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[Thymosin beta 10 prompted the VEGF-C expression in lung cancer cell]
Zixuan Li1, Lianyue Qu2, Hongshan Zhong3
1Department of Pathology, the First Affiliated Hospital of China Medical University and College of Basic Medical Sciences, China Medical University, Shenyang 110001, China;Department of Radiology and Key Laboratory of Diagnostic Imaging and Interventional Radiology of Liaoning Province, the First Affiliated Hospital of China Medical University, Shenyang 110001, China.
Background And Objective:
Our previous study found that thymosin β10 overexpressed in lung cancer and positively correlated with differentiation, lymph node metastasis and stage of lung cancer. In this reasearch we aim to study the effects and mechanism of exogenous human recombinant Tβ10 on the expression of VEGF-C on non-small cell lung cancer.
Methods:
After SPC, A549 and LK2 cells were treated with 100 ng/mL recombinant human Tβ10, the mRNA level of VEGF-C were detected by RT-PCR. The mean while the protein expression of VEGF-C, P-AKT and AKT were determined by Western blot assay.
Results:
Exogenous recombinant human Tβ10 were significantly promote the expression levels of VEGF-C mRNA and protein while promoting the phosphorylation of AKT. Exogenous Tβ10 can promote the expression of VEGF-C mRNA and protein in lung cancer cell lines A549 and LK2 (P<0.05), and this effect can be inhibited by use AKT inhibitor LY294002 (P<0.05).
Conclusions:
Tβ10 human recombinant proteins can promote the expression of VEGF-C by activating AKT phosphorylation in lung cancer cell lines.
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