CD163 as a novel target gene of STAT3 is a potential therapeutic target for gastric cancer

Cheng, Zhenguo; Gong, Baocheng; Wang, Pengliang; Liu, Funan

doi:10.18632/oncotarget.20244

Cited by 42 publications

(30 citation statements)

References 45 publications

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“…We have also detected an enrichment on the macrophage chemotaxis protein set. Therefore, our results suggest that both regulatory macrophages and dexa-tolDC might be triggering similar tolerogenic mechanisms, probably through the STAT3 and Wnt5a signaling pathway, as its interaction with CD163 has already been reported in cancer studies 31 , 32 . Regarding C1QB and C1QC genes, their overexpression is aligned with the up-modulation of the complement activation protein set.…”

Section: Discussionsupporting

confidence: 69%

Comparative transcriptomic profile of tolerogenic dendritic cells differentiated with vitamin D3, dexamethasone and rapamycin

Navarro‐Barriuso

Mansilla

Naranjo-Gómez³

et al. 2018

Sci Rep

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Tolerogenic dendritic cell (tolDC)-based therapies have become a promising approach for the treatment of autoimmune diseases by their potential ability to restore immune tolerance in an antigen-specific manner. However, the broad variety of protocols used to generate tolDC in vitro and their functional and phenotypical heterogeneity are evidencing the need to find robust biomarkers as a key point towards their translation into the clinic, as well as better understanding the mechanisms involved in the induction of immune tolerance. With that aim, in this study we have compared the transcriptomic profile of tolDC induced with either vitamin D3 (vitD3-tolDC), dexamethasone (dexa-tolDC) or rapamycin (rapa-tolDC) through a microarray analysis in 5 healthy donors. The results evidenced that common differentially expressed genes could not be found for the three different tolDC protocols. However, individually, CYP24A1, MUCL1 and MAP7 for vitD3-tolDC; CD163, CCL18, C1QB and C1QC for dexa-tolDC; and CNGA1 and CYP7B1 for rapa-tolDC, constituted good candidate biomarkers for each respective cellular product. In addition, a further gene set enrichment analysis of the data revealed that dexa-tolDC and vitD3-tolDC share several immune regulatory and anti-inflammatory pathways, while rapa-tolDC seem to be playing a totally different role towards tolerance induction through a strong immunosuppression of their cellular processes.

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Section: Discussionsupporting

confidence: 69%

Comparative transcriptomic profile of tolerogenic dendritic cells differentiated with vitamin D3, dexamethasone and rapamycin

Navarro‐Barriuso

Mansilla

Naranjo-Gómez³

et al. 2018

Sci Rep

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“…[33][34][35] Furthermore, we also found that CD163 was positively associated with fibroblasts ( Figure 4(a,b), lower panel), which was consistent with the previous reports that the expression of CD163 was positively associated with fibroblasts. [36][37][38] These data suggested that CD163 may participate in the regulation of stromal cells in the tumor microenvironment.…”

Section: Relationship Between Cd163 and Infiltrated Cells In The Tumomentioning

confidence: 80%

Molecular and clinical characterization of CD163 expression via large-scale analysis in glioma

Zhang

Maimela

et al. 2019

OncoImmunology

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The expression and function of CD163 in glioma are not fully understood. In this report, we collected totally 1323 glioma samples from the Chinese Glioma Genome Atlas (CGGA) dataset, including 325 RNA-seq data and 301 mRNA microarray data, and 697 glioma samples from The Cancer Genome Atlas (TCGA) dataset to characterize the molecular and clinical features of CD163 in glioma by conducting a large-scale study. We found that CD163 expression was positively associated with the grade of malignancy of glioma. CD163 expression was up-regulated in IDH wild-type glioma and mesenchymal subtype. Gene ontology analysis suggested that CD163-related genes were more involved in immune response and angiogenesis in glioma. Moreover, CD163 showed a positive relationship with stromal and immune cell populations. Kaplan-Meier curves analysis revealed that higher CD163 expression indicated significantly poor survival in glioma and glioblastoma multiforme (GBM). Pearson correlation analysis revealed that CD163 was robustly associated with the immune checkpoints and other macrophage markers. These results demonstrated that CD163 predicts poor prognosis in glioma patients. Additionally, combination of CD163 and immune checkpoints may impair angiogenesis and reverse dysfunctional phenotypes of T cells, which suggest that CD163 may be a promising biomarker and target for immunotherapeutic strategies.

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“…However, in the tumor microenvironment, macrophages are also known to produce inflammatory mediators and reactive oxygen species that can induce angiogenesis and promote tumor progression [30][31][32]. To investigate the M2/antiinflammatory macrophage distribution in KS tissues, we evaluated the distribution of CD163, a hemoglobinhaptoglobin acute phase marker which is often correlated with myeloid suppressor phenotypes [33]. While CD163 + myeloid cells were evident in biopsied tissue, the majority were localized in LANAregions (P = 0.0002) ( Figure 6A and 6B).…”

Section: Cd163 Expressing Cells Are In Lana Negative Regionmentioning

confidence: 99%

Lack of CD8+ T-cell co-localization with Kaposi’s sarcoma-associated herpesvirus infected cells in Kaposi’s sarcoma tumors

et al. 2020

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Despite the close association between Kaposi's sarcoma (KS) and immune dysfunction, it remains unclear whether tumor infiltrating immune cells (TIIC), by their absence, presence, or dysfunction, are mechanistically correlated with KS pathogenesis. Therefore, their potential capacity to serve as prognostic biomarkers of KS disease progression or control is unclear. Because epidemic-KS (EpKS) occurs with HIV-1 co-infection, it is particularly important to compare TIIC between EpKS and HIV-negative African endemic-KS (EnKS) to dissect the roles of HIV-1 and Kaposi Sarcoma-associated herpesvirus (KSHV) in KS pathogenesis. This cross-sectional study of 13 advanced KS (4 EnKS, 9 EpKS) patients and 3 healthy controls utilized single-color immunohistochemistry and dual-color immunofluorescence assays to characterize and quantify KSHV infected cells in relation to various TIIC in KS biopsies. Analysis of variance (ANOVA) and Mann-Whitney tests were used to assess differences between groups where P-values < 0.05 were considered significant. The abundance of KSHV infected cells was heterogeneous in KS biopsies. Despite the presence of T-cell chemoattractant chemokine CxCL-9 in biopsies, CD8 + T-cells were sparsely distributed in regions with evident KSHV infected cells but were readily detectable in regions devoid of KSHV infected cells (P < 0.0001). CD68 + (M1) macrophages were evenly and diffusely distributed in KS biopsies, whereas, the majority of CD163 + (M2) macrophages were localized in regions devoid of KSHV infected cells (P < 0.0001). Overall, the poor immune cell infiltration or co-localization in KS biopsies independent of HIV-1 co-infection suggests a fundamental tumor immune evasion mechanism that warrants further investigation.

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CD163 as a novel target gene of STAT3 is a potential therapeutic target for gastric cancer

Cited by 42 publications

References 45 publications

Comparative transcriptomic profile of tolerogenic dendritic cells differentiated with vitamin D3, dexamethasone and rapamycin

Comparative transcriptomic profile of tolerogenic dendritic cells differentiated with vitamin D3, dexamethasone and rapamycin

Molecular and clinical characterization of CD163 expression via large-scale analysis in glioma

Lack of CD8+ T-cell co-localization with Kaposi’s sarcoma-associated herpesvirus infected cells in Kaposi’s sarcoma tumors

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