CD155 contributes to the mesenchymal phenotype of triple‐negative breast cancer

Zheng, Qianqian; Gao, Jian; Yin, Ping; Wang, Wei; Wang, Biao; Li, Yan; Zhao, Chenghai

doi:10.1111/cas.14276

Cited by 21 publications

(16 citation statements)

References 57 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our observation of a more rounded, less mesenchymal morphology in CD155-depleted cells has been described previously in glioma cells 14 , and studies in triple-negative aggressive breast cancer cells demonstrated CD155 contribution to the mesenchymal cell state 63 . Depletion of CD155 in these cells triggered mesenchymal to epithelial transition and repressed migration and invasion in vitro and in vivo., suggesting that CD155 expression in MB cells could also contribute to migration control indirectly via transcriptional reprogramming.…”

Section: Discussionsupporting

confidence: 86%

CD155 and EndoA1 mediate growth and tissue invasion downstream of MAP4K4 in medulloblastoma cells

Capdeville

Russo

Pentón

et al. 2021

Preprint

View full text Add to dashboard Cite

How the phenotype of Medulloblastoma (MB) tumor cells adapts in response to growth factor cues is poorly understood. We systematically determined alterations in the plasma membrane (PM)-associated proteome in growth factor-activated MB cells. We found that ligand-induced activation of c-MET receptor tyrosine kinase triggers specific internalization of c-MET and of membrane-associated and transmembrane proteins including nucleoside and ion transporters. In contrast, c-MET activation caused increased PM association of the PVR/CD155 adhesion and immunomodulatory receptor, promoting MB cell motility and tumor cell growth in the cerebellar tissue. Both increased and decreased PM association of a number of these proteins including PVR/CD155 is regulated by the Ser/Thr MAP4K4. We further identified Endophilin A proteins as potential regulators of this process downstream of MAP4K4 to contribute to HGF-induced invasion control. Together, our findings describe a novel link between MAP4K4 overexpression in MB and the maintenance of a cellular phenotype associated with growth and invasiveness.

show abstract

Section: Discussionsupporting

confidence: 86%

CD155 and EndoA1 mediate growth and tissue invasion downstream of MAP4K4 in medulloblastoma cells

Capdeville

Russo

Pentón

et al. 2021

Preprint

View full text Add to dashboard Cite

show abstract

“…CD155 functions as a multi‐functional molecule in human cancers 24 . Previous studies reported that CD155 promoted cell proliferation through Ras‐Raf‐MEK‐ERK signaling pathway 25 and contributed to mesenchymal phenotype in breast cancer 26 . In addition, CD155 overexpression could induce tumor immune escape via interacting with co‐inhibitory receptors on T cells and NK cells 12,27 .…”

Section: Discussionmentioning

confidence: 99%

High serum soluble CD155 level predicts poor prognosis and correlates with an immunosuppressive tumor microenvironment in hepatocellular carcinoma

Jin

Yang

et al. 2022

Clinical Laboratory Analysis

View full text Add to dashboard Cite

Background Hepatocellular carcinoma (HCC) is one of the most prevalent malignancies with poor prognosis. There is no research about the clinical significance of serum soluble CD155 (sCD155) level for HCC. We aim to explore the prognostic and diagnostic value of sCD155 in HCC patients undergoing curative resection. Methods Serum sCD155 level in HCC patients was determined by enzyme‐linked immunosorbent assay. The prognostic significance of sCD155 was evaluated by Cox regression and Kaplan–Meier analyses. CD155 expression and biomarkers of immune cells in HCC tissues were detected by immunohistochemistry staining. The diagnostic significance of sCD155 was evaluated using receiver operating characteristic curve. Results Serum sCD155 level was significantly increased in HCC patients and predicted poor prognosis. The prognostic value of sCD155 remained in low recurrent risk subgroups of HCC. Serum sCD155 level was positively related to CD155 expression in HCC tissues. High serum sCD155 level was associated with decreased numbers of CD8+T cells and CD56+NK cells and increased number of CD163+M2 macrophages. Serum sCD155 level had better performance in distinguishing HCC patients from healthy donors and patients with chronic liver conditions than α‐fetoprotein. Among patients with α‐fetoprotein ≤ 20 ng/ml, serum sCD155 level could differentiate HCC patients from non‐HCC patients. Conclusion Serum sCD155 level represents a promising biomarker for diagnosis and prognosis of HCC. High serum sCD155 level may reflect an immunosuppressive tumor microenvironment in HCC.

