Aim
This study was aimed to explore the role of growth differentiation factor 15 (GDF15) in hepatocellular carcinoma (HCC).
Conclusion
GDF15 could promote cell viability, invasion, migration, and angiogenesis of HepG2 cells. GDF15 overexpression might be a potential risk factor of HCC.
Methods
Human liver carcinoma cell line HepG2 was used and transfected with vector and/or short hairpin RNA (shRNA) against GDF15. Then, the transfection efficiency was ascertained by real-time reverse transcription-polymerase chain reaction (RT-PCR) and Western blot. Cell viability was measured by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyltetrazolium bromide (MTT). Cell invasion and migration were measured by Transwell assay and Scratch assay. In addition, human umbilical vein endothelial cell (HUVEC) tube formation assay was performed to analysis the angiogenesis. Further, the protein expressions of epithelial-mesenchymal transition (EMT)-related factors were measured by Western blot. Result: We found that GDF15 overexpression significantly facilitated cell viability, cell invasion, migration, and angiogenesis (P<0.05 or P<0.01). The protein expressions of N-Cadherin, Vimentin and Twist1 were up-regulated by GDF15 overexpression, while E-Cadherin was down-regulated. Reciprocally, using a GDF15-shRNA strategy, we observed that GDF15 downregulation inhibited both basal and GDF15-induced cell viability, migration, invasion and angiogenesis in HepG2 cells.