Mesenchymal plasticity of devil facial tumour cells during in vivo vaccine and immunotherapy trials

2021 ◽  
Author(s):  
Amanda L. Patchett ◽  
Cesar Tovar ◽  
Nicholas B. Blackburn ◽  
Gregory M. Woods ◽  
A. Bruce Lyons
Keyword(s):  
Tumour Cells

Role of non-conventional natural killer cells in resistance against syngeneic tumour cells in vivo

Nature ◽  
1977 ◽  
Vol 270 (5638) ◽  
pp. 609-611 ◽  
Author(s):  
O. HALLER ◽  
M. HANSSON ◽  
R. KIESSLING ◽  
H. WIGZELL
Keyword(s):  
Natural Killer Cells ◽  
Natural Killer ◽  
Tumour Cells ◽  
Killer Cells

Apoptosis, cell proliferation and in vivo biological behaviour of primary and metastatic tumour cells of an AKR lymphoma variant

APOPTOSIS ◽  
1997 ◽  
Vol 2 (2) ◽  
pp. 214-220 ◽  
Author(s):  
N. Donin ◽  
D. Katzenelson ◽  
J. Ravia ◽  
J. Hiss ◽  
G. Schiby ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tumour Cells ◽  
Metastatic Tumour ◽  
Biological Behaviour

Very high dilutions of dexamethasone inhibit its pharmacological effects in vivo

2001 ◽  
Vol 90 (04) ◽  
pp. 198-203 ◽  
Author(s):  
LV Bonamin ◽  
KS Martinho ◽  
AL Nina ◽  
F Caviglia ◽  
RGW Do Rio
Keyword(s):  
Inflammatory Cells ◽  
Experimental Models ◽  
Tumour Cells ◽  
Pharmacological Effects ◽  
Trypan Blue Exclusion ◽  
Male Adult ◽  
Trypan Blue Exclusion Method ◽  
High Dilutions ◽  
Ascitic Tumour

AbstractWe evaluated the interaction of dexamethasone 10−17 and 10−33 M (equivalent to 7cH and 15cH) with dexamethasone in pharmacological concentrations, using as experimental models: acute inflammation induced by carrageenan, Ehrlich ascitic tumour, and migration of tumour infiltrating leukocytes (TIL). Male adult BALB/c mice (n=7 per group) were used in all experiments. Carrageenan (1%) was injected into the footpad for oedema evaluation and into the peritoneal cavity (i.p.), for differential counting of inflammatory cells. Ehrlich ascitic tumour cells (107 viable cells/ml) were injected i.p. and tumour cells were counted after 6 days, by the Trypan blue exclusion method. The differential TIL was counted using smears stained by hematoxylin–eosin. Treatments were made immediately after carrageenan inoculation or once a day, during Ehrlich tumour development, until the animals were killed. Animals were treated with the following preparations: (1) phosphate buffer saline (PBS) solution; (2) dexamethasone (0.5 mg/kg for inflammation model or 4 mg/kg for tumour model) mixed with dexamethasone 7cH or 15cH; (3) dexamethasone (same doses) mixed in PBS. Homeopathic dexamethasone partially blocked the anti-inflammatory effect of pharmacological dexamethasone with regard to paw oedema (two-way ANOVA, P≤0.0008) and polymorphonuclear cell migration (χ2, P=0.0001). No important differences were observed between experimental and control groups, in relation to Ehrlich tumour cells viability or count, or bodyweight, but potentised dexamethasone restored control levels of TIL viability, compared to mice treated with pharmacological doses of dexamethasone (χ2, P≤0.001). The results demonstrate that a potentised substance may change its own pharmacological effects and suggest that ultradilutions effects act mostly on host response.

