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Fig. 4 | Molecular Cancer

Fig. 4

From: Na,K-ATPase β1-subunit is a target of sonic hedgehog signaling and enhances medulloblastoma tumorigenicity

Fig. 4

Activation of Shh signaling prevents Na,K-ATPase β1-subunit upregulation during CGP differentiation. a. Phase contrast images showing proliferation of CGP cells after six days of treatment with 0.1 μM SAG. Scale bar, 100 μm. b. In vitro cultured CGP cells were incubated with either DMSO or 0.1 μM SAG for the indicated period of time and β1-subunit levels were determined by immunoblotting. α-tubulin was used to ensure equal loading. c. β1-subunit mRNA levels in CGP cells cultured from WT mice. mRNA levels are from CGP cells treated with DMSO or 0.1 μM SAG for seven days, and CGP cells cultured from Smo/Smo mice. The mRNA levels were normalized to control cells treated with DMSO. The differences in β1-subunit mRNA levels between DMSO and SAG treated and DMSO and Smo/Smo CGP cells were significant (** = p < 0.005). d. Immunoblots for β1-subunit and Gli1 in ONS-76 cells treated for 48 h with 0.1 μM SAG. α-tubulin served as loading control. e. Immunoblots for β1-subunit and Gli1 in DAOY cells treated for 48 h with 0.1 μM SAG. α-tubulin served as loading control. The β1-subunit level relative to the level of α-tubulin in SAG-treated cells was reduced to 60 % of the β1-subunit level in DMSO-treated control cells. f. β1-subunit and Gli1 mRNA levels in DAOY cells treated for 2 h with 0.1 μM SAG. β-actin was used as the endogenous control. The difference between the mRNA levels of β1-subunit and Gli1 was significant (* = p < 0.05). g. β1-subunit levels in Gli1 overexpressing cells. 293 T cells were transfected with pEGFPC1-Gli1 or pEGFPC1 vector as control for 72 h. Immunoblots for β1-subunit and Gli1 are shown. α-tubulin served as loading control. The β1-subunit level relative to the level of α-tubulin in Gli-transfected cells was only 70 % of the β1-subunit level in vector only-transfected cells

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