diffuse large B-cell lymphoma by MYH9-mediated regulation of Wnt–β-catenin–STAT3 signaling

Fig. 2

A GO analysis of PTGDS associated genes based on the GEO database (GSE31312). B and C The treatment with rhPTGDS and PGD2 promoted cell proliferation in a dose-dependent manner. D Relative expression of PTGDS protein was confirmed by western blotting in lentivirus transfected cells. E–G PTGDS overexpression promoted cell proliferation, and PTGDS knockdown inhibited cell viability, proliferation, and c-myc expression. H–K In a xenograft DLBCL mouse model, the growth rate, weight, volume, and bioluminescence of tumor were higher in the LV-PTGDS group than sh-PTGDS group (n = 6 per group). L and M PTGDS knockdown induced cell cycle arrest at G0/G1 phase and inhibited the expression of Cyclin D1 and CDK2. N and O PTGDS knockdown increased cell apoptosis and regulated the expression of apoptosis-associated proteins. P and Q PTGDS knockdown suppressed cell invasion and the expression of zeb1 and vimentin. After culture for 24–48 h, the percentage of cells in the lower chamber to input cells represented the level of cell invasion. Data are shown as the mean ± SD. *p < 0.05; **p < 0.01; ***p < 0.001.

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