scholarly journals Nigrospora sphaerica products from the flowering dogwood exhibit antitumorigenic effects via the translational regulator, pS6 ribosomal protein

2018 ◽  
Vol 2 (3) ◽  
Author(s):  
Asha Maheshwari ◽  
Margaret Mmbaga ◽  
Quincy Quick
Keyword(s):  
Cell Migration ◽  
Tumor Cell ◽  
Translational Control ◽  
Disease Recurrence ◽  
Chemotherapeutic Agents ◽  
Boyden Chamber ◽  
Tumor Cell Migration ◽  
Flowering Dogwood ◽  
Anticancer Properties ◽  
Migration Analysis

The utility of diverse species of endophytic fungi as a viable source for drug agents with clinical applicability for the treatment of human diseases continues to expand. In this study we examined secondary metabolites of Nigrospora sphaerica isolated from the flowering dogwood, Cornus florida L., for their anticancer properties on lung cancer and glioblastoma.  Molecular identification of N. sphaerica was determined using ITS-rDNA sequence.  The expression of translational pathway proteins were examined after exposure to various crude extract concentrations (2µg/ml, 4µg/ml, 8µg/ml) using immunoblotting procedures, while tumor cell migration analysis was performed using boyden chamber assays.  Crude N. sphaerica extracts exhibited antiproliferative and antimigratory effects on solid tumors as determined by cell proliferation and cell migration assays, respectively.  The antitumorigenic effects of N. sphaerica were as a consequence of negatively regulating the PI3K/Akt/mTOR translational control signaling pathway, a canonical mechanistic axis that contributes to the maintenance and progression of several human cancers.  To our knowledge this is the first evidence that demonstrates N. sphaerica from C. florida inhibits tumor cell migration, and thus disease recurrence a major factor in the therapeutic resistance of cancers to chemotherapeutic agents.

scholarly journals Prodigiosin Inhibits Proliferation, Migration, and Invasion of Nasopharyngeal Cancer Cells

2018 ◽  
Vol 48 (4) ◽  
pp. 1556-1562 ◽  
Author(s):  
Yongze Liu ◽  
Han Zhou ◽  
Xiaofeng Ma ◽  
Chuanyao Lin ◽  
Ling Lu ◽  
...  
Keyword(s):  
Cell Migration ◽  
Nasopharyngeal Carcinoma ◽  
Tumor Cell ◽  
Cancer Cells ◽  
Cell Invasion ◽  
Nasopharyngeal Cancer ◽  
Migration And Invasion ◽  
Boyden Chamber ◽  
Cell Cycle Distribution ◽  
Tumor Cell Migration

Background/Aims: Nasopharyngeal carcinoma remains a devastating and difficult disease to treat. This study explores the antineoplastic effect of prodigiosin on nasopharyngeal cancer cells. Methods: Human nasopharyngeal carcinoma CNE2 cells and human normal nasopharyngeal epithelial NP69 cells were obtained and treated with prodigiosin or fluorouracil (5-FU). Colony formation assay was performed to screen for the optimal experimental concentrations of prodigiosin and 5-FU, and MTT assay was used to examine cell proliferative ability. Flow cytometry was used to examine cell cycle distribution, the scratch test was employed to examine cell migration, and Transwell migration assay (Boyden chamber) was used to study cell invasion. Results: The optimal concentrations of prodigiosin and 5-FU for treatment were 4 mg/L and 0.35 mg/L, respectively. Both prodigiosin and 5-FU inhibited tumor cell proliferation. The percentage of cells in G0/G1 phase was higher and the percentage of cells in S phase was lower in the prodigiosin and 5-FU groups than in the untreated groups. Both prodigiosin and 5-FU inhibited tumor cell migration and tumor cell invasion. Conclusions: Our results suggest that prodigiosin can inhibit proliferation, migration, and invasion of nasopharyngeal carcinoma cells.

Hyaluronan stimulates tumor cell migration by modulating the fibrin fiber architecture

1999 ◽  
Vol 112 (13) ◽  
pp. 2241-2251 ◽  
Author(s):  
W. Hayen ◽  
M. Goebeler ◽  
S. Kumar ◽  
R. Riessen ◽  
V. Nehls
Keyword(s):  
Cell Migration ◽  
Tumor Cell ◽  
Laser Scanning ◽  
Three Dimensional ◽  
Laser Scanning Microscopy ◽  
Boyden Chamber ◽  
Fibrin Polymerization ◽  
Fibrin Gels ◽  
Tumor Cell Migration ◽  
And Migration

