scholarly journals Posidonia oceanica (L.) Delile Dampens Cell Migration of Human Neuroblastoma Cells

Marine Drugs ◽  
2021 ◽  
Vol 19 (10) ◽  
pp. 579
Author(s):  
Marzia Vasarri ◽  
Manuela Leri ◽  
Emanuela Barletta ◽  
Carlo Pretti ◽  
Donatella Degl’Innocenti
Keyword(s):  
Cell Migration ◽  
Cancer Cell ◽  
Neuroblastoma Cells ◽  
Gelatin Zymography ◽  
Posidonia Oceanica ◽  
In Vivo Studies ◽  
Cancer Cell Migration ◽  
Western Blot Assay ◽  
Human Neuroblastoma

Neuroblastoma (NB) is a common cancer in childhood, and lethal in its high-risk form, primarily because of its high metastatic potential. Targeting cancer cell migration, and thus preventing metastasis formation, is the rationale for more effective cancer therapy against NB. Previous studies have described the leaf extract from Posidonia oceanica marine plant (POE) as an antioxidant, anti-inflammatory agent and inhibitor of cancer cell migration. This study aims to examine the POE anti-migratory role in human SH-SY5Y neuroblastoma cells and the underlying mechanisms of action. Wound healing and gelatin zymography assays showed that POE at early times inhibits cell migration and reduces pro-MMP-2 release into culture medium. By monitoring expression level of key autophagy markers by Western blot assay, a correlation between POE-induced cell migration inhibition and autophagy activation was demonstrated. Cell morphology and immunofluorescence analyses showed that POE induces neurite formation and neuronal differentiation at later times. These results suggest POE might act against cell migration by triggering early nontoxic autophagy. The POE-induced cellular morphological change toward cell differentiation might contribute to prolonging the phytocomplex anti-migratory effect to later times. Overall, these results encourage future in vivo studies to test POE applicability in neuroblastoma treatment.

scholarly journals Comparison of Chitosan Nanoparticles and Soluplus Micelles to Optimize the Bioactivity of Posidonia oceanica Extract on Human Neuroblastoma Cell Migration

Pharmaceutics ◽  
2019 ◽  
Vol 11 (12) ◽  
pp. 655 ◽  
Author(s):  
Vieri Piazzini ◽  
Marzia Vasarri ◽  
Donatella Degl’Innocenti ◽  
Asia Guastini ◽  
Emanuela Barletta ◽  
...  
Keyword(s):  
Cell Migration ◽  
Cancer Cell ◽  
Chitosan Nanoparticles ◽  
In Vitro Release ◽  
Posidonia Oceanica ◽  
Inhibitory Effect ◽  
Human Neuroblastoma Cell ◽  
Prolonged Release ◽  
Cancer Cell Migration ◽  
Human Neuroblastoma

Posidonia oceanica (L.) Delile is a marine plant endemic of Mediterranean Sea endowed with interesting bioactivities. The hydroalcholic extract of P. oceanica leaves (POE), rich in polyphenols and carbohydrates, has been shown to inhibit human cancer cell migration. Neuroblastoma is a common childhood extracranial solid tumor with high rate of invasiveness. Novel therapeutics loaded into nanocarriers may be used to target the migratory and metastatic ability of neuroblastoma. Our goal was to improve both the aqueous solubility of POE and its inhibitory effect on cancer cell migration. Methods: Chitosan nanoparticles (NP) and Soluplus polymeric micelles (PM) loaded with POE have been developed. Nanoformulations were chemically and physically defined and characterized. In vitro release studies were also performed. Finally, the inhibitory effect of both nanoformulations was tested on SH-SY5Y cell migration by wound healing assay and compared to that of unformulated POE. Results: Both nanoformulations showed excellent physical and chemical stability during storage, and enhanced the solubility of POE. PM-POE improved the inhibitory effect of POE on cell migration probably due to the high encapsulation efficiency and the prolonged release of the extract. Conclusions: For the first time, a phytocomplex of marine origin, i.e., P. oceanica extract, has enhanced in terms of acqueous solubility and bioactivity once encapsulated inside nanomicelles.