Mode of action of amphotericin B on chick embryo fibroblasts and on mouse Ehrlich tumour cells: a cytological and cytochemical analysis

1975 ◽  
Vol 18 (3) ◽  
pp. 441-451
Author(s):  
F. De Paermentier ◽  
R. Bassleer ◽  
A. Lepoint ◽  
C. Desaive ◽  
G. Goessens ◽  
...  
Keyword(s):  
Chick Embryo ◽  
Amphotericin B ◽  
Tumour Cells ◽  
Total Protein Content ◽  
Cell Multiplication ◽  
Cytochemical Analysis ◽  
Ehrlich Ascites ◽  
Embryo Fibroblasts

Chick embryo fibroblasts cultivated in vitro and Ehrlich ascites tumor cells (in vivo or in vitro) have been treated with amphotericin B. Cell multiplication is strongly inhibited. Large clear zones appear in the fibroblast nucleoi (phase-contrast and electron-microscope observations). Many treated fibroblasts and tumour cells have a high DNA content (pre-mitotic or polyploid level; measurements by cytophotometry). However, the RNA content (cytophotometry) and the total protein content (cytophotometry and micro-interferometry) are relatively low in the tumour cells. As shown by autoradiography, DNA synthesis is active but RNA synthesis and, in some cases, protein synthesis are inhibited. Due to this unbalanced growth, the cells cannot divide.

lncRNA SNHG14 promotes the proliferation, migration, and invasion of thyroid tumour cells by regulating miR-93-5p

Zygote ◽  
2021 ◽  
pp. 1-11
Author(s):  
Fang Tian ◽  
Huimin Ying ◽  
Shuaiju Liao ◽  
Yuanyuan Wang ◽  
Quansheng Wang
Keyword(s):  
Wound Healing ◽  
Xenograft Model ◽  
Tumour Cells ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Thyroid Tumour ◽  
Invasion And Migration ◽  
Vital Functions ◽  
And Migration

Summary Long non-coding RNAs (lncRNAs) exert vital functions in the occurrence and development of various tumours. The aim of this study was to examine the regulatory effect and underlying molecular mechanism of lncRNA small nucleolar RNA host gene 14 (SNHG14) on the proliferation, invasion and migration of thyroid tumour cells. The expression of SNHG14 in thyroid tumour cell lines was determined using qRT-PCR. CCK-8 and western blot were used to detect the effects of SNHG14 on proliferation and apoptosis of thyroid tumour cells. The effect of SNHG14 on the migration and invasion of thyroid tumour cells was analyzed using immunofluorescence, wound-healing and transwell assays. A targeting relationship between SNHG14 and miR-93-5p was determined using bioinformatics software and luciferase reporter assays. In addition, CCK-8, immunofluorescence, wound-healing and transwell assays were applied to demonstrate that SNHG14 promoted the proliferation, migration and invasion of thyroid tumour cells by targeting miR-93-5p. The biological function of SNHG14 in vivo was explored through a xenograft model and immunohistochemistry. SNHG14 was upregulated in thyroid tumour cells compared with normal cells. Downregulation of SNHG14 effectively reduced the proliferation, migration and invasion of TPC-1 cells, and induced cell apoptosis. Moreover, SNHG14 directly targeted miR-93-5p and there was a negative correlation between them. Further functional experiments illustrated that miR-93-5p overexpression dramatically reversed the promoting role of SNHG14 in proliferation, migration and invasion of TPC-1 cells. Our results demonstrated that SNHG14 promotes the proliferation, invasion and migration of thyroid tumour cells by downregulating miR-93-5p.

NF-kappa B activation in vivo in both host and tumour cells by the antivascular agent 5,6-dimethylxanthenone-4-acetic acid (DMXAA)

2003 ◽  
Vol 39 (8) ◽  
pp. 1176-1183 ◽  
Author(s):  
S.-T Woon ◽  
S Zwain ◽  
M.A Schooltink ◽  
A.L Newth ◽  
B.C Baguley ◽  
...  
Keyword(s):  
Acetic Acid ◽  
Tumour Cells ◽  
Nf Kappa B

Expression of anionic sites on tumour cells at different stages of tissue invasion in vivo: a comparative study by X-ray microanalysis

1989 ◽  
Vol 94 (3) ◽  
pp. 561-566
Author(s):  
P.M. Evans ◽  
D.K. Suker ◽  
I. ap Gwynn
Keyword(s):  
Iron Hydroxide ◽  
Tumour Cells ◽  
Ehrlich Carcinoma ◽  
Similar Degree ◽  
Anionic Sites ◽  
Colloidal Iron ◽  
Cell Behaviour ◽  
X Ray ◽  
Invasion Stage

