Skip to main content
Fig. 1 | Journal of Experimental & Clinical Cancer Research

Fig. 1

From: TMEM52B suppression promotes cancer cell survival and invasion through modulating E-cadherin stability and EGFR activity

Fig. 1

TMEM52B expression in cell lines. (A) Top, real-time quantitative PCR analysis of TMEM52B in various human cancer cell lines. β-actin was used as an internal control for input RNA. Middle, semi-quantitative RT-PCR analysis of TMEM52B. Densitometric quantification was performed on gel images. Bottom, gel images of semi-quantitative RT-PCR. All determinations were performed in three independent experiments. Values represent mean ± standard deviation (SD). *P < 0.05. (B) Immunoblot analysis of TMEM52B in human cancer cells. GAPDH was used as an internal control. (C) HEK293E cells were transfected with a GFP-fused TMEM52B-expression vector for 48 h before visualizing GFP. Scale bar, 10 μm. (D) Immunoblot analysis of subcellular localization of TMEM52B in SW480sub cells. WCL, whole-cell lysates; C, cytosolic fraction; N, nuclear fraction; M, plasma membrane-enriched fraction; CS, cytoskeletal fraction. GAPDH, Histone H3, EGFR, and vimentin were used as internal controls for the cytosolic, nuclear, and plasma membrane, and cytoskeletal fractions, respectively

Back to article page