Neutrophil granulocytes influence on extracellular matrix in cancer progression

Strøbech, Jan E.; Giuriatti, Pietro; Erler, Janine T.

doi:10.1152/ajpcell.00122.2022

Cited by 8 publications

(5 citation statements)

References 90 publications

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“…Nevertheless, they can additionally promote the dissemination of cancer cells from initial locations to different regions of the organism. 35 , 36 , 37 NET‐DNA receptor CCDC25, as indicated by recent research conducted by Yang et al, plays a role in promoting the migration of cancer cells via NETs. 38 The presence of CCDC25 was discovered to aid in the ingestion of cancer cells from in vitro samples of human breast cancer cells or primary breast cancer cells, leading to a noteworthy decrease in the in vitro migration of cancer cells.…”

Section: Discussionmentioning

confidence: 99%

“…In the human circulatory system, neutrophils, which are the primary white blood cells (WBC), play a vital role in the initial protection against infections. Nevertheless, they can additionally promote the dissemination of cancer cells from initial locations to different regions of the organism 35–37 . NET‐DNA receptor CCDC25, as indicated by recent research conducted by Yang et al, plays a role in promoting the migration of cancer cells via NETs 38 .…”

Section: Discussionmentioning

confidence: 99%

“…dissemination of cancer cells from initial locations to different regions of the organism [35][36][37]. NET-DNA receptor CCDC25, as indicated by recent research conducted by Yang et al, plays a role in promoting the migration of cancer cells via NETs 38.…”

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confidence: 99%

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Integrated analysis of NET‐DNA receptor CCDC25 in malignant tumors: Pan‐cancer analysis

Cheng,

Yin,

Song

2023

Health Science Reports

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BackgroundPreviously, it was reported that the coiled‐coil domain containing 25 (CCDC25) plays a role in the formation of neutrophil extracellular traps (NETs). This study systematically analyzed the expression profiles of CCDC25 in 30 different types of cancer and one type of blood cancer, acute myeloid leukemia.MethodsThe GTEx and CCLE databases were used to evaluate the distribution of CCDC25 expression in both normal tissue and cancer cell lines. A comparison was performed between normal tissue and tumor tissue to analyze the differential expression of CCDC25. We assessed the impact of CCDC25 on the clinical outlook in the TCGA pan‐cancer data set by analyzing the Kaplan–Meier survival plot and conducting COX regression analysis. Moreover, the association between the expression levels of CCDC25 and the tumor microenvironment in multiple cancers was conducted. Additionally, the investigation also examined the link between CCDC25 and immune neoantigen, tumor mutational burden, microsatellite instability, mismatch repair genes (MMRs), HLA‐related genes, and DNA methyltransferase (DNMT).ResultsCCDC25 was expressed in nearly all of the 31 normal tissues while exhibiting a moderate to low level of expression in cancer cell lines. While abnormal expression was detected in the majority of malignancies, there was no link found between elevated CCDC25 levels and overall survival, disease‐free survival, recurrence‐free survival, and disease‐free interval in the TCGA comprehensive cancer data set. Nevertheless, the expression of CCDC25 exhibited a notable link with the infiltration levels of activated CD4 memory T cells, quiescent mast cells, dendritic cells in an activated state, T cells that assist in follicle development, M2 macrophages, and neutrophils in various tumors.ConclusionsIn most cancers, the results indicate that there is no link between CCDC25 and prognosis. However, CCDC25 can be targeted for therapeutic purposes concerning metastasis and immune infiltration.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Integrated analysis of NET‐DNA receptor CCDC25 in malignant tumors: Pan‐cancer analysis

Cheng,

Yin,

Song

2023

Health Science Reports

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“…M2-like TAMs have been shown to secrete LOX which further enhances stiffness. Neutrophils, similar to macrophages, also contribute to ECM remodeling by secreting neutrophil extracellular traps (NET), which contain proteases such as NE, MMP9, and cathepsin G, promoting tumorigenesis via ECM remodeling ( 17 ). Sustained inflammation can activate neutrophils to form NETs, which cleave laminin 111, further awaking dormant breast cancer cells by stimulating their proliferation via activation of α3β1 integrin signaling in preclinical models ( 18 ).…”

Section: Cellular Reciprocity Regulating Ecm Remodelingmentioning

confidence: 99%

The Interplay between Extracellular Matrix Remodeling and Cancer Therapeutics

Prakash,

Shaked

2024

Cancer Discovery

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The extracellular matrix (ECM) is an abundant noncellular component of most solid tumors known to support tumor progression and metastasis. The interplay between the ECM and cancer therapeutics opens up new avenues in understanding cancer biology. While the ECM is known to protect the tumor from anticancer agents by serving as a biomechanical barrier, emerging studies show that various cancer therapies induce ECM remodeling, resulting in therapy resistance and tumor progression. This review discusses critical issues in this field including how the ECM influences treatment outcome, how cancer therapies affect ECM remodeling, and the challenges associated with targeting the ECM. Significance: The intricate relationship between the extracellular matrix (ECM) and cancer therapeutics reveals novel insights into tumor biology and its effective treatment. While the ECM may protect tumors from anti-cancer agents, recent research highlights the paradoxical role of therapy-induced ECM remodeling in promoting treatment resistance and tumor progression. This review explores the key aspects of the interplay between ECM and cancer therapeutics.

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“…A high neutrophil to lymphocyte ratio has long been a poor prognostic marker for patient survival and has dictated treatment regimens ( 10 , 11 ). Neutrophils have been implicated to play a role in the establishment of the metastatic niche and are involved in rearranging the ECM ( 7 , 12 ).…”

Section: Introductionmentioning

confidence: 99%

FES null mice demonstrate a reduction in neutrophil dependent pancreatic cancer metastatic burden

et al. 2023

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Patients with pancreatic ductal adenocarcinoma (PDAC) have a dismal 5-year survival rate of less than 10%, predominantly due to delayed diagnosis and a lack of effective treatment options. In the PDAC tumor microenvironment (TME), neutrophils are among the immune cell types that are most prevalent and are linked to a poor clinical prognosis. However, treatments that target tumor-associated neutrophils are limited despite recent developments in our understanding of neutrophil function in cancer. The feline sarcoma oncogene (FES) is a nonreceptor tyrosine kinase previously associated with leukemia and hematopoietic homeostasis. Here we describe a newly derived FES null mouse with no distinct phenotype and no defects in hematopoietic homeostasis including neutrophil viability. The immune cell composition and neutrophil population were analyzed with flow cytometry, colony-forming unit (CFU) assay, and a neutrophil viability assay, while the response to PDAC was examined with an in vivo cancer model. In an experimental metastasis model, the FES null model displayed a reduced PDAC hepatic metastatic burden and a reduction in neutrophils granulocytes. Accordingly, our results indicate FES as a potential target for PDAC TME modulation.

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Neutrophil granulocytes influence on extracellular matrix in cancer progression

Cited by 8 publications

References 90 publications

Integrated analysis of NET‐DNA receptor CCDC25 in malignant tumors: Pan‐cancer analysis

Integrated analysis of NET‐DNA receptor CCDC25 in malignant tumors: Pan‐cancer analysis

The Interplay between Extracellular Matrix Remodeling and Cancer Therapeutics

FES null mice demonstrate a reduction in neutrophil dependent pancreatic cancer metastatic burden

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