Wnt Signaling in the Tumor Microenvironment

Ruan, Yongsheng; Ogana, Heather; Gang, Eun Ji; Kim, Hye Na; Kim, Yong-Mi

doi:10.1007/978-3-030-47189-7_7

Cited by 22 publications

(14 citation statements)

References 136 publications

(144 reference statements)

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“…25 Targeting Rho-ROCK signaling by noncoding RNAs might be an effective way to modulate angiogenesis in the TME. 26,27 In this study, we revealed that circ_TNFRSF21 facilitated tube formation of HUVECs by sponging miR-3619-5p and upregulating ROCK2. Moreover, our results indicated that ROCK2 was directly prohibited by miR-3619-5p, which was consistent with a previous report.…”

Section: Discussionmentioning

confidence: 65%

M2 macrophage facilitated angiogenesis in cutaneous squamous cell carcinoma via circ_TNFRSF21/miR‐3619‐5p/ROCK axis

Huang

Gao

et al. 2022

The Kaohsiung J of Med Scie

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In recent years, the role of circular RNA in cancer cells has been studied broadly; however, the functional significance of circular RNA in the regulation of the tumor microenvironment (TME) is not fully understood. In this study, we aimed to reveal the role of circ_TNFRSF21 in M2 macrophage‐induced cutaneous squamous cell carcinoma (cSCC) angiogenesis. Quantitative polymerase chain reaction and Western blotting were performed to determine the levels of the indicated genes. Direct binding between circ_TNFRSF21 and miR‐3619‐5p, miR‐3619‐5p, and ROCK2 was verified by dual‐luciferase activity. The migration and invasion of human umbilical vein endothelial cells were evaluated by wound healing and transwell assays. Tube formation was performed to detect in vitro angiogenesis. Circ_TNFRSF21 and ROCK2 were upregulated in cSCC tissue, while miR‐3619‐5p was downregulated. Circ_TNFRSF21 negatively regulated the expression of miR‐3619‐5p, while miR‐3619‐5p negatively regulated the expression of ROCK2. miR‐3619‐5p suppressed tube formation by inhibiting ROCK signaling. M2 macrophages facilitated tube formation via the circ_TNFRSF21/miR‐3619‐5p/ROCK2 axis. Our present study revealed that circ_TNFRSF21 was elevated in M2 macrophages and mediated M2 macrophage‐induced tube formation in vitro.

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Section: Discussionmentioning

confidence: 65%

M2 macrophage facilitated angiogenesis in cutaneous squamous cell carcinoma via circ_TNFRSF21/miR‐3619‐5p/ROCK axis

Huang

Gao

et al. 2022

The Kaohsiung J of Med Scie

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“…It is involved in leucocyte maintenance and renewal while promoting immune tolerance, immune evasion and limits the antitumor immune response. 52 Furthermore, Wnt/β-catenin signaling also plays a crucial role in EMT, thus, it enhances cancer stem cell maintenance. Based on these findings, we postulate that MIR155HG modulates tumor-immune interactions via the Wnt/β-catenin signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

Epigenetic Activation of lncRNA MIR155HG Mediated by Promoter Hypomethylation and SP1 is Correlated with Immune Infiltration in Glioma

Wu¹,

Wan²,

Wang³

et al. 2022

OTT

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Purpose The lncRNA MIR155 host gene (MIR155HG) plays a role in the progression of several malignant cancers. However, the specific mechanisms of MIR155HG in glioma progression have not been clearly established. The purpose of this study was to investigate the function of MIR155HG in glioma at the transcriptome level and relationship with immune infiltration. Patients and Methods Totally, 697 RNA-seq and 594 DNA methylation data were retrieved from The Cancer Genome Atlas (TCGA) dataset while 325 RNA-seq data were retrieved from the Chinese Glioma Genome Atlas (CGGA) dataset. The DNA methylation levels of MIR155HG CpG islands were assessed through bisulfite amplicon sequencing (BSAS). The regulatory mechanism of SP1 on MIR155HG was examined by chromatin immunoprecipitation (ChIP) and luciferase reporter assays. R language was used as the main tool for statistical analysis and graphical work. Results MIR155HG was predominantly expressed in the isocitrate dehydrogenase (IDH) wild-type as well as mesenchymal subtype gliomas. Promoter methylation levels of MIR155HG in glioblastoma (GBM) were remarkably decreased compared with those in lower-grade glioma (LGG). In addition, there were negative correlations between promoter methylation levels and MIR155HG expressions but positive correlations with patients’ overall survival. In vitro studies further revealed that MIR155HG expression was regulated by DNA promoter methylation and transcription factor (SP1) binding to the promoter. Moreover, there was a close association between MIR155HG expression and immune as well as stromal cell infiltrations, inflammatory activities, and immune checkpoints. Clinically, univariate and multivariate Cox analyses revealed that MIR155HG is an independent prognostic marker for glioma patients. Conclusion Our results established that MIR155HG is a potential biomarker for prognosis and an immunotherapeutic target in glioma.

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“…CAMs mediate the adhesion of cancer cells not only to each other but also to stromal cells and ECM, namely, the tumor microenvironment (TME). The TME mainly comprises stable nonmalignant cells, including surrounding immune cells, extracellular matrix, fibroblasts, endothelial cells (ECs), blood vessels, and stromal cells ( 33 ).…”

Section: Cams In Cancers and Their Microenvironmentmentioning

confidence: 99%

“…SRGN is an ECM factor that binds to CD44 in an autocrine manner and acts by triggering MAPK and Wnt/β-catenin signaling in breast CSCs ( 80 ). Thus, CD44 is closely regulated by Wnt signaling ( 33 , 81 ).…”

Section: Cd44 and Endocrine-related Cancersmentioning

confidence: 99%

Mechanisms of Cell Adhesion Molecules in Endocrine-Related Cancers: A Concise Outlook

et al. 2022

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Chemotherapy is a critical treatment for endocrine-related cancers; however, chemoresistance and disease recurrence remain a challenge. The interplay between cancer cells and the tumor microenvironment via cell adhesion molecules (CAMs) promotes drug resistance, known as cell adhesion-mediated drug resistance (CAM-DR). CAMs are cell surface molecules that facilitate cell-to-cell or cell-to-extracellular matrix binding. CAMs exert an adhesion effect and trigger intracellular signaling that regulates cancer cell stemness maintenance, survival, proliferation, metastasis, epithelial–mesenchymal transition, and drug resistance. To understand these mechanisms, this review focuses on the role of CD44, cadherins, selectins, and integrins in CAM-DR in endocrine-related cancers.

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Wnt Signaling in the Tumor Microenvironment

Cited by 22 publications

References 136 publications

M2 macrophage facilitated angiogenesis in cutaneous squamous cell carcinoma via circ_TNFRSF21/miR‐3619‐5p/ROCK axis

M2 macrophage facilitated angiogenesis in cutaneous squamous cell carcinoma via circ_TNFRSF21/miR‐3619‐5p/ROCK axis

Epigenetic Activation of lncRNA MIR155HG Mediated by Promoter Hypomethylation and SP1 is Correlated with Immune Infiltration in Glioma

Mechanisms of Cell Adhesion Molecules in Endocrine-Related Cancers: A Concise Outlook

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