DDIAS is a target of NFATc1 and is associated with cisplatin resistance in lung cancer cells.

Study reports a progressive decrease of NFATc1 in lung tumor tissue and in tumor-infiltrating lymphocytes (TIL) of patients suffering from advanced-stage non-small cell lung cancer and reveals a role of NFATc1 in the activation and cytotoxic functions of T cells, in the development of memory CD8+ T-cell subsets, and in the regulation of T-cell exhaustion.

High NFAT2 expression is associated with carboplatin resistance in lung cancer.

MiR-338 regulates NFATc1 expression and inhibits the proliferation and epithelial-mesenchymal transition of human non-small-cell lung cancer cells.

Mice harboring conditionally inactivated NFATc1 in T cells (NFATc1DeltaCD4) showed increased lung tumor growth associated with impaired T-cell activation and function. In the absence of NFATc1 reduced IL2 influenced the development of memory CD8+ T cells.