IDO1 Promotes the Progression of NSCLC by Regulating the Polarization of M2 Macrophages.

Int J Gen Med

Department of Pulmonary and Critical Care Medicine, Qilu Hospital of Shandong University, Jinan, People's Republic of China.

Published: May 2023

Purpose: Non-small cell lung cancer (NSCLC) is currently a problem in the clinic and in society. Tumor-related macrophages (TAMs) in the tumor microenvironment (TME) play a vital role in the development of NSCLC.

Patients And Methods: Bioinformatics was used to analyze the role of Indoleamine 2,3-dioxygenase 1 (IDO1) in NSCLC and the correlation of its expression with CD163 expression. The expression of CD163 and IDO1 was measured by immunohistochemistry, and their colocalization was assessed by immunofluorescence. M2 macrophage polarization was induced, and a coculture model of NSCLC cells and macrophages was established.

Results: Bioinformatics analysis showed that IDO1 promoted the metastasis and differentiation of NSCLC and inhibited DNA repair. Moreover, the expression of IDO1 was positively correlated with CD163 expression. We discovered that IDO1 expression was related to M2 macrophage differentiation. In vitro, we showed that increased IDO1 expression promoted the invasion, proliferation, and metastasis of NSCLC cells.

Conclusion: In conclusion, we determined that IDO1 can regulate the M2 polarization of TAMs and promote the progression of NSCLC, which provides partial theoretical evidence for the use of IDO1 inhibitors in the treatment of NSCLC.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10178912PMC
http://dx.doi.org/10.2147/IJGM.S398908DOI Listing

Publication Analysis

Top Keywords

ido1
9
nsclc
8
progression nsclc
8
expression cd163
8
cd163 expression
8
ido1 expression
8
expression
7
ido1 promotes
4
promotes progression
4
nsclc regulating
4

Similar Publications

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!