scholarly journals The Heterogeneity of Neutrophil Recruitment in the Tumor Microenvironment and the Formation of Premetastatic Niches

2021 ◽  
Vol 2021 ◽  
pp. 1-6
Author(s):  
Xin Xing ◽  
Yongrui Bai ◽  
Jian Song
Keyword(s):  
Tumor Microenvironment ◽  
Tumor Cell ◽  
Tumor Cells ◽  
Cell Invasion ◽  
Stromal Cells ◽  
Tumor Metastasis ◽  
Neutrophil Recruitment ◽  
Tumor Cell Invasion ◽  
Primary Cancer ◽  
Neutrophil Chemotaxis

The recruitment of neutrophil to the primary cancer has been shown to be steered by neoplastic cells or tumor-educated mesenchymal stromal cells and has a prometastatic effect. However, the neutrophil chemotaxis and their interaction with tumor cells in the distal metastasized tissues remain elusive. In this review, we discussed emerging research on the interaction between neutrophil recruitment and tumor metastasis, which is essential for studying tumor cell invasion and related immunotherapy.

scholarly journals Aspirin inhibits platelets from reprogramming breast tumor cells and promoting metastasis

2019 ◽  
Vol 3 (2) ◽  
pp. 198-211 ◽  
Author(s):  
Kelly E. Johnson ◽  
Julia R. Ceglowski ◽  
Harvey G. Roweth ◽  
Jodi A. Forward ◽  
Mason D. Tippy ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Tumor Cells ◽  
Cell Invasion ◽  
Breast Tumor ◽  
Tumor Metastasis ◽  
Tumor Cell Invasion ◽  
Akt Pathway ◽  
Breast Tumor Cells ◽  
Invasive Capacity ◽  
Platelet Releasate

Abstract It is now recognized that compounds released from tumor cells can activate platelets, causing the release of platelet-derived factors into the tumor microenvironment. Several of these factors have been shown to directly promote neovascularization and metastasis, yet how the feedback between platelet releasate and the tumor cell affects metastatic phenotype remains largely unstudied. Here, we identify that breast tumor cells secrete high levels of interleukin 8 (IL-8, CXCL8) in response to platelet releasate, which promotes their invasive capacity. Furthermore, we found that platelets activate the Akt pathway in breast tumor cells, and inhibition of this pathway eliminated IL-8 production. We therefore hypothesized inhibiting platelets with aspirin could reverse the prometastatic effects of platelets on tumor cell signaling. Platelets treated with aspirin did not activate the Akt pathway, resulting in reduced IL-8 secretion and impaired tumor cell invasion. Of note, patients with breast cancer receiving aspirin had lower circulating IL-8, and their platelets did not increase tumor cell invasion compared with patients not receiving aspirin. Our data suggest platelets support breast tumor metastasis by inducing tumor cells to secrete IL-8. Our data further support that aspirin acts as an anticancer agent by disrupting the communication between platelets and breast tumor cells.

scholarly journals Pathological Investigation of Meningioma Capsule with respect to Tumor Cell Invasion

2021 ◽  
Author(s):  
Takashi Sugawara ◽  
Daisuke Kobayashi ◽  
Taketoshi Maehara
Keyword(s):  
Tumor Cell ◽  
Tumor Cells ◽  
Cell Invasion ◽  
Tumor Invasion ◽  
Recurrence Risk ◽  
Tumor Cell Invasion ◽  
Brain Surface ◽  
Eloquent Cortex ◽  
The Brain

Abstract OBJECTIVE No previous study has pathologically investigated whether the meningioma capsule presents with tumor cells. We investigated which types of tumor capsules include tumor cells to help decide the kind of capsules which can be left intraoperatively without recurrence risk. METHODS We investigated 22 specimens of 14 newly diagnosed meningiomas between February 2011 and June 2021. Capsules were classified into three types: tumor capsule (TC), capsule-like thickened arachnoid membrane (CAM), and extended membrane (EM). Capsule properties were scored as hardness (soft = 1, medium = 2, hard = 3) and transparency (high = 1, medium = 2, low = 3). Hardness, transparency, and score sum was compared between capsules with/without tumor invasion in CAM and EM types. RESULTS The mean follow-up duration was 28.1 months, and there was only one recurrence in a remote location from the residual capsule. Nine capsules were classified as TC, seven as CAM, and six as EM. 88.9% of TCs, 42.9% of CAMs, and 50% of EMs were invaded by tumor cells. Hardness, transparency, and score sum in CAM with tumor invasion was lower than in CAM without, but not significant (p = 0.114, p = 0.114, p = 0.057). CONCLUSION Thickened TC or soft and highly transparent CAM imply a high risk of tumor cell invasion, thus such cases should be followed up long and carefully. The hard and low transparent residual CAMs may have low risk of tumor invasion, thus these kinds of residual capsules might not increase the recurrence risk. Thus, leaving such capsules tightly adhered to the eloquent cortex is theoretically justified to avoid damaging the brain surface.

