Neutrophil elastase in the tumor microenvironment

Lerman, Irina; Hammes, Stephen R.

doi:10.1016/j.steroids.2017.11.006

Cited by 110 publications

(118 citation statements)

References 91 publications

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“…Most of the neutrophil-induced pro-tumor effects are associated with the release of NE, CG and PR3, which activate MMPs, and thus mediate tumor invasiveness via their degrading activity against extracellular matrix proteins. In line with this, preclinical studies revealed that genetic deletion or pharmacological inhibition of NE reduces tumor burden and metastatic potential ( Sun and Yang, 2004 ; Ghaedi et al, 2011 ; Lerman and Hammes, 2017 ).…”

Section: The Role Of Aat/neutrophil Interplay In Tumorigenesis and Mementioning

confidence: 73%

The Multifaceted Effects of Alpha1-Antitrypsin on Neutrophil Functions

et al. 2018

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Neutrophils are the predominant immune cells in human blood possessing heterogeneity, plasticity and functional diversity. The activation and recruitment of neutrophils into inflamed tissue in response to stimuli are tightly regulated processes. Alpha1-Antitrypsin (AAT), an acute phase protein, is one of the potent regulators of neutrophil activation via both -protease inhibitory and non-inhibitory functions. This review summarizes our current understanding of the effects of AAT on neutrophils, illustrating the interplay between AAT and the key effector functions of neutrophils.

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Section: The Role Of Aat/neutrophil Interplay In Tumorigenesis and Mementioning

confidence: 73%

The Multifaceted Effects of Alpha1-Antitrypsin on Neutrophil Functions

et al. 2018

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“… 21 The underlying mechanism(s) may largely depend on the fact that NE has a similar ability as MMPs in causing tissue damage by degrading the structural components of ECM. 22 Moreover, NE can cooperate with MMPs and amplify the effect of ECM degradation. 23 In addition to matrix degradation, NE can also promote peri-bronchial fibrosis by enhancing fibroblast proliferation.…”

Section: Introductionmentioning

confidence: 99%

Role of inflammatory cells in airway remodeling in COPD

Wang¹,

Xu²,

Meng³

et al. 2018

COPD

252

184

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COPD is characterized by chronic bronchitis, chronic airway obstruction, and emphysema, leading to a progressive and irreversible decline in lung function. Inflammation is central for the development of COPD. Chronic inflammation in COPD mainly involves the infiltration of neutrophils, macrophages, lymphocytes, and other inflammatory cells into the small airways. The contribution of resident airway structural cells to the inflammatory process is also important in COPD. Airway remodeling consists of detrimental changes in structural tissues and cells including airway wall thickening, epithelial metaplasia, goblet cell hypertrophy, and smooth muscle hyperplasia. Persistent airway inflammation might contribute to airway remodeling and small airway obstruction. However, the underlying mechanisms remain unclear. In this review, we will provide an overview of recent insights into the role of major immunoinflammatory cells in COPD airway remodeling.

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“…Other strategies that have been investigated to target neutrophils in the TME involve inhibition of enzymes and mediators known to induce pro-tumorigenic properties, namely NE ( 182 ), a2 isoform V-ATPase ( 146 ), arachidonate 5-lipoxygenase ( 155 ), IL-23 ( 139 ), and IL-17 ( 183 ). Again, the latter can also promote anti-tumor activities ( 158 ), illustrating that the role of TANs appears to be highly context-dependent, determined by the histological origin and stage of the tumor as well as the therapies applied in the treatment.…”

Section: Neutrophilsmentioning

confidence: 99%

Diamonds in the Rough: Harnessing Tumor-Associated Myeloid Cells for Cancer Therapy

et al. 2018

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Therapeutic approaches that engage immune cells to treat cancer are becoming increasingly utilized in the clinics and demonstrated durable clinical benefit in several solid tumor types. Most of the current immunotherapies focus on manipulating T cells, however, the tumor microenvironment (TME) is abundantly infiltrated by a heterogeneous population of tumor-associated myeloid cells, including tumor-associated macrophages (TAMs), tumor-associated dendritic cells (TADCs), tumor-associated neutrophils (TANs), and myeloid-derived suppressor cells (MDSCs). Educated by signals perceived in the TME, these cells often acquire tumor-promoting properties ultimately favoring disease progression. Upon appropriate stimuli, myeloid cells can exhibit cytoxic, phagocytic, and antigen-presenting activities thereby bolstering antitumor immune responses. Thus, depletion, reprogramming or reactivation of myeloid cells to either directly eradicate malignant cells or promote antitumor T-cell responses is an emerging field of interest. In this review, we briefly discuss the tumor-promoting and tumor-suppressive roles of myeloid cells in the TME, and describe potential therapeutic strategies in preclinical and clinical development that aim to target them to further expand the range of current treatment options.

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Neutrophil elastase in the tumor microenvironment

Cited by 110 publications

References 91 publications

The Multifaceted Effects of Alpha1-Antitrypsin on Neutrophil Functions

The Multifaceted Effects of Alpha1-Antitrypsin on Neutrophil Functions

Role of inflammatory cells in airway remodeling in COPD

Diamonds in the Rough: Harnessing Tumor-Associated Myeloid Cells for Cancer Therapy

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