Physiological Mechanisms of Tumor-Cell Invasion and Migration

Physiology ◽  
2005 ◽  
Vol 20 (3) ◽  
pp. 194-200 ◽  
Author(s):  
David H. Geho ◽  
Russell W. Bandle ◽  
Timothy Clair ◽  
Lance A. Liotta
Keyword(s):  
Tumor Invasion ◽  
Developmental Regulation ◽  
Cell Types ◽  
Tumor Cell Invasion ◽  
Physiological Mechanisms ◽  
Invasion And Migration ◽  
Extracellular Signaling ◽  
Multiple Cell ◽  
Pharmacological Blockade ◽  
And Migration

Recent advances in understanding the complex biology of the microenvironment that underlies tumor invasion and migration have revealed novel and promising therapeutic targets. Pharmacological blockade of intra- and extracellular signaling events that regulate migration and survival of multiple cell types may disrupt the host-tumor conspiracy that allows escape from normal developmental regulation.

scholarly journals MENA promotes esophageal squamous cell carcinoma cell invasion and migration via MMP-2, MMP-9 and AKT activation

2020 ◽  
Author(s):  
Yueheng Li ◽  
Na Gao ◽  
Jing Li ◽  
Zhengfan Gao ◽  
Zhenzhen Yang ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Cell Invasion ◽  
Tumor Cell Invasion ◽  
Wound Healing Assay ◽  
Transwell Assay ◽  
Invasion And Migration ◽  
Akt Activation ◽  
Qrt Pcr ◽  
And Migration ◽  
Migration Capacity

Abstract Background: Esophageal squamous cell carcinoma (ESCC) is a fatal disease with poor prognosis. The predominant reason for ESCC-related death is metastasis caused by tumor cell invasion. Human MENA protein is a member of Ena/Vasp family, which plays a critical role during tumor cell invasion. However, the biological effect of MENA in ESCC cell lines remains unclear Methods: In this study, fluorescent quantitative real-time PCR (qRT-PCR) were conducted to detect the mRNA expression of MENA in tumor and para-cancer tissue, CCK-8 assay and clone formation assay were conducted to evaluate cell proliferation activity, Transwell assay and wound-healing assay were conducted to detect the changes of cell invasion and migration capacity, siRNA and MENA expression vector were constructed to explore biological function of MENA in ESCC cell lines. Western blot analysis were conducted to detect the expressions of MENA , molecular markers of epithelial-mesenchymal transition (EMT), Akt, p-Akt, MMP-2 and MMP-9 respectively in ESCC cell line. Results: The qRT-PCR experiment results showed that MENA expression in ESCC tissue of 35 patients was relatively higher than that in tissue adjacent to cancer. CCK-8 assay suggested that tumor cell proliferation capacity was suppressed followed by the knockdown of MENA expression in Mena high ESCC cell TE13 and was potentiated by the overexpression of MENA in Mena low ESCC cell TE1. Transwell assay and wound healing assay demonstrated that interfering in MENA could inhibit TE13 cells invasion and migration capacity by affecting the expressions of Matrix metalloproteinase-2(MMP-2) and Matrix metalloproteinase-9 (MMP-9), in contrast, overexpression of MENA in Mena low ESCC cell TE1 could promote invasion and migration by up-regulated expression of MMP-2 and MMP-9. Western blot analysis indicated that interfering of MENA expression could affect EMT-related molecular markers (E-cadherin, N-cadherin, Snail, Slug), Akt and p-Akt Conclusions: Our study reveal that MENA could promote the ESCC cell invasion and migration by upregulate MMP-2, MMP-9 expression and Akt activation. Meanwhile, interfering of MENA expression could affect EMT in ESCC cells. This indicated that MENA may be a potential molecular therapeutic target for ESCC metastasis

scholarly journals Clofarabine commandeers the RNR-α—ZRANB3 nuclear signaling axis