scholarly journals P11.65 Insights into the mechanisms of primary brain tumor invasion

2019 ◽  
Vol 21 (Supplement_3) ◽  
pp. iii58-iii59
Author(s):  
A Bikfalvi ◽  
T Daubon ◽  
C Billottet
Keyword(s):  
Extracellular Matrix ◽  
Tumor Cell ◽  
Tumor Cells ◽  
Conformational Changes ◽  
Cell Invasion ◽  
Immune Cell ◽  
Tumor Cell Invasion ◽  
Migration And Invasion ◽  
Matricellular Proteins

Abstract We have made progress in unravelling the mechanisms of tumor cell invasion by focusing the attention on two molecular pathways including chemokines and extracellular matrix molecules. Chemokines are important mediators of cell signaling that operate both on normal cells and tumor cells and in the immune-cell compartment (Billottet et al, 2013). Among the chemokine receptors, CXCR3 mediate diverse biological functions and comes in two major isoforms the A and B isoform. We found that ligand affinities and conformational changes are very different for the A and B form. We have recently elucidated the role and mechanism of CXCR3A in GBM invasion (Boyé et al, 2017b). We demonstrated that agonist stimulation enhances in vitro cell migration and invasion in GBM cells. A major finding was that CXCR3A forms a complex with the trafficking receptor Lipoprotein-related receptor-1 (LRP1). Silencing of LRP1 leads to an increase in the magnitude of ligand-induced conformational change with CXCR3-A focalized at the cell membrane, leading to sustained receptor activity and increase in the migration. This was also clinically validated. Our study defines LRP1 as a new regulator of CXCR3 and indicates that targeting CXCR3-A in GBM may constitute a promising strategy to halt tumor cell invasion. The extracellular matrix (ECM) has morphogenic roles in tumors. Important ECM components are the matricellular proteins, called thrombospondins(THBS1-5) (Adams and Lawler 2011). We recently elucidated the complex role of THSB1 in GBM invasion (Daubon et al.2019). Global expression analysis revealed that THBS1 is up-regulated in GBMs and associated with a poor prognosis. We, furthermore, demonstrated that THBS1 did not activate TGFβ in GBM but that TGFβ1 induced the expression of THBS1 via SMAD3. Furthermore, GBM invasion is compromised when THBS1 is silenced in tumor cells. Thus, our data clearly show that THBS1 is not only involved in the regulation of angiogenesis in GBM, but also impacts the invasive behaviour of glioma cells by interacting with a molecule called CD47 expressed on the surface of GBM cells. RNA-sequencing after microdissection of central and peripheral tumour areas in a human PDX model demonstrated that THBS1 was the gene with the highest connectivity in the peripheral invasive tumour areas. Taken together, these data indicate that THBS1 plays important role in the infiltrative process in GBM. REFERENCES: Adams JC, Lawler J. Cold Spring Harb Perspect Biol. 2011;3:a009712 Billottet C, Quemener C, Bikfalvi A. Biochim Biophys Acta. 2013;1836:287- Boyé K et al. Sci Rep. 2017;7:10703 Boyé K et al. Nat Commun. 2017;8:1571 Daubon T et al, Nature Communications. Nat Commun. 2019 Mar 8;10(1):1146 Murphy-Ullrich JE, Poczatek M. Cytokine Growth Factor Rev. 2000 11:59

The role of tumor microenvironment in collective tumor cell invasion

2017 ◽  
Vol 13 (11) ◽  
pp. 991-1002 ◽  
Author(s):  
Jia-shun Wu ◽  
Su-rui Sheng ◽  
Xin-hua Liang ◽  
Ya-ling Tang
Keyword(s):  
Tumor Microenvironment ◽  
Tumor Cell ◽  
Cell Invasion ◽  
Tumor Cell Invasion

scholarly journals Dynamin 2 interacts with α-actinin 4 to drive tumor cell invasion

