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Fig. 4 | Acta Neuropathologica Communications

Fig. 4

From: Tenascin-C expression contributes to pediatric brainstem glioma tumor phenotype and represents a novel biomarker of disease

Fig. 4

Altered TNC expression affects glioma cell proliferation, invasion and morphology in vitro. TNC expression was altered in pediatric supratentorial high-grade glioma (HGG n = 1) and brainstem glioma (DIPG n = 3) cell lines via lentiviral transfection of two distinct shRNA TNC constructs and one TNC cDNA. a TNC shRNA knockdown results in decreased cell proliferation, in all lines compared to empty vector controls (*p < 0.05, **p < 0.01, data for TNC shRNA 234 shown). X-axis: Time in days, day zero defined as day of plating. Y-axis: Cell proliferation calculated as number of cells collected on days 2, 4, 6, 8, relative to cell count on day 0 (percent). b TNC knockdown (shRNA) inhibits scratch gap closure on wound healing assay in all cell lines, with a mean decrease in cell motility of 17.7% compared to empty-vector controls (****p < 0.0001). TNC overexpression (via cDNA) did not significantly increase cell motility compared to empty vector controls. Y-axis: Cell migration rate relative to hour 0 (percent). c Top row: TNC knockdown results in decreased cell invasion compared to empty-vector controls (*p = 0.016, **p = 0.0067). Bottom row: Overexpressing TNC results in increased cell invasion compared to empty-vector controls (*p = 0.0227, SF9427 **p = 0.006, KNS42 **p = 0.0035) Y-axis: Cell count normalized to empty-vector controls. d Light microscopy demonstrates alteration of cell morphology after TNC cDNA transfection. SF8628 TNC cDNA cells appear larger and spread widely relative to control. DIPGIV cells changed from attached to suspended with TNC cDNA transfection. Cells stained by crystal violet. Scale bar = 100 μm. Error bars represent standard error of the mean

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