scholarly journals Lactobacilli inhibit cervical cancer cell migration in vitro and reduce tumor burden in vivo through upregulation of E-cadherin

2017 ◽  
Vol 38 (3) ◽  
pp. 1561-1568 ◽  
Author(s):  
Xiaoxi Li ◽  
Hong Wang ◽  
Xingxing Du ◽  
Wenna Yu ◽  
Jingwen Jiang ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Migration ◽  
Cancer Cell ◽  
Tumor Burden ◽  
Cervical Cancer Cell ◽  
Cancer Cell Migration ◽  
Reduce Tumor Burden ◽  
E Cadherin

scholarly journals CRMP2 as a Candidate Target to Interfere with Lung Cancer Cell Migration

Biomolecules ◽  
2021 ◽  
Vol 11 (10) ◽  
pp. 1533
Author(s):  
Xabier Morales ◽  
Rafael Peláez ◽  
Saray Garasa ◽  
Carlos Ortiz de Solórzano ◽  
Ana Rouzaut
Keyword(s):  
Cell Migration ◽  
Lung Adenocarcinoma ◽  
Cancer Cell ◽  
Adaptor Protein ◽  
Mechanistic Explanation ◽  
In Vitro Assays ◽  
Cancer Cell Migration ◽  
Cortical Actin

Collapsin response mediator protein 2 (CRMP2) is an adaptor protein that adds tubulin dimers to the growing tip of a microtubule. First described in neurons, it is now considered a ubiquitous protein that intervenes in processes such as cytoskeletal remodeling, synaptic connection and trafficking of voltage channels. Mounting evidence supports that CRMP2 plays an essential role in neuropathology and, more recently, in cancer. We have previously described a positive correlation between nuclear phosphorylation of CRMP2 and poor prognosis in lung adenocarcinoma patients. In this work, we studied whether this cytoskeleton molding protein is involved in cancer cell migration. To this aim, we evaluated CRMP2 phosphorylation and localization in the extending lamella of lung adenocarcinoma migrating cells using in vitro assays and in vivo confocal microscopy. We demonstrated that constitutive phosphorylation of CRMP2 impaired lamella formation, cell adhesion and oriented migration. In search of a mechanistic explanation of this phenomenon, we discovered that CRMP2 Ser522 phospho-mimetic mutants display unstable tubulin polymers, unable to bind EB1 plus-Tip protein and the cortical actin adaptor IQGAP1. In addition, integrin recycling is defective and invasive structures are less evident in these mutants. Significantly, mouse xenograft tumors of NSCLC expressing CRMP2 phosphorylation mimetic mutants grew significantly less than wild-type tumors. Given the recent development of small molecule inhibitors of CRMP2 phosphorylation to treat neurodegenerative diseases, our results open the door for their use in cancer treatment.

scholarly journals Wnt5a induces ROR1 to recruit cortactin to promote breast-cancer migration and metastasis

2019 ◽  
Vol 5 (1) ◽  
Author(s):  
Md Kamrul Hasan ◽  
George F. Widhopf ◽  
Suping Zhang ◽  
Sharon M. Lam ◽  
Zhouxin Shen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Migration ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Surface Protein ◽  
Cancer Cell Migration ◽  
Breast Cancer Cell Migration ◽  
Promote Breast Cancer

Abstract ROR1 is a conserved oncoembryonic surface protein expressed in breast cancer. Here we report that ROR1 associates with cortactin in primary breast-cancer cells or in MCF7 transfected to express ROR1. Wnt5a also induced ROR1-dependent tyrosine phosphorylation of cortactin (Y421), which recruited ARHGEF1 to activate RhoA and promote breast-cancer-cell migration; such effects could be inhibited by cirmtuzumab, a humanized mAb specific for ROR1. Furthermore, treatment of mice bearing breast-cancer xenograft with cirmtuzumab inhibited cortactin phosphorylation in vivo and impaired metastatic development. We established that the proline at 841 of ROR1 was required for it to recruit cortactin and ARHGEF1, activate RhoA, and enhance breast-cancer-cell migration in vitro or development of metastases in vivo. Collectively, these studies demonstrate that the interaction of ROR1 with cortactin plays an important role in breast-cancer-cell migration and metastasis.

