Molecular therapy oncolytics | VOL. 25
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Human lung adenocarcinoma CD47 is upregulated by interferon-γ and promotes tumor metastasis.

Publication Date Jun 16, 2022

Abstract

Tumor cells can evade attack by phagocytes by upregulating the self-marker CD47. The mechanisms underlying tumor CD47 upregulation, however, remain unclear. Here, we report that human lung adenocarcinoma CD47 is upregulated by interferon-γ (IFN-γ), the level in the tumor microenvironment of which is markedly increased after tumor metastasis and chemotherapy. The IFN-γ receptor is expressed in various human lung adenocarcinoma tissues regardless of the CD47 protein expression, and lung adenocarcinoma CD47 expression is significantly enhanced following tumor metastasis or chemotherapy treatment. In line with this, CD47 expression in various lung cancer cells is markedly increased by IFN-γ treatment. Mechanistically, IFN-γ promotes CD47 expression by activating interferon regulatory factor-1 (IRF-1), which binds to an IRF-1-binding domain within the CD47 promoter region and increases CD47 transcription. Functionally, IFN-γ-enhanced CD47 expression facilitates human lung cancer cell invasion both invitro and invivo, whereas IFN-γ-induced CD47 upregulation and cancer metastasis are blocked by mutating the IRF-1-binding site within the CD47 promoter. Our results reveal IFN-γ-enhanced CD47 expression as a novel mechanism promoting human lung adenocarcinoma progression.

Concepts
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Human Lung Cancer Cell Invasion
CD47 Expression
Human Lung Adenocarcinoma Tissues
Human Lung Adenocarcinoma
CD47 Upregulation
Interferon Regulatory Factor-1
Human CD47
Promotes Tumor Metastasis
Tumor Metastasis
IFN-γ Receptor

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