2019 ◽  
Author(s):  
Marcus J. C. Long ◽  
Yi Zhao ◽  
Yimon Aye
Keyword(s):  
Dna Synthesis ◽  
Tumor Invasion ◽  
Early Time ◽  
Cell Types ◽  
Drug Induced ◽  
Nuclear Signaling ◽  
Signaling Axis ◽  
Multiple Cell ◽  
Essential Enzyme ◽  
Approved Drugs

SummaryRibonucleotide reductase (RNR) is an essential enzyme in DNA-biogenesis and a target of several chemotherapeutics. Here we investigate how anti-leukemic drugs [e.g., clofarabine (ClF)] that target one of the two subunits of RNR, RNR-α, affect non-canonical RNR-α functions. We discovered that these clinically-approved RNR-inhibiting dATP-analogs inhibit growth by also targeting ZRANB3—a newly-identified DNA-synthesis promoter and nuclear-localized interactor of RNR-α. Remarkably, in early time points following drug treatment, ZRANB3-targeting accounted for most of the drug-induced DNA-synthesis suppression and multiple cell types featuring ZRANB3-knockout/knockdown were resistant to these drugs. Additionally, ZRANB3 plays a major role in regulating tumor-invasion and H-rasG12V-promoted transformation in a manner dependent on the recently-discovered interactome of RNR-α involving select cytosolic-/nuclear-localized protein-players. The H-rasG12V-promoted transformation—which we show requires ZRANB3-supported DNA-synthesis—was efficiently suppressed by ClF. Such overlooked mechanisms-of-action of approved drugs and a new example of non-oncogene addiction, which is suppressed by RNR-α, may advance cancer interventions.

Six‐transmembrane epithelial antigen of the prostate 1 is associated with tumor invasion and migration in endometrial carcinomas

2019 ◽  
Vol 120 (7) ◽  
pp. 11172-11189 ◽  
Author(s):  
Jiali Sun ◽  
Guoxin Ji ◽  
Jie Xie ◽  
Zhi Jiao ◽  
Haozheng Zhang ◽  
...  
Keyword(s):  
Tumor Invasion ◽  
Invasion And Migration ◽  
And Migration ◽  
Endometrial Carcinomas

scholarly journals miR-720 inhibits tumor invasion and migration in breast cancer by targeting TWIST1

2013 ◽  
Vol 35 (2) ◽  
pp. 469-478 ◽  
Author(s):  
Lin-Zi Li ◽  
Chris Zhiyi Zhang ◽  
Li-Li Liu ◽  
Chun Yi ◽  
Shi-Xun Lu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Invasion ◽  
Invasion And Migration ◽  
And Migration

scholarly journals E2F1 promotes tumor cell invasion and migration through regulating CD147 in prostate cancer

2016 ◽  
Vol 48 (4) ◽  
pp. 1650-1658 ◽  
Author(s):  
YU-XIANG LIANG ◽  
JIAN-MING LU ◽  
RU-JUN MO ◽  
HUI-CHAN HE ◽  
JIAN XIE ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Tumor Cell ◽  
Cell Invasion ◽  
Tumor Cell Invasion ◽  
Invasion And Migration ◽  
And Migration

scholarly journals The CCN family: a new stimulus package

2003 ◽  
Vol 178 (2) ◽  
pp. 169-175 ◽  
Author(s):  
DR Brigstock
Keyword(s):  
Clinical Endocrinology ◽  
Cell Types ◽  
Tissue Growth ◽  
Ccn Proteins ◽  
Ccn Family ◽  
Igf Binding Proteins ◽  
Igf Binding ◽  
Multiple Cell ◽  
Activate Cell ◽  
And Migration

