Extracellular Matrix Enzymes and Immune Cell Biology

McMahon, Meagan; Ye, Siying; Pedrina, Jess; Dlugolenski, Daniel; Stambas, John

doi:10.3389/fmolb.2021.703868

Cited by 33 publications

(25 citation statements)

References 105 publications

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“…Excessive expression of MMP-1 plays a central role in tissue destruction in various vascular diseases. Upregulated VEGF-A, an endothelial cell (EC) activation marker, increases vascular permeability [ 137 ]. Excessive MMP-1 and hyperactivation of ECs occur in COVID-19 patients and are associated with the severity of COVID-19.…”

Section: Discussionmentioning

confidence: 99%

Computational exploration of the dual role of the phytochemical fortunellin: Antiviral activities against SARS-CoV-2 and immunomodulatory abilities against the host

Agrawal

Pathak

Mishra

et al. 2022

Computers in Biology and Medicine

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Section: Discussionmentioning

confidence: 99%

Computational exploration of the dual role of the phytochemical fortunellin: Antiviral activities against SARS-CoV-2 and immunomodulatory abilities against the host

Agrawal

Pathak

Mishra

et al. 2022

Computers in Biology and Medicine

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“…The stiffening effect is often caused by collagen deposition and crosslinking, mediated by increased secretion of lysyl oxidase (LOX) [ 30 , 40 ] and overproduction of other ECM components such as heparan sulfate proteoglycans (HSPGs) [ 41 , 42 ]. Due to this physical constraint, primary tumor growth and cell migration within the TME are greatly dependent on matrix metalloproteinases (MMP) and heparinase enzymes to degrade and reorganize the crosslinked networks [ 43 , 44 , 45 , 46 , 47 , 48 ]. However, T cells do not often secrete enzymes to degrade ECM, but rather choose the path of least resistance [ 49 ] or follow contact guidance imposed by architectural features of the surrounding ECM [ 50 , 51 ].…”

Section: Car T Cell Trafficking and Infiltrationmentioning

confidence: 99%

CAR T Cell Locomotion in Solid Tumor Microenvironment

Nguyen

Ogando‐Rivas

Liu

et al. 2022

Cells

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The promising outcomes of chimeric antigen receptor (CAR) T cell therapy in hematologic malignancies potentiates its capability in the fight against many cancers. Nevertheless, this immunotherapy modality needs significant improvements for the treatment of solid tumors. Researchers have incrementally identified limitations and constantly pursued better CAR designs. However, even if CAR T cells are armed with optimal killer functions, they must overcome and survive suppressive barriers imposed by the tumor microenvironment (TME). In this review, we will discuss in detail the important role of TME in CAR T cell trafficking and how the intrinsic barriers contribute to an immunosuppressive phenotype and cancer progression. It is of critical importance that preclinical models can closely recapitulate the in vivo TME to better predict CAR T activity. Animal models have contributed immensely to our understanding of human diseases, but the intensive care for the animals and unreliable representation of human biology suggest in vivo models cannot be the sole approach to CAR T cell therapy. On the other hand, in vitro models for CAR T cytotoxic assessment offer valuable insights to mechanistic studies at the single cell level, but they often lack in vivo complexities, inter-individual heterogeneity, or physiologically relevant spatial dimension. Understanding the advantages and limitations of preclinical models and their applications would enable more reliable prediction of better clinical outcomes.

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“…Furthermore, complex ECM remodeling processes are required for cancer cells to invade stromal tissue and create a microenvironment that promotes tumor progression and metastasis [ 99 ]. ECM remodeling is influenced by proteinases, MMPs and PA–plasmin systems [ 100 , 101 ]. Plasmin, either directly or indirectly through MMPs, degrades components of the ECM, thus contributing to cancer cell invasion and metastases [ 102 ].…”

Section: Notch Signaling Regulates Bc Progressionmentioning

confidence: 99%

Notch Signaling in Breast Tumor Microenvironment as Mediator of Drug Resistance

Chimento

D’Amico

Pezzi

et al. 2022

IJMS

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Notch signaling dysregulation encourages breast cancer progression through different mechanisms such as stem cell maintenance, cell proliferation and migration/invasion. Furthermore, Notch is a crucial driver regulating juxtracrine and paracrine communications between tumor and stroma. The complex interplay between the abnormal Notch pathway orchestrating the activation of other signals and cellular heterogeneity contribute towards remodeling of the tumor microenvironment. These changes, together with tumor evolution and treatment pressure, drive breast cancer drug resistance. Preclinical studies have shown that targeting the Notch pathway can prevent or reverse resistance, reducing or eliminating breast cancer stem cells. In the present review, we will summarize the current scientific evidence that highlights the involvement of Notch activation within the breast tumor microenvironment, angiogenesis, extracellular matrix remodeling, and tumor/stroma/immune system interplay and its involvement in mechanisms of therapy resistance.

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Extracellular Matrix Enzymes and Immune Cell Biology

Cited by 33 publications

References 105 publications

Computational exploration of the dual role of the phytochemical fortunellin: Antiviral activities against SARS-CoV-2 and immunomodulatory abilities against the host

Computational exploration of the dual role of the phytochemical fortunellin: Antiviral activities against SARS-CoV-2 and immunomodulatory abilities against the host

CAR T Cell Locomotion in Solid Tumor Microenvironment

Notch Signaling in Breast Tumor Microenvironment as Mediator of Drug Resistance

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