mproved cell survival by upregulating p38 in the MAPK cascade and increasing p-AKT in the AKT cascade, in particular in lung cancer cell lines. Overall, the results from the present study demonstrated that ENO1 may contribute to the development of lung cancers, but not esophageal cancers. Copyright © Chen et al.The role of forkhead box O3 (FOXO3) as a tumor suppressor gene and its association with the human lifespan is well documented. However, several studies have indicated that high expression of FOXO3 is also significantly associated with tumorigenesis. The aim of the present study was to determine the clinical significance of FOXO3 in the development and prognosis of hepatocellular carcinoma (HCC). mRNA expression data of FOXO3 from The Cancer Genome Atlas database was analyzed through the UALCAN online tool to compare the expression of FOXO3 between HCC and normal liver tissues. Subsequently, the expression of FOXO3 at the protein level was investigated via immunohistochemical staining of 314 HCC and 150 non-cancerous liver tissue samples. The association between protein expression and clinicopathological parameters was analyzed using the χ2 test, and the effect of FOXO3 expression on survival was assessed via Kaplan-Meier analysis. The expression of FOXO3 mRNA was significantly higher in HCC in comparison with healthy tissues. High FOXO3 protein expression was revealed in 43/150 non-cancerous liver tissues, and in 238/314 HCC samples. A significant association was demonstrated between FOXO3 expression and metastasis, Tumor-Node-Metastasis stage, Edmondson grade, α-fetoprotein level and overall survival. In conclusion, the high expression of FOXO3 predicts a poor prognosis in patients with HCC, indicating this protein as a potential therapeutic target in HCC. Copyright © Song et al.The present study investigated whether microRNA (miR)-132-3p targeted transcription factor SOX-4 (Sox4) for the inhibition of proliferation, migration, invasion and promotion of apoptosis in liver cancer (LC) cells. The expression of miR132-3p and Sox4 mRNA was evaluated by quantitative PCR and protein expression was determined by western blot analysis. Cell proliferation, apoptosis, migration, and invasion were assessed at different time points by the MTT assay, flow cytometry analysis, wound healing assay and Transwell migration assay, respectively. Bioinformatics prediction and luciferase assays were performed to validate and confirm Sox4as a potential target of miR-132p. There was a reduced expression of miR-132-3p in HepG2 and Huh7 cell lines compared with HccLM3 cells. Overexpression of miR-132-3p resulted in significant inhibition of proliferation and induction of apoptosis in LC cells. Moreover, migration and invasion of HepG2 cells were suppressed by over expressing miR-132-3p. However, downregulation of miR-132-3p in Hep-G2 cells promoted cell growth, invasion and migration and inhibited apoptosis.  https://www.selleckchem.com/pharmacological_epigenetics.html  Bioinformatics analysis predicted Sox4 as a potential target of miR-132-3p, which was further confirmed by the luciferase reporter assay. In addition, an inverse association was observed between miR-132-3p and Sox4 expression. miR-132-3p may regulate the proliferation, apoptosis, migration and invasion of HepG2 cells by targeting Sox4. Copyright © Huang et al.Paeoniflorin (PF) has been demonstrated to exert tumor suppressive functions in various types of human cancer. However, the mechanisms of PF-mediated anti-tumor activity have not been fully elucidated. S-phase kinase associated protein 2 (Skp2) has been characterized as an oncoprotein that contributes to carcinogenesis. Therefore, the inhibition of Skp2 may be a useful approach for the treatment of various types of human cancer. The present study explored whether PF inhibited the expression of Skp2 in liver cancer cells, leading to cell viability inhibition, induction of apoptosis, and suppression of migration and invasion. PF treatment led to inhibition of Skp2 expression in liver cancer cells. The overexpression of Skp2 abolished PF-mediated anti-cancer activity, whereas the downregulation of Skp2 enhanced this type of activity. The data indicated that PF may be considered as a novel inhibitor of Skp2 in liver cancer cells. Copyright © Liu et al.Renal cell carcinoma (RCC) is the most common type of cancer of the adult kidney. It is generally asymptomatic even at advanced stages, so opportune diagnosis is rare, making it almost impossible to study this cancer at its early stages. RCC tumors induced by ferric nitrilotriacetate (FeNTA) in rats histologically correspond to the human clear cell RCC subtype (ccRCC) and the exposure to this carcinogen during either one or two months leads to different early stages of neoplastic development. High levels of nuclear factor kappa B (NF-κB) and epidermal growth factor receptor (EGFR) as well as low levels of NF-κB inhibitor alpha (IκBα) are frequent in human RCC, but their status in FeNTA-induced tumors and their evolution along renal carcinogenesis is unclear. On this basis, in the present study NF-κB, IκBα and EGFR behavior was analyzed at different stages of the experimental renal carcinogenesis model. Similar to patients with RCC, neoplastic tissue showed high levels of p65, one of the predominant subunits of NF-κB in ccRCC and of EGFR (protein and mRNA), as well as a decrease in the levels of NF-κB's main inhibitor, IκBα, resulting in a classic oncogenic combination. Conversely, different responses were observed at early stages of carcinogenesis. After one month of FeNTA-exposure, NF-κB activity and EGFR levels augmented; but unexpectedly, IκBα also did. While after two months, NF-κB activity diminished, but EGFR and IκBα levels remained elevated. In conclusion, FeNTA-induced tumors and RCC human neoplasms are analogues regarding to the classic NF-κB, IκBα and EGFR behavior, and distinctive non-conventional combination of changes is developed at each early stage studied. The results obtained suggest that the dysregulation of the analyzed molecules could be related to different signaling pathways and therefore, to particular effects depending on the phase of the carcinogenic process. Copyright © Pariente-Pérez et al.