Changes in energy metabolism are a decisive biochemical feature of cancer cells. Normal cells usually use oxygen to burn fuel to produce most of the energy they need. The energy production of cancer depends on glucose, a process called glycolysis.
Scientists say: "Cell cancer cells rely on anaerobic fermentation to convert glucose into lactic acid. This state of glycolysis is catalyzed by LDH-A enzyme. In cancer cells, LDH-A is elevated, which makes tumor cells immune. Oxygen limitation converts most glucose stores into lactic acid. This shifts the function of glucose products from simple energy production to accelerated cell growth and proliferation." Therefore, LDH-A has been identified as a cancer therapy that focuses on preventing cancer cell proliferation. A promising target.
Non-small cell lung cancer (NSCLC) accounts for 85% of lung cancer and is a leading cause of cancer death, which is highly dependent on glycolysis. NSCLC promotes glycolysis through two key proteins, K-RAS and EGFR mutations. Therefore, the researchers constructed a mouse model of inducible LDH-A non-small cell lung cancer that expresses oncogenic K-RAS and EGFR.
Next, the researchers obtained a small molecule LDH-A inhibitor drug, and similar effects were observed in cell culture experiments. These results further confirm that blocking glycolysis can affect cancer-initiating cells, and that such tumor-forming and self-renewing cancer cell populations are associated with invasive and poor prognosis.
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