show abstract

“…Collectively, these changes, when they are accompanied by the expression of specific transcription factors and molecular modifications [ 40 ] are referred to as tumor cell epithelial-mesenchymal transition (EMT) [ 41 , 42 ]. Indeed, the causal relationship between ICPML expression on tumor cells and EMT has been shown in several instances with a variety of technical approaches (e.g., siRNA, CRISPR/Cas) [ 43 , 44 , 45 , 46 , 47 ]. Expression of ICPMLs on tumor cells can be both a consequence [ 48 ], as well as a cause of tumor cell EMT [ 43 , 44 , 49 , 50 , 51 ], suggesting the existence of a positive feedback loop between the expression of ICPMLs and EMT [ 9 ].…”

Section: The Consequences Of the Expression Of Icpmls On The Biology Of Tumor Cellsmentioning

confidence: 99%

“…Indeed, the causal relationship between ICPML expression on tumor cells and EMT has been shown in several instances with a variety of technical approaches (e.g., siRNA, CRISPR/Cas) [ 43 , 44 , 45 , 46 , 47 ]. Expression of ICPMLs on tumor cells can be both a consequence [ 48 ], as well as a cause of tumor cell EMT [ 43 , 44 , 49 , 50 , 51 ], suggesting the existence of a positive feedback loop between the expression of ICPMLs and EMT [ 9 ]. Interestingly, tumor cell EMT can also have immunosuppressive effects [ 52 ] and it has recently been shown that loss of the epithelial marker E-cadherin, a hallmark of EMT, reduces responsiveness to ICIs in a mouse melanoma model [ 53 ].…”

Section: The Consequences Of the Expression Of Icpmls On The Biology Of Tumor Cellsmentioning

confidence: 99%

“…As regards individual ICPMLs, the following have been reported to be associated with tumor cell EMT: PD-1 [ 54 , 55 ] PD-L1 [ 54 , 55 , 56 , 57 ], PD-L2 [ 54 , 55 ], B7-H3 [ 55 ], B7-H4 [ 43 , 58 ], CTLA-4 [ 54 , 55 ], OX40 [ 54 ], CD47 [ 59 , 60 , 61 ], CD137 ligand [ 62 ], CD155 [ 44 ], FGL1 [ 46 ], T-cell immunoglobulin and mucin-domain containing-3 (TIM-3) [ 55 , 63 ] and B- and T-lymphocyte attenuator (BTLA, CD272) [ 55 ]. Other ICPMLs, while not having been formally associated with EMT (e.g., CD70, galectin-9), are expressed by tumor cells displaying EMT-related functionalities [ 64 , 65 , 66 , 67 ].…”

Section: The Consequences Of the Expression Of Icpmls On The Biology Of Tumor Cellsmentioning

confidence: 99%

See 1 more Smart Citation

Depleting Tumor Cells Expressing Immune Checkpoint Ligands—A New Approach to Combat Cancer

Marcucci

Rumio

2021

Cells

View full text Add to dashboard Cite

Antibodies against inhibitory immune checkpoint molecules (ICPMs), referred to as immune checkpoint inhibitors (ICIs), have gained a prominent place in cancer therapy. Several ICIs in clinical use have been engineered to be devoid of effector functions because of the fear that ICIs with preserved effector functions could deplete immune cells, thereby curtailing antitumor immune responses. ICPM ligands (ICPMLs), however, are often overexpressed on a sizeable fraction of tumor cells of many tumor types and these tumor cells display an aggressive phenotype with changes typical of tumor cells undergoing an epithelial-mesenchymal transition. Moreover, immune cells expressing ICPMLs are often endowed with immunosuppressive or immune-deviated functionalities. Taken together, these observations suggest that compounds with the potential of depleting cells expressing ICPMLs may become useful tools for tumor therapy. In this article, we summarize the current state of the art of these compounds, including avelumab, which is the only ICI targeting an ICPML with preserved effector functions that has gained approval so far. We also discuss approaches allowing to obtain compounds with enhanced tumor cell-depleting potential compared to native antibodies. Eventually, we propose treatment protocols that may be applied in order to optimize the therapeutic efficacy of compounds that deplete cells expressing ICPMLs.

show abstract

CD155 contributes to the mesenchymal phenotype of triple‐negative breast cancer

Cited by 21 publications

References 57 publications

CD155 and EndoA1 mediate growth and tissue invasion downstream of MAP4K4 in medulloblastoma cells

CD155 and EndoA1 mediate growth and tissue invasion downstream of MAP4K4 in medulloblastoma cells

High serum soluble CD155 level predicts poor prognosis and correlates with an immunosuppressive tumor microenvironment in hepatocellular carcinoma

Depleting Tumor Cells Expressing Immune Checkpoint Ligands—A New Approach to Combat Cancer

Contact Info

Product

Resources

About