The CCN family comprises cysteine-rich 61 (CYR61/CCN1), connective tIssue growth factor (CTGF/CCN2), nephroblastoma overexpressed (NOV/CCN3), and Wnt-induced secreted proteins-1 (WISP-1/CCN4), -2 (WISP-2/CCN5) and -3 (WISP-3/CCN6). These proteins stimulate mitosis, adhesion, apoptosis, extracellular matrix production, growth arrest and migration of multiple cell types. Many of these activities probably occur through the ability of CCN proteins to bind and activate cell surface integrins. Accumulating evidence supports a role for these factors in endocrine pathways and endocrine-related processes. To illustrate the broad role played by the CCN family in basic and clinical endocrinology, this Article highlights the relationship between CCN proteins and hormone action, skeletal growth, placental angiogenesis, IGF-binding proteins and diabetes-induced fibrosis.

scholarly journals circEPS15 Overexpression in Hepatocellular Carcinoma Modulates Tumor Invasion and Migration

2020 ◽  
Author(s):  
Maolin Tian ◽  
Gang Li ◽  
Bin Jiang ◽  
Sadula Abuduhaibaier ◽  
Dianrong Xiu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Cycle ◽  
Tumor Invasion ◽  
Expression Profiles ◽  
The Cancer Genome Atlas ◽  
Circular Rnas ◽  
Invasion And Migration ◽  
Qrt Pcr ◽  
Cerna Network ◽  
And Migration

Abstract Background: Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related deaths worldwide. Recent evidence indicates that circular RNAs (circRNAs) play important roles in tissue development, gene regulation, and carcinogenesis. However, whether circRNAs are involved in HCC progression and encode functional proteins remains largely unknown.Methods: Circular RNA microarrays were performed using three pathologically diagnosed HCC samples and their paired adjacent normal liver tissues. Cell invasion, migration, cell cycle, and apoptosis after circRNA overexpression were measured using a transwell culture system, a wound healing assay, and flow cytometry . Full-length, mutated, and truncated sequences of circEPS15 with a FLAG tag were inserted inside a circular expression vector. Western blotting was used to confirm circEPS15 expression and the requirement of internal ribosomal entry site (IRES) elements within the circRNA. The miRNA and mRNA expression profiles were obtained by analyzing data retrieved from The Cancer Genome Atlas (TCGA) database. We then constructed a ceRNA network of mRNAs, miRNAs, and circEPS15. Using tissue samples from own patients, we also verified certain analytical results with quantitative real-time PCR (qRT-PCR).Results: The expression of circEPS15 was downregulated in HCC tissues, and the survival curves showed that low circEPS15 levels were associated with poor overall survival in HCC patients. Overexpression of circEPS15 suppressed tumor invasion and migration by inhibiting the TJP1/CDH2/VIM signaling pathway and retarded cell cycle progression, but it had no effect on cell apoptosis. ceRNA analysis and qRT-PCR showed that there might be a circRNA (circEPS15)-miRNA (miR-24-3p)-mRNA (CIDEA) network in HCC. The spanning junction open reading frame in circEPS15 driven by IRES encoded a novel protein.Conclusions: Endogenous circEPS15 plays a novel role in repressing HCC through the ceRNA network and encoding a functional protein.

scholarly journals Fibronectin Promotes Survival and Migration of Primary Neural Stem Cells Transplanted into the Traumatically Injured Mouse Brain

2002 ◽  
Vol 11 (3) ◽  
pp. 283-295 ◽  
Author(s):  
Matthew C. Tate ◽  
Deborah A. Shear ◽  
Stuart W. Hoffman ◽  
Donald G. Stein ◽  
David R. Archer ◽  
...  
Keyword(s):  
Stem Cells ◽  
Neural Stem Cells ◽  
Cellular Therapy ◽  
Cell Types ◽  
Survival Times ◽  
Germinal Zone ◽  
Cortical Contusion ◽  
Multiple Cell ◽  
And Migration

