Background: Rosmarinic acid (RA) is a natural phenolic compound that acts as a Fyn inhibitor by 53 homology modeling of the human Fyn structure. Therefore, the apoptosis mechanism related to NF-κB signaling pathway induced by RA in HepG2 was investigated. Methods: The cell growth, apoptosis, and proliferation of HepG2 regulated by various concentrations of RA were studied. The proteins expression of MMP-2, MMP-9, PI3K, AKT, NF-κB, and apoptosis-related proteins Bax, Bcl-2, cleaved caspase-3 were detected. Results: RA significantly reduced proliferation rates, inhibited migration and invasion, and decreased the expressions of invasion-related factors, such as matrix metalloproteinase (MMP)-2 and MMP-9. TUNEL staining revealed that RA resulted in a dose-dependent increase of HepG2 cell apoptosis. In line with this finding, the expression of apoptosis suppressor protein Bcl-2 was downregulated and that of the pro-apoptotic proteins Bax and cleaved caspase-3 was increased. In addition, we found that the phosphatidylinositol 3-kinase (PI3K)/Akt/nuclear factor kappa B (NF-κB) signaling pathway was involved in RA-mediated inhibition of HepG2 cell metastasis. Conclusion: Our study identified that RA as a drug candidate for the treatment of HCC.

Background AQP-9 is the key element of apoptosis, but its mechanism related to glucose metabolism in colon cancer was unclear. Therefore, the role of miR-539 in regulating expression of AQP-9 and its bio-functions were investigated. Methods The target gene of miR-539 was verified. The cell growth, apoptosis, and proliferation of SW480 regulated by AQP-9 and miR-539 were explored. The proteins expression associated with glucose metabolism pathway and apoptosis-related proteins were determined. Moreover, the glucose oxidase colorimetric method was used to measure the production of glucose in SW480. Results AQP9 was the target gene of miR-539. Interference on AQP-9 expression inhibited cell proliferation and growth of SW480, promoted its apoptosis by regulating Bcl-2 family members. Meanwhile, it caused down-expression of GOT1, GK and G6PC. Through inhibiting the expression of AQP-9 in SW480 could reduced cellular glucose production process. The above bio-functions could be achieved by utilization of miR-539 to suppress the expression of AQP-9, too. Conclusion Our work identified that the utilization of siRNA of AQP-9 with miR-539 could cause inhibition of proliferation, growth and induce apoptosis in SW480, which was associated with gluconeogenesis genes GOT1, GK, and G6PC in the progression of cellular glucose metabolism.