CMTM family proteins 1–8: roles in cancer biological processes and potential clinical value

Wu, Jie; Li, Lan; Wu, Siyi; Xu, Bin

doi:10.20892/j.issn.2095-3941.2020.0032

Cited by 37 publications

(23 citation statements)

References 77 publications

(156 reference statements)

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“…Even though partially conflicting findings between our model and published data can be reconciled, it is also likely that additional mechanisms by which PD-L1 and EMT mutually influence each other play a role depending on the studied cell line or cancer. For instance, PD-L1 expression can induce EMT by activating the TF SREBP-1c in hepatocellular and renal cell carcinoma (Wang et al, 2015;Xu et al, 2020), ZEB1 can bind and silence IRF1, a TF of PD-L1 (Jun Yang et al, 2017), and activity of the CMTM family, which stabilizes PD-L1, correlates with EMT-TFs such as SLUG (Jie Wu, 2020;Li et al, 2021).…”

Section: Renal Cell Carcinomamentioning

confidence: 99%

Bidirectional crosstalk between epithelial-mesenchymal plasticity and IFNγ-induced PD-L1 expression promotes tumor progression

Burger

Nesenberend

Lems

et al. 2022

Preprint

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Epithelial-Mesenchymal Transition (EMT) and immunoevasion through upregulation of Programmed Death-Ligand 1 (PD-L1) are important drivers of cancer progression. While EMT has been proposed to facilitate PD-L1-mediated immunosuppression, the molecular mechanisms of their interaction remain obscure. Here we provide insight into these mechanisms by proposing a mathematical model that describes the crosstalk between EMT and Interferon gamma (IFNγ)-induced PD-L1 expression. Our model shows that via interaction with microRNA-200 (miR-200), the multistability of the EMT regulatory circuit is mirrored in the PD-L1 levels, which are further amplified by IFNγ stimulation. This IFNγ-mediated effect is most prominent for cells in a fully mesenchymal state, and less strong for those in an epithelial or partially mesenchymal state. Additionally, bi-directional crosstalk between miR-200 and PD-L1 implies that IFNγ stimulation allows cells to undergo EMT for lower amounts of inducing signal, and that IFNγ presence accelerates EMT and decelerates Mesenchymal-Epithelial Transition (MET). Overall, our model agrees with published findings and provides insight into possible mechanisms behind EMT-mediated immune-evasion; and primary, adaptive, or acquired resistance to immunotherapy. Our model can be used as a starting point to explore additional crosstalk mechanisms, as an improved understanding of these mechanisms is indispensable for developing better diagnostic and therapeutic options for cancer patients.

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Section: Renal Cell Carcinomamentioning

confidence: 99%

Bidirectional crosstalk between epithelial-mesenchymal plasticity and IFNγ-induced PD-L1 expression promotes tumor progression

Burger

Nesenberend

Lems

et al. 2022

Preprint

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“…Several biological processes, such as DNA methylation and microRNAs, as well as transcriptional regulation molecules, such as NF-κB, p53, and SOX10, regulate the expression of CMTM family members. 26 , 27 DNA methylation is another important regulator of CMTM family member expression. For example, CpG methylation can inactivate the CMTM5 gene in various carcinoma cell lines, such as oral squamous cell carcinoma, 28 breast carcinoma, 29 and myeloid leukemia.…”

Section: Characteristics Of Cmtm Familymentioning

confidence: 99%

CMTM Family and Gastrointestinal Tract Cancers: A Comprehensive Review

Li¹,

Wang²,

Wang³

et al. 2022

CMAR

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“…CMTM members are widely expressed in the immune system and are involved in several pathological processes ( Delic et al, 2015 ). A recent study found that abnormal expression of CMTMs was implicated in the process of tumor growth and metastasis ( Wu et al, 2019b ; Wu et al, 2020 ). However, the specific role and mechanism remain elusive.…”

Section: Introductionmentioning

confidence: 99%

CMTM Family Genes Affect Prognosis and Modulate Immunocytes Infiltration in Grade II/III Glioma Patients by Influencing the Tumor Immune Landscape and Activating Associated Immunosuppressing Pathways

Wang

Zhang

et al. 2022

Front. Cell Dev. Biol.

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Lower-grade glioma (LGG) is one of the most common primary tumor types in adults. The chemokine-like factor (CKLF)-like Marvel transmembrane domain-containing (CMTM) family is widely expressed in the immune system and can modulate tumor progression. However, the role of the CMTM family in LGG remains unknown. A total of 508 LGG patients from The Cancer Genome Atlas (TCGA) database were used as a training cohort, and 155 LGG patients from the Chinese Glioma Genome Atlas (CGGA) array database, 142 LGG patients from the CGGA RNA-sequencing database, and 168 LGG patients from the GSE108474 database were used as the validation cohorts. Patients were subdivided into two groups using consensus clustering. The ENET algorithm was applied to build a scoring model based on the cluster model. Finally, ESTIMATE, CIBERSORT, and xCell algorithms were performed to define the tumor immune landscape. The expression levels of the CMTM family genes were associated with glioma grades and isocitrate dehydrogenase (IDH) status. Patients in cluster 2 and the high-risk score group exhibited a poor prognosis and were enriched with higher grade, wild-type IDH (IDH-WT), 1p19q non-codeletion, MGMT promoter unmethylation, and IDH-WT subtype. Patients in cluster 1 and low-risk score group were associated with high tumor purity and reduced immune cell infiltration. Enrichment pathways analysis indicated that several essential pathways involved in tumor progression were associated with the expression of CMTM family genes. Importantly, PD-1, PD-L1, and PD-L2 expression levels were increased in cluster 2 and high-risk groups. Therefore, the CMTM family contributes to LGG progression through modulating tumor immune landscape.

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CMTM family proteins 1–8: roles in cancer biological processes and potential clinical value

Cited by 37 publications

References 77 publications

Bidirectional crosstalk between epithelial-mesenchymal plasticity and IFNγ-induced PD-L1 expression promotes tumor progression

Bidirectional crosstalk between epithelial-mesenchymal plasticity and IFNγ-induced PD-L1 expression promotes tumor progression

CMTM Family and Gastrointestinal Tract Cancers: A Comprehensive Review

CMTM Family Genes Affect Prognosis and Modulate Immunocytes Infiltration in Grade II/III Glioma Patients by Influencing the Tumor Immune Landscape and Activating Associated Immunosuppressing Pathways

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