Abstract
Lactate dehydrogenase A (LDH-A) is a key enzyme during glycolysis, which increases the synthesis of related proteins and has elevated activity in cancer cells. The role of LDH-A in lung adenocarcinoma (LUAD) progression was investigated in the present study. Expression levels of LDH-A were assessed in LUAD samples, and the relationship between LDH-A expression status and the prognosis of LUAD patients was confirmed. The effect of LDH-A on proliferation, invasion, migration, and colony formation of cancer cells was assessed. We further determined the role of LDH-A in tumor growth in vivo by using xenograft LUAD tumor models. The potential mechanism of LDH-A promotion in LUAD progression was explored. LDH-A showed an abnormally high expression in LUAD, which is closely associated with poor prognosis in patients with LUAD. In in vitro experiments, silencing LDH-A expression in LUAD cells could effectively inhibit proliferation, invasion, migration, and colony formation of cancer cells. In in vivo experiments, tumor growth was markedly inhibited by LDH-A silencing in a xenograft model of LUAD. Notably, LDH-A could also promote tumor progression by regulating epithelial–mesenchymal transition (EMT)-related molecules. LDH-A can promote the malignant biological behaviors of LUAD cells, and thus can be a potential target for LUAD treatment.
Highlights
Lung cancer is a malignant tumor with the highest morbidity and mortality worldwide
According to the IHC results, Lactate dehydrogenase A (LDH-A) protein was mainly located in the cytoplasm of lung adenocarcinoma (LUAD) cells (Figure 1A,B)
The results indicated that LDH-A expression level in cancer tissues was remarkably higher than para-carcinoma tissues, and the difference was statistically significant (P < 0.05; Figure 1C)
Summary
Lung cancer is a malignant tumor with the highest morbidity and mortality worldwide. Among all primary lung cancers, lung adenocarcinoma (LUAD) is the main pathological subtype [1]. With the extensive application of targeted medicine in the clinic, the survival time of LUAD patients has been extended. Several studies have indicated that the cancer cell is a specialized cell type, characterized by active proliferation and vigorous growth. These cells possess some features that either cannot be seen, or can rarely be seen in normal cells [3]. Cancer cells have poor mitochondrial function and oxidative phosphorylation impairments, which preferentially generate energy through glycolysis. This result in abundant lactic acid production. This phenomenon is referred to as the Warburg effect, which is prevalent in cancer cells [4]
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