Deregulation of interferon-gamma receptor 1 expression and its implications for lung adenocarcinoma progression

Abstract

Interferon-gamma (IFN-γ) plays a dual role in cancer; it is both a pro- and an antitumorigenic cytokine, depending on the type of cancer. The deregulation of the IFN-γ canonic pathway is associated with several disorders, including vulnerability to viral infections, inflammation, and cancer progression. In particular, the interplay between lung adenocarcinoma (LUAD) and viral infections appears to exist in association with the deregulation of IFN-γ signaling. In this mini-review, we investigated the status of the IFN-γ signaling pathway and the expression level of its components in LUAD. Interestingly, a reduction in IFNGR1 expression seems to be associated with LUAD progression, affecting defenses against viruses such as severe acute respiratory syndrome coronavirus 2. In addition, alterations in the expression of IFNGR1 may inhibit the antiproliferative action of IFN-γ signaling in LUAD.

Keywords: Interferon-gamma; IFNGR1; JAK1; Antiviral; Anti-tumor; Lung adenocarcinoma

Core Tip: IFNGR1 is a transmembrane receptor required for interferon-gamma (IFN-γ) signaling. IFNGR1 expression is deregulated in lung adenocarcinoma, affecting IFN-γ signaling to promote cancer progression and reduce antiviral responses. Thus, the status of IFNGR1 expression may be critical in the detection of this cancer, and the restoration of its homeostasis may help control tumor progression and improve defense against viral infections.