Fig. 2: Venlafaxine (VEN) inhibits the norepinephrine (NE)-enhanced cell viability and vascular endothelial growth factor (VEGF) expression in colon cancer cells. | Cell Death Discovery

Fig. 2: Venlafaxine (VEN) inhibits the norepinephrine (NE)-enhanced cell viability and vascular endothelial growth factor (VEGF) expression in colon cancer cells.

From: Venlafaxine antagonizes the noradrenaline-promoted colon cancer progression by inhibiting the norepinephrine transporter

Fig. 2: Venlafaxine (VEN) inhibits the norepinephrine (NE)-enhanced cell viability and vascular endothelial growth factor (VEGF) expression in colon cancer cells.

Colon cancer cells (CT26, HCT116, and SW480) were treated with control, VEN (10 μM), NE (10 μM), and drug combination [NE (10 μM) + VEN (10 μM)] for 24 h and 48 h separately. A The effects of NE/VEN on colon cancer cell proliferation were determined by 3-(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide (MTT) assay. B Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) assay was performed and revealed an increase in the VEGF mRNA with NE treatment, while VEN inhibited the NE-increased VEGF mRNA in colon cancer cells. C Western blotting was performed and revealed increases in VEGF protein and Akt activation with NE treatment, while VEN inhibited these NE-induced changes in colon cancer cells. The band intensities of VEGF, pAkt, and Akt relative to glyceraldehyde-3-phosphate dehydrogenase (GAPDH) were quantified and normalized to the Ctrl. group. The quantification graphs of normalized band intensities of different replicates were shown in Fig. S8. Data are expressed as mean ± SD, *P < 0.05, **P < 0.01, or ***P < 0.001 in (A) and (B).

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