scholarly journals Roles of the Na+/H+ Exchanger Isoform 1 and Urokinase in Prostate Cancer Cell Migration and Invasion

2021 ◽  
Vol 22 (24) ◽  
pp. 13263
Author(s):  
Xiuju Li ◽  
Benjamin Buckley ◽  
Konstantin Stoletov ◽  
Yang Jing ◽  
Marie Ranson ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Migration ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Colony Formation ◽  
Prostate Cancer Cell ◽  
Cancer Cell Migration ◽  
Prostate Cancer Cells

Prostate cancer is a leading cause of cancer-associated deaths in men over 60 years of age. Most patients are killed by tumor metastasis. Recent evidence has implicated a role of the tumor microenvironment and urokinase plasminogen activator (uPA) in cancer cell migration, invasion, and metastasis. Here, we examine the role of the Na+/H+ exchanger isoform 1 (NHE1) and uPA in DU 145 prostate cancer cell migration and colony formation. Knockout of NHE1 reduced cell migration. The effects of a series of novel NHE1/uPA hexamethylene-amiloride-based inhibitors with varying efficacy towards NHE1 and uPA were examined on prostate cancer cells. Inhibition of NHE1—alone, or with inhibitors combining NHE1 or uPA inhibition—generally did not prevent prostate cancer cell migration. However, uPA inhibition—but not NHE1 inhibition—prevented anchorage-dependent colony formation. Application of inhibitors at concentrations that only saturate uPA inhibition decreased tumor invasion in vivo. The results suggest that while knockout of NHE1 affects cell migration, these effects are not due to NHE1-dependent proton translocation. Additionally, while neither NHE1 nor uPA activity was critical in cell migration, only uPA activity appeared to be critical in anchorage-dependent colony formation of DU 145 prostate cancer cells and invasion in vivo.

scholarly journals Breast Fibroblasts and ECM Components Modulate Breast Cancer Cell Migration through the Secretion of MMPs in a 3D Microfluidic Co-Culture Model

Cancers ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1173 ◽  
Author(s):  
Karina M. Lugo-Cintrón ◽  
Max M. Gong ◽  
José M. Ayuso ◽  
Lucas A. Tomko ◽  
David J. Beebe ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Migration ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Progression ◽  
Cancer Cell Migration ◽  
Migration Distance ◽  
Breast Fibroblasts

The extracellular matrix (ECM) composition greatly influences cancer progression, leading to differential invasion, migration, and metastatic potential. In breast cancer, ECM components, such as fibroblasts and ECM proteins, have the potential to alter cancer cell migration. However, the lack of in vitro migration models that can vary ECM composition limits our knowledge of how specific ECM components contribute to cancer progression. Here, a microfluidic model was used to study the effect of 3D heterogeneous ECMs (i.e., fibroblasts and different ECM protein compositions) on the migration distance of a highly invasive human breast cancer cell line, MDA-MB-231. Specifically, we show that in the presence of normal breast fibroblasts, a fibronectin-rich matrix induces more cancer cell migration. Analysis of the ECM revealed the presence of ECM tunnels. Likewise, cancer-stromal crosstalk induced an increase in the secretion of metalloproteinases (MMPs) in co-cultures. When MMPs were inhibited, migration distance decreased in all conditions except for the fibronectin-rich matrix in the co-culture with human mammary fibroblasts (HMFs). This model mimics the in vivo invasion microenvironment, allowing the examination of cancer cell migration in a relevant context. In general, this data demonstrates the capability of the model to pinpoint the contribution of different components of the tumor microenvironment (TME).

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