Multipotential stem cells are an attractive choice for cell therapy after traumatic brain injury (TBI), as replacement of multiple cell types may be required for functional recovery. In the present study, neural stem cells (NSCs) derived from the germinal zone of E14.5 GFP-expressing mouse brains were cultured as neurospheres in FGF2-enhanced medium. When FGF2 was removed in vitro, NSCs expressed phenotypic markers for neurons, astrocytes, and oligodendrocytes and exhibited migratory behavior in the presence of adsorbed fibronectin (FN). NSCs (105 cells) were transplanted into mouse brains 1 week after a unilateral, controlled, cortical contusion (depth = 1 mm, velocity = 6 m/s, duration = 150 ms) (n = 19). NSCs were injected either directly into the injury cavity with or without an injectable FN-based scaffold [collagen I (CnI)/ FN gel; n = 14] or into the striatum below the injury cavity (n = 5). At all time points examined (1 week to 3 months posttransplant), GFP+ cells were confined to the ipsilateral host brain tissue. At 1 week, cells injected into the injury cavity lined the injury penumbra while cells inserted directly into the striatum remained in or around the needle track. Striatal transplants had a lower number of surviving GFP+ cells relative to cavity injections at the 1 week time point (p < 0.01). At the longer survival times (3 weeks–3 months), 63–76% of transplanted cells migrated into the fimbria hippocampus regardless of injection site, perhaps due to cues from the degenerating hippocampus. Furthermore, cells injected into the cavity within a FN-containing matrix showed increased survival and migration at 3 weeks (p < 0.05 for both) relative to injections of cells alone. These results suggest that FGF2-responsive NSCs present a promising approach for cellular therapy following trauma and that the transplant location and environment may play an important role in graft survival and integration.

Antineoplastic Effects of NF-κB Inhibition by DHMEQ (Dehydroxymethylepoxyquinomicin) Alone and in Co-treatment with Radio-and Chemotherapy in Medulloblastoma Cell Lines

2018 ◽  
Vol 18 (4) ◽  
pp. 541-549 ◽  
Author(s):  
Priscila M.M. Ramos ◽  
Julia A. Pezuk ◽  
Angel M. Castro-Gamero ◽  
Harley F. Oliveira ◽  
Carlos A. Scrideli ◽  
...  
Keyword(s):  
Cell Lines ◽  
Cell Invasion ◽  
Cell Types ◽  
Chemotherapeutic Agents ◽  
Anticancer Effect ◽  
Invasion And Migration ◽  
And Migration ◽  
Tumor Types ◽  
Medulloblastoma Cell Lines ◽  
Potential Antitumor

Background: NF-κB is a transcription factor involved in the transcriptional regulation of a large number of genes related to tumorigenesis in several cancer cell types, and its inhibition has been related to anticancer effect. DHMEQ (Dehydroxymethylepoxyquinomicin) is a compound that blocks the translocation of NF-κB from the cytoplasm to the nucleus, thus inhibiting its activity as a transcriptional activator. Several studies have shown the antineoplastic effects of DHMEQ in numerous tumor types, however, there are no surveys that tested their effects in MB. Objectives: The aim of the present study was to evaluate the effects of DHMEQ as NF-κB inhibitor in pediatric MB cell lines. Method: We used the UW402, UW473 and ONS-76 medulloblastoma (MB) cell lines to verify the effect of DHMEQ on proliferation, clonogenic capacity, apoptosis, cell invasion and migration, and evaluated the effect of the combination with other drugs and the potential as a radiosensitizator. Results: A significant decrease in the cell growth, a strong inhibition of the clonogenic capacity, migration and cell invasion was observed after NF-κB inhibition in the three MB cell lines. Conversely, increased level of apoptosis rates were demonstrated. Additionally, treatments with DHMEQ combined with other chemotherapeutic agents were synergic in most points, and a strong radiosensitization by this compound was observed in the three MB cell lines. Conclusion: DHMEQ has potential antitumor effect on MB cells, and it may be considered a new therapeutic agent to improve treatment approaches in MB.

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