MicroRNAs (miRs) have been proposed as minimally invasive prognostic markers for various types of cancer, including liver cancer, which is one of the most common cancers worldwide. In the present study, the expression of miR-34a in human liver cancer tissues and cell lines was evaluated and the effects of miR-34a on cell proliferation, invasion and glycolysis in hepatocellular carcinoma (HCC) cells were determined. The results indicated that miR-34a was downregulated in human liver cancer tissues. Overexpression of miR-34a significantly inhibited liver cancer cell proliferation and clone formation. In terms of the underlying mechanism, miR-34a was indicated to negatively regulate the expression of lactate dehydrogenase A (LDHA), which consequently inhibited LDHA-dependent glucose uptake in the cancer cells, as well as cell proliferation and invasion. Collectively, these data suggest that miR-34a functions as a negative regulator of glucose metabolism and may serve as a novel marker for liver cancer prognosis.
Type 2 diabetes mellitus (T2DM) is a metabolic disease closely related to obesity. Elevated levels of blood glucose lead to serious damage to the heart, brain, blood vessels, nervous system, and digestive system, and even threaten the life of the patients over time
Liver fibrosis is the main pathological feature of various chronic liver diseases that can progress to cirrhosis. However, no effective treatment strategy for liver fibrosis is available. Phytic acid (PA) is a natural plant compound found in cereals, legumes, and rapeseed. Currently, there are few reports on its relationship with liver fibrosis. Herein, we explored the effects of PA on liver fibrosis. In this study, the liver fibrosis model was constructed by intraperitoneal injection of CCl4 and intragastric administration of sodium phytate (100 mg/kg) or silymarin (100 mg/kg) five times a week. The CCl4 injection could significantly increase the content of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in serum and induce the damage of liver cells, infiltration of inflammatory factors, and deposition of collagen fibers in the liver tissue. Compared to the CCl4 group, PA significantly reduced AST and ALT. Also, PA alleviated liver damage and reduced inflammatory cell infiltration, collagen deposition area, and hydroxyproline (Hyp) content in the liver tissue, as well as downregulated α-smooth muscle actin (α-SMA) and collagen I (Col-1). Mechanistically, PA downregulated PI3K, p-AKT, p-p65, and p-IκBα in the liver tissue and reduced the release of inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6). In conclusion, PA might ameliorate liver fibrosis by inhibiting the NF-κB and PI3K/AKT signaling pathways.
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