Abstract
Lung cancer is a leading cause of global cancer deaths. Na/K-ATPase has been studied as a target for cancer treatment. Cardiotonic steroids (CS) trigger intracellular signalling upon binding to Na/K-ATPase. Normal lung and tumour cells frequently express different pump isoforms. Thus, Na/K-ATPase is a powerful target for lung cancer treatment. Drugs targeting Na/K-ATPase may induce apoptosis and autophagy in transformed cells. We argue that Na/K-ATPase has a role as a potential target in chemotherapy in lung cancer treatment. We discuss the effects of Na/K-ATPase ligands and molecular pathways inducing deleterious effects on lung cancer cells, especially those leading to apoptosis and autophagy.
Highlights
Many new cancer treatments have arisen, but the search for a suitable drug that acts on cancers that are chemo-resistant to common cancer drugs remains a huge challenge
We argue that Na/K-ATPase has a role as a potential target in chemotherapy in lung cancer treatment
We discuss the effects of Na/K-ATPase ligands and the molecular pathways inducing deleterious effects on lung cancer cells, especially those leading to apoptosis and autophagy
Summary
Many new cancer treatments have arisen, but the search for a suitable drug that acts on cancers that are chemo-resistant to common cancer drugs remains a huge challenge. Cardiotonic steroids (CS), when bound to Na/K-ATPase, trigger several cell-signalling pathways, resulting in the proliferation, differentiation and promotion of autophagy or apoptosis. These effects vary depending on the cell type as well as the type and concentration of CS. Na/K-ATPase is a powerful target for lung cancer treatment. We argue that Na/K-ATPase has a role as a potential target in chemotherapy in lung cancer treatment. We discuss the effects of Na/K-ATPase ligands and the molecular pathways inducing deleterious effects on lung cancer cells, especially those leading to apoptosis and autophagy
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