Quantification of colloidal iron hydroxide (CIH) labelling by X-ray microanalysis was used to investigate anionic sites at the surface of Ehrlich carcinoma cells from different locations in the mouse host. Individual tumour cells from peritoneal ascites suspensions (pre-invasion stage) varied up to threefold in their ability to bind CIH and a similar degree of intra-tumour heterogeneity was observed in different experimental animals. Pretreatment of the cells with neuraminidase confirmed that binding was at least partly due to surface sialic acid. Invasive cells isolated from mesenteric tumour nodules were also heterogeneous with regard to the availability of surface anionic sites, as were tumour cells adhering to the surface of the mesentery; however, in both these populations CIH binding was significantly greater on average than for free ascites tumour cells. The results suggest that surface anionic sites are determinants of the invasiveness of malignant cells in vivo, and that both the number and topography of these sites may be important in modulating tumour cell behaviour.

scholarly journals Pre-metastatic niche triggers SDF-1/CXCR4 axis and promotes organ colonisation by hepatocellular circulating tumour cells via downregulation of Prrx1

2019 ◽  
Vol 38 (1) ◽  
Author(s):  
Yujun Tang ◽  
Yishi Lu ◽  
Yuan Chen ◽  
Lei Luo ◽  
Lei Cai ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Cell Line ◽  
Lentiviral Vector ◽  
Tumour Cells ◽  
Clinical Samples ◽  
Circulating Tumour Cells ◽  
Metastatic Niche ◽  
Metastatic Sites

Abstract Background Circulating tumour cells (CTCs), especially mesenchymal CTCs, are important determinants of metastasis, which leads to most recurrence and mortality in hepatocellular carcinoma (HCC). However, little is known about the underlying mechanisms of CTC colonisation in pre-metastatic niches. Methods Detection and classification of CTCs in patients were performed using the CanPatrol™ system. A lentiviral vector expressing Prrx1-targeting shRNA was constructed to generate a stable HCC cell line with low expression of Prrx1. The effect of Prrx1 knockdown on stemness, migration, and drug resistance of the cell line was assessed, including involvement of SDF-1/CXCR4 signalling. Promising clinical applications of an inhibitor of STAT3 tyrosine phosphorylation, C188–9, and specific blockade with CXCR4 antibody were explored. Results The number of mesenchymal CTCs in blood was closely associated with tumour recurrence or metastasis. Pre-metastatic niche-derived SDF-1 could downregulate Prrx1, which induced the stemness, drug resistance, and increased expression of CXCR4 in HCC cells through the STAT3 pathway in vitro. In vivo, mice bearing tumours of Prrx1 low-expressing cells had significantly shorter survival. In xenograft tumours and clinical samples, loss of Prrx1 was negatively correlated with increased expression of CXCR4 in lung metastatic sites compared with that in the primary foci. Conclusions These findings demonstrate that decreased expression of Prrx1 stimulates SDF-1/CXCR4 signalling and contributes to organ colonisation with blood CTCs in HCC. STAT3 inhibition and specific blockade of CXCR4 have clinical potential as therapeutics for eliminating organ metastasis in advanced HCC.

scholarly journals Exploring the effect of nsSNPs in human YPEL3 gene in cellular senescence

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Abhishek Singh ◽  
Mukesh Thakur ◽  
Sujeet Kumar Singh ◽  
Lalit Kumar Sharma ◽  
Kailash Chandra
Keyword(s):  
Conformational Changes ◽  
Cellular Senescence ◽  
Health Professionals ◽  
Md Simulation ◽  
Tumour Cells ◽  
In Vivo Studies ◽  
Native Conformation ◽  
Altered Expression

Abstract YPEL3 that induces cellular senescence in both normal and tumour cells of humans may show altered expression under the influence of incidental mutations. In this study, we proposed the first structure of Native YPEL3 protein and its five possible deleterious mutants—V40M, C61Y, G98R, G108S, and A131T and predicted their deleterious effects to alter stability, flexibility and conformational changes in the protein. The MD simulation (RMSD, RMSF, Rg, h-bond and SASA) analysis revealed that the variants V40M, G98R and G108S increased the flexibility in protein, and variant V40M imparted more compactness to the protein.. In general, variants attributed changes in the native conformation and structure of the YPEL3 protein which might affect the native function of cellular senescence. The study provides opportunities for health professionals and practitioners in formulating précised medicines to effectively cure various cancers. We propose in-vitro or in-vivo studies should consider these reported nsSNPs while examining any malfunction in the YPEL3 protein.

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