2020 ◽  
Vol 31 (6) ◽  
pp. 439-451 ◽  
Author(s):  
Kevin M. Burton ◽  
Hong Cao ◽  
Jing Chen ◽  
Li Qiang ◽  
Eugene W. Krueger ◽  
...  
Keyword(s):  
Cell Migration ◽  
Tumor Cell ◽  
Tumor Cells ◽  
Cell Invasion ◽  
Tumor Cell Invasion ◽  
Related Protein ◽  
Invasive Tumor ◽  
Invasive Cell ◽  
Dynamin 2

Dyn2 and α-actinin 4 interact directly to regulate invasive cell migration and the stabilization of invadopodia. Intriguingly, this is specific for α-actinin 4, and not the highly related protein α-actinin 1. These findings elucidate a novel mechanism of regulating cell migration, with important implications for invasive tumor cells.

scholarly journals Microfluidic modeling of the biophysical microenvironment in tumor cell invasion

Lab on a Chip ◽  
2017 ◽  
Vol 17 (19) ◽  
pp. 3221-3233 ◽  
Author(s):  
Yu Ling Huang ◽  
Jeffrey E. Segall ◽  
Mingming Wu
Keyword(s):  
Tumor Microenvironment ◽  
Tumor Cell ◽  
Cell Invasion ◽  
Tumor Cell Invasion ◽  
Extracellular Matrices

Microfluidic model for the physical tumor microenvironment: intramural and interstitial flows and extracellular matrices (ECMs).

scholarly journals Latrunculin A and Its C-17-O-Carbamates Inhibit Prostate Tumor Cell Invasion and HIF-1 Activation in Breast Tumor Cells⊥

2008 ◽  
Vol 71 (3) ◽  
pp. 396-402 ◽  
Author(s):  
Khalid A. El Sayed ◽  
Mohammad A. Khanfar ◽  
Hassan M. Shallal ◽  
A. Muralidharan ◽  
Bhushan Awate ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Tumor Cells ◽  
Cell Invasion ◽  
Breast Tumor ◽  
Prostate Tumor ◽  
Tumor Cell Invasion ◽  
Breast Tumor Cells ◽  
Latrunculin A ◽  
Prostate Tumor Cell

scholarly journals Morphological features of invasion of tumor cells of invasive ductal breast cancer

Morphologia ◽  
2021 ◽  
Vol 15 (3) ◽  
pp. 119-124
Author(s):  
L.A. Naleskina ◽  
T.V. Zadvornyi ◽  
L.M. Kunska ◽  
N.Y. Lukianova
Keyword(s):  
Breast Cancer ◽  
Connective Tissue ◽  
Tumor Cell ◽  
Tumor Cells ◽  
Cell Invasion ◽  
Tumor Cell Invasion ◽  
Invasive Front ◽  
Invasive Ductal Breast Cancer ◽  
Pathological Characteristics ◽  
Ductal Breast Cancer

Background. Nowadays, it has been proven that along with the invasion of individual tumor cells, their group migration occurs in the invasive front of the tumor, and this is an important factor in tumor progression. Objective: to determine the features of tumor cell invasion in the invasive front (IF) of invasive ductal breast cancer (BCa) without special specific features (IC NST) and to establish associative links between them and the clinical and pathological characteristics of the disease. Methods. The study was performed on BCa samples (after hematoxylin and eosin stained) from 120 patients with invasive ductal BCa I-II stage with G2 grade of tumor differentiation that didn’t receive neoadjuvant chemotherapy. Results. Tumors were divided into 3 groups: with predominance of parenchymal component (PC), with the larger component of connective tissue, and relatively equivalent ratio of these components. Within the IF of the studied tumors of patients with ІІ stage of the tumor process, group invasion of tumor structures was mainly determined, both separately and in combination. In particular, an increase in solid structures in tumors with a predominance of the PC, and in neoplasms with expressed desmoplastic changes in connective tissue and their advantage, - alveolar, tubular, discrete. Conclusion. In tumors of patients with invasive ductal BCa in the invasive front is dominated by collective migration of tumor cells, which is the starting mechanism of tumor progression and the first step of the metastatic process. Defined associative links between the features of tumor cell invasion and the clinical and pathological characteristics of the tumor process in BCa patients can be used in predicting this form of cancer.

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