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Suprabasin as a novel tumor endothelial cell marker.

Alam MT, Nagao-Kitamoto H, Ohga N, Akiyama K, Maishi N, Kawamoto T, Shinohara N, Taketomi A, Shindoh M, Hida Y, Hida K - Cancer Sci. (2014)

Bottom Line: SBSN knockdown inhibited the migration and tube formation ability of TEC.We also showed that the AKT pathway was a downstream factor of SBSN.These findings suggest that SBSN is involved in the angiogenic potential of TEC and may be a novel TEC marker.

View Article: PubMed Central - PubMed

Affiliation: Vascular Biology, Frontier Research Unit, Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan; Department of Oral Pathology and Biology, Graduate School of Dental Medicine, Hokkaido University, Sapporo, Japan.

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Suprabasin (SBSN) expression after growth factor treatment. NEC were incubated in 0.5% EBM2 medium for 12 h, followed by treatment with endothelial growth factor (EGF), vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) for 12 h. The cells were cultured at 37°C in a humidified atmosphere of 5% CO2. *P < 0.05 versus control; two-sided student's t-test. After 12 h of incubation, mRNA was extracted from the cells and used in the RT-PCR analysis of SBSN expression.
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fig04: Suprabasin (SBSN) expression after growth factor treatment. NEC were incubated in 0.5% EBM2 medium for 12 h, followed by treatment with endothelial growth factor (EGF), vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) for 12 h. The cells were cultured at 37°C in a humidified atmosphere of 5% CO2. *P < 0.05 versus control; two-sided student's t-test. After 12 h of incubation, mRNA was extracted from the cells and used in the RT-PCR analysis of SBSN expression.

Mentions: The PI3K/AKT pathway plays an essential role in the survival of TEC.(29) We previously reported that activation of AKT was involved in cell migration of mTEC;(13,23) and, therefore, we explored the interaction between the AKT pathway and SBSN. Phosphorylation of AKT in mTEC was suppressed by the PI3K inhibitor LY294002 treatment (Suppl. Fig. S5a). Moreover, we showed that the protein level of phosphorylated AKT was reduced by siSBSN treatment compared with control siRNA in both types of mTEC (melanoma and renal) (Fig. 3a), but not in NEC or in other cell types (Suppl. Fig. S5b). Moreover, we demonstrated that LY294002 inhibited tube formation in mTEC in a concentration-dependent manner (Fig. 3b). These findings indicate that SBSN regulated the migration and tube formation of mTEC via the AKT pathway. In addition, SBSN-positive blood vessels in human colon cancer tissues were positively stained by anti-AKT, but not those of normal colon tissues (Fig. 3c). This result suggests that SBSN may also be involved in AKT activation in human tumor blood vessels. To address how SBSN expression is regulated, endothelial cells were treated with growth factors such as endothelial growth factor (EGF), VEGF and fibroblast growth factor-2 (FGF-2). Among these growth factors, EGF significantly induced SBSN mRNA expression in NEC (Fig. 4).


Suprabasin as a novel tumor endothelial cell marker.

Alam MT, Nagao-Kitamoto H, Ohga N, Akiyama K, Maishi N, Kawamoto T, Shinohara N, Taketomi A, Shindoh M, Hida Y, Hida K - Cancer Sci. (2014)

Suprabasin (SBSN) expression after growth factor treatment. NEC were incubated in 0.5% EBM2 medium for 12 h, followed by treatment with endothelial growth factor (EGF), vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) for 12 h. The cells were cultured at 37°C in a humidified atmosphere of 5% CO2. *P < 0.05 versus control; two-sided student's t-test. After 12 h of incubation, mRNA was extracted from the cells and used in the RT-PCR analysis of SBSN expression.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4317965&req=5

fig04: Suprabasin (SBSN) expression after growth factor treatment. NEC were incubated in 0.5% EBM2 medium for 12 h, followed by treatment with endothelial growth factor (EGF), vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) for 12 h. The cells were cultured at 37°C in a humidified atmosphere of 5% CO2. *P < 0.05 versus control; two-sided student's t-test. After 12 h of incubation, mRNA was extracted from the cells and used in the RT-PCR analysis of SBSN expression.
Mentions: The PI3K/AKT pathway plays an essential role in the survival of TEC.(29) We previously reported that activation of AKT was involved in cell migration of mTEC;(13,23) and, therefore, we explored the interaction between the AKT pathway and SBSN. Phosphorylation of AKT in mTEC was suppressed by the PI3K inhibitor LY294002 treatment (Suppl. Fig. S5a). Moreover, we showed that the protein level of phosphorylated AKT was reduced by siSBSN treatment compared with control siRNA in both types of mTEC (melanoma and renal) (Fig. 3a), but not in NEC or in other cell types (Suppl. Fig. S5b). Moreover, we demonstrated that LY294002 inhibited tube formation in mTEC in a concentration-dependent manner (Fig. 3b). These findings indicate that SBSN regulated the migration and tube formation of mTEC via the AKT pathway. In addition, SBSN-positive blood vessels in human colon cancer tissues were positively stained by anti-AKT, but not those of normal colon tissues (Fig. 3c). This result suggests that SBSN may also be involved in AKT activation in human tumor blood vessels. To address how SBSN expression is regulated, endothelial cells were treated with growth factors such as endothelial growth factor (EGF), VEGF and fibroblast growth factor-2 (FGF-2). Among these growth factors, EGF significantly induced SBSN mRNA expression in NEC (Fig. 4).

Bottom Line: SBSN knockdown inhibited the migration and tube formation ability of TEC.We also showed that the AKT pathway was a downstream factor of SBSN.These findings suggest that SBSN is involved in the angiogenic potential of TEC and may be a novel TEC marker.

View Article: PubMed Central - PubMed

Affiliation: Vascular Biology, Frontier Research Unit, Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan; Department of Oral Pathology and Biology, Graduate School of Dental Medicine, Hokkaido University, Sapporo, Japan.

Show MeSH
Related in: MedlinePlus