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Pancreatic ductal adenocarcinoma is prone to distant metastasis and is expected to become the second leading cause of cancer-related death. In an extremely nutrient-deficient and hypoxic environment resulting from uncontrolled growth, vascular disturbances and desmoplastic reactions, pancreatic cancer cells utilize "metabolic reprogramming" to satisfy their energy demand and support malignant behaviors such as metastasis. Notably, pancreatic cancer cells show extensive enhancement of glycolysis, including glycolytic enzyme overexpression and increased lactate production, and this is caused by mitochondrial dysfunction, cancer driver genes, specific transcription factors, a hypoxic tumor microenvironment and stromal cells, such as cancer-associated fibroblasts and tumor-associated macrophages. The metabolic switch from oxidative phosphorylation to glycolysis in pancreatic cancer cells regulates the invasion–metastasis cascade by promoting epithelial–mesenchymal transition, tumor angiogenesis and the metastatic colonization of distant organs. In addition to aerobic glycolysis, oxidative phosphorylation also plays a critical role in pancreatic cancer metastasis in ways that remain unclear. In this review, we expound on the intracellular and extracellular causes of the enhancement of glycolysis in pancreatic cancer and the strong association between glycolysis and cancer metastasis, which we expect will yield new therapeutic approaches targeting cancer metabolism. [ABSTRACT FROM AUTHOR]

Accumulating researches identify microRNA-26a (miR-26a) as a tumor suppressor in hepatocellular carcinoma (HCC). F-box protein 11 (FBXO11), a predicted target gene of miR-26a, is an E3 ubiquitin ligase and a type II methyltransferase, and functions as a key regulator of tumor initiation and progression. This study was aimed to investigate the regulatory role of miR-26a in FBXO11 expression and explored the clinical significance as well as functional role of FBXO11 in HCC. The expression levels of miR-26a were prominently downregulated in HCC tissues compared to matched tumor-adjacent tissues. MiR-26a inversely regulated FBXO11 abundance in HCC cells. Hereby, miR-26a could directly target 3′UTR of FBXO11 mRNA to suppress its expression. Gene Expression Omnibus (GEO) database (GSE54236 and GSE45436) and our data demonstrated that the expression of FBXO11 was up-regulated in HCC tissues. The level of FBXO11 mRNA was inversely correlated with miR-26a expression in HCC specimens. High FBXO11 expression was positively correlated with large tumor size, venous infiltration and advanced tumor stage of HCC patients. Clinical prognostic analysis illustrated that high FBXO11 expression predicted a poor survival of HCC patients. In vitro , FBXO11 knockdown inhibited cell proliferation, colony formation, migration and invasion of HCC cells. Additionally, miR-26a overexpression showed a consistent effect with FBXO11 knockdown on these malignant behaviors of HCC cells. Notably, FBXO11 restoration reversed the inhibitory effect of miR-26a on HCC cell proliferation, colony formation, migration and invasion. In summary, these results indicated that miR-26a regulation of FBXO11 exhibited an oncogenic role in HCC. Inhibition of FBXO11 might serve as a therapeutic target for HCC. [ABSTRACT FROM AUTHOR]