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Fig. 2 | BMC Cancer

Fig. 2

From: Identification of V-ATPase as a molecular sensor of SOX11-levels and potential therapeutic target for mantle cell lymphoma

Fig. 2

Wild-type V-ATPase level is a pre-requisite for SOX11-dependent bafilomycin A1-induced growth inhibition. Cell lines with altered expression of SOX11 (high/SOX11IND-, low/SOX11IND+) were transfected with (a) a pool of siRNAs targeting V-ATPase or (b) a control siRNA (SCR), and treated with different concentrations of bafilomycin A1 for up to 48 h. The data here represents the 48 h time-point. a Following treatment with bafilomycin A1, cells with knocked V-ATPase fail to show SOX11-dependent bafilomycin A1-induced growth inhibition. b Cells with functional V-ATPase show SOX11-dependent, bafilomycin A1-induced growth reduction at 50 and 500 nM. Thus, we conclude that the SOX11-dependent, V-ATPase inhibitor-induced growth inhibition is related to the function of V-ATPase. Mean values are normalized against corresponding non-treated control samples, and error bars indicate SEM. The significance was determined by Student’s t-test (*P <0.05, **P <0.005). V-ATPaseTR refers to transient knock-down of V-ATPase, and SCRTR refers to scrambled control used in transient knock-down experiments

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