Chen Xiao, Yao Jie, Zhang Meng-Yu, Li Rui, Liu Xiao, Qu Yi-Qing
Department of Pulmonary and Critical Care Medicine, Qilu Hospital of Shandong University, Jinan, People's Republic of China.
Department of Respiratory Medicine, Tai'an City Central Hospital, Tai'an, People's Republic of China.
Int J Gen Med. 2023 May 8;16:1713-1733. doi: 10.2147/IJGM.S398908. eCollection 2023.
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.
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.
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.
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.
非小细胞肺癌(NSCLC)目前是临床和社会面临的一个问题。肿瘤微环境(TME)中的肿瘤相关巨噬细胞(TAM)在NSCLC的发展中起着至关重要的作用。
采用生物信息学分析吲哚胺2,3-双加氧酶1(IDO1)在NSCLC中的作用及其表达与CD163表达的相关性。通过免疫组织化学检测CD163和IDO1的表达,并通过免疫荧光评估它们的共定位。诱导M2巨噬细胞极化,并建立NSCLC细胞与巨噬细胞的共培养模型。
生物信息学分析表明,IDO1促进NSCLC的转移和分化,并抑制DNA修复。此外,IDO1的表达与CD163的表达呈正相关。我们发现IDO1的表达与M2巨噬细胞分化有关。在体外,我们表明IDO1表达的增加促进了NSCLC细胞的侵袭、增殖和转移。
总之,我们确定IDO1可以调节TAM的M2极化并促进NSCLC的进展,这为使用IDO1抑制剂治疗NSCLC提供了部分理论依据。