Aerobic glycolysis is critical for tumor growth and metastasis. Previously, we have found that the overexpression of the inhibitor of growth 5 (ING5) inhibits lung cancer aggressiveness and epithelial–mesenchymal transition (EMT). However, whether ING5 regulates lung cancer metabolism reprogramming remains unknown. Here, by quantitative proteomics, we showed that ING5 differentially regulates protein phosphorylation and identified a new site (Y163) of the key glycolytic enzyme PDK1 whose phosphorylation was upregulated 13.847-fold. By clinical study, decreased p-PDK1Y163 was observed in lung cancer tissues and correlated with poor survival. p-PDK1Y163 represents the negative regulatory mechanism of PDK1 by causing PDHA1 dephosphorylation and activation, leading to switching from glycolysis to oxidative phosphorylation, with increasing oxygen consumption and decreasing lactate production. These effects could be impaired by PDK1Y163F mutation, which also impaired the inhibitory effects of ING5 on cancer cell EMT and invasiveness. Mouse xenograft models confirmed the indispensable role of p-PDK1Y163 in ING5-inhibited tumor growth and metastasis. By siRNA screening, ING5-upregulated TIE1 was identified as the upstream tyrosine protein kinase targeting PDK1Y163. TIE1 knockdown induced the dephosphorylation of PDK1Y163 and increased the migration and invasion of lung cancer cells. Collectively, ING5 overexpression—upregulated TIE1 phosphorylates PDK1Y163, which is critical for the inhibition of aerobic glycolysis and invasiveness of lung cancer cells.

A study published in National Science Review reveals that carbon-14 (C-14) from algae can integrate into zebrafish biomolecules through a food chain transfer pathway, causing metabolic changes and neurological alterations.

Heart failure is the terminal stage of various cardiovascular diseases, usually characterized by pathological myocardial hypertrophy. So far, the pathogenesis of heart failure is not fully understood. The global burden of cardiovascular disease and epidemiological evidence indicate that in addition to traditional risk factors such as genetic inheritance and hypertension, exposure to exogenous environmental pollutants is a new risk factor. In recent years, the use of antimicrobials has increased, resulting in more exposure of these substances to humans, raising concerns about potential risks to human and environmental health. According to the findings of this study, the exposure to antibacterial agent TCC may be a new risk factor for metabolic cardiovascular diseases. This conclusion is supported by physiological indicator tests and a combined analysis of metabolomics and transcriptomics in cardiac organoids.

Much of our knowledge of the protein PD-1, a leading cancer treatment target, comes from studies in mice. In a comprehensive assessment of PD-1, researchers have found that PD-1 in mice is significantly weaker than the human version, providing new information on how cancer treatments are developed.