The glycosaminoglycan hyaluronan, which supports tumor cell migration and metastasis, interferes with fibrin polymerization and leads to increased fiber size and porosity of fibrin clots. Here we have studied the proportionate effect of fibrin polymerization on hyaluronan-mediated migration of glioblastoma cells. The structural and physical properties of hyaluronan-containing fibrin gels were analyzed by turbidity measurement, laser scanning microscopy, compaction assay, and calculation of pore size by liquid permeation. When fibrin polymerized in the presence of hyaluronan or dextran, the resulting gels strongly stimulated cell migration, and migration significantly correlated with fiber mass-to-length ratios and pore diameters. In contrast, cell migration was not induced by addition of hyaluronan to supernatants of already polymerized gels. Hyaluronan-mediated migration was inhibited in fibrin gels by antibodies to alphav- and beta1integrins and the disintegrin echistatin, but not by antibodies to the hyaluronan receptor CD44 (up to 50 microg/ml). As a control, we show that anti-CD44 (10 microg/ml) inhibited cell migration on a pure hyaluronan matrix using a two-dimensional Boyden chamber system. In contrast to three-dimensional migration, the migration of cells on the surfaces of variably structured fibrin gels was not significantly different, indicating that increased gel permeability (porosity) may account for hyaluronan-mediated migration. We conclude that, in complex three-dimensional substrates, the predominant effect of hyaluronan on cell migration might be indirect and requires modulation of fibrin polymerization.

scholarly journals Eosinophilic inflammation promotes CCL6-dependent metastatic tumor growth

2021 ◽  
Vol 7 (22) ◽  
pp. eabb5943
Author(s):  
Fei Li ◽  
Xufei Du ◽  
Fen Lan ◽  
Na Li ◽  
Chao Zhang ◽  
...  
Keyword(s):  
Cell Migration ◽  
Bone Metastasis ◽  
Tumor Cell ◽  
Cancer Metastasis ◽  
Inflammatory Diseases ◽  
Metastatic Tumor ◽  
Eosinophil Infiltration ◽  
Tumor Cell Migration ◽  
Promote Tumor Cell ◽  
Chemokine Ligand

Compelling evidence suggests that inflammatory components contribute to cancer development. However, eosinophils, involved in several inflammatory diseases, were not fully explored in cancer metastasis. We show that airway inflammatory eosinophilia and colonic inflammation with eosinophil infiltration are both associated with increased metastasis in mice. Eosinophilia is responsible for increased bone metastasis in eosinophil-enriched Cd3δ-Il-5 transgenic (Il-5 Tg) mice. We also observe increased eosinophils in the malignant pleural effusion of cancer patients with pleural metastasis. Mechanistically, eosinophils promote tumor cell migration and metastasis formation through secreting C-C motif chemokine ligand 6 (CCL6). Genetic knockout of Ccl6 in Il-5 Tg mice remarkably attenuates bone metastasis. Moreover, inhibition of C-C chemokine receptor 1 (CCR1, the receptor of CCL6) in tumor cells reduces tumor cell migration and metastasis. Thus, our study identifies a CCL6-dependent prometastatic activity of eosinophils, which can be inhibited by targeting CCR1 and represent an approach to preventing metastatic disease.

scholarly journals Compensation mechanism in tumor cell migration

2003 ◽  
Vol 160 (2) ◽  
pp. 267-277 ◽  
Author(s):  
Katarina Wolf ◽  
Irina Mazo ◽  
Harry Leung ◽  
Katharina Engelke ◽  
Ulrich H. von Andrian ◽  
...  
Keyword(s):  
Cell Migration ◽  
Tumor Cell ◽  
Shape Change ◽  
Proteolytic Degradation ◽  
Amoeboid Movement ◽  
Tumor Cell Migration ◽  
Tumor Dissemination ◽  
Β1 Integrins

Invasive tumor dissemination in vitro and in vivo involves the proteolytic degradation of ECM barriers. This process, however, is only incompletely attenuated by protease inhibitor–based treatment, suggesting the existence of migratory compensation strategies. In three-dimensional collagen matrices, spindle-shaped proteolytically potent HT-1080 fibrosarcoma and MDA-MB-231 carcinoma cells exhibited a constitutive mesenchymal-type movement including the coclustering of β1 integrins and MT1–matrix metalloproteinase (MMP) at fiber bindings sites and the generation of tube-like proteolytic degradation tracks. Near-total inhibition of MMPs, serine proteases, cathepsins, and other proteases, however, induced a conversion toward spherical morphology at near undiminished migration rates. Sustained protease-independent migration resulted from a flexible amoeba-like shape change, i.e., propulsive squeezing through preexisting matrix gaps and formation of constriction rings in the absence of matrix degradation, concomitant loss of clustered β1 integrins and MT1-MMP from fiber binding sites, and a diffuse cortical distribution of the actin cytoskeleton. Acquisition of protease-independent amoeboid dissemination was confirmed for HT-1080 cells injected into the mouse dermis monitored by intravital multiphoton microscopy. In conclusion, the transition from proteolytic mesenchymal toward nonproteolytic amoeboid movement highlights a supramolecular plasticity mechanism in cell migration and further represents a putative escape mechanism in tumor cell dissemination after abrogation of pericellular proteolysis.

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