Molecular mediators of interactions with extracellular matrix components in metastasis and angiogenesis

Bernstein, Lori R.; Liotta, Lance A.

doi:10.1097/00001622-199401000-00015

Cited by 144 publications

(95 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…MeWo cells were compared before and after transfection with the KCREB mutant gene to assess the role of CREB in melanoma cell penetration through the basement membrane, an important component in the process of tumor invasion and metastasis (Bernstein and Liotta, 1994;Lester and McCarthy, 1992). MeWo parental and neo-transfected cells exhibited high potential to penetrate through Matrigel-coated ®lters (Table 2).…”

Section: Resultsmentioning

confidence: 99%

“…The process of metastasis includes detachment of tumor cells from the primary tumor mass, degradation of and migration through the surrounding connective tissue into the vascular system, transport and extravasation (Aslakson and Miller, 1992;Bernstein and Liotta, 1994). An important factor in regulating dissemination is the ability of the tumor cells to adhere to and migrate through the extracellular matrix Lester and McCarthy 1992).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Dominant-negative CREB inhibits tumor growth and metastasis of human melanoma cells

et al. 1997

View full text Add to dashboard Cite

The ATF/CREB family of eukaryotic transcription factors contain the bZIP structural motif and mediate their transcriptional activities via heterodimerization with ATF and AP-1 family members. Quenching of CREBassociated proteins by a dominant-negative CREB (KCREB) that is mutated within its DNA-binding domain decreases radiation resistance of human melanoma cells. The purpose of this study was to determine the role of CREB in tumor growth and metastasis of human melanoma using KCREB. Highly metastatic MeWo human melanoma cells were transfected with the KCREB expression vector and subsequently analysed for changes in their tumorigenic and metastatic potential. Expression of KCREB in MeWo human cells decreased their tumorigenic and metastatic potential in nude mice compared with parental and control transfected cells. The KCREB-transfected cells displayed downregulation of 72 kDa collagenase type IV (MMP-2) mRNA expression and activity and decreased invasiveness through Matrigel-coated ®lters. Moreover, transcriptional activities mediated by the CAT gene driven by the MMP-2 promoter were decreased by 14 ± 45-fold in KCREB-transfected cells. In addition, the cell-surface adhesion molecule MCAM/MUC18 that is involved in metastasis of human melanoma was downregulated in the KCREB-transfected cells. These data indicate that, through their transcriptional activities, CREB and its associated proteins play an important role in the acquisition of the metastatic phenotype of human melanoma cells.

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Dominant-negative CREB inhibits tumor growth and metastasis of human melanoma cells

et al. 1997

View full text Add to dashboard Cite

show abstract

“…5E). Numerous observations suggest that cell-cell or cell-matrix adhesion through adhesion molecules, such as integrins and cadherins, regulates cell survival, tumor invasion, and metastasis (24,25). Interestingly, the ability of p53 to regulate cell survival in response to DNA damage is also regulated by cellcell interaction via adhesion molecules (26).…”

Section: Lack Of Ninj1 Up-regulates P53 Expression Potentially Throughmentioning

confidence: 99%

Ninjurin1, a target of p53, regulates p53 expression and p53-dependent cell survival, senescence, and radiation-induced mortality

Cho

Rossi

Jung

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

The tumor suppressor protein p53 plays a crucial role in coordinating cellular processes, such as cell cycle arrest, apoptosis, and senescence. The nerve injury-induced protein 1 (Ninjurin1, Ninj1) is a homophilic adhesion molecule and involved in nerve regeneration. Interestingly, Ninj1 is found to be overexpressed in human cancer, but its role in tumorigenesis is not clear. Here, we found that Ninj1 is transcriptionally regulated by p53 and can be induced by DNA damage in a p53-dependent manner. We also found that knockout or knockdown of Ninj1 increases p53 expression potentially through enhanced p53 mRNA translation. In addition, we found that Ninj1 deficiency suppresses cell proliferation but enhances apoptosis and premature senescence in a p53-dependent manner. Consistent with this, we found that mice heterozygous in ninj1 are hypersensitive to ionizing radiation-induced lethality, along with increased expression of p53 in thymus. Taken together, we provided evidence that Ninj1 is a p53 target and modulates p53 mRNA translation and p53-dependent premature senescence, cell proliferation, apoptosis, and radiationinduced mortality in vitro and in vivo. Thus, we postulate that as a membrane adhesion molecule, Ninj1 is an ideal target to regulate p53 activity via the p53-Ninj1 loop. cellular senescence | radiosensitivity

show abstract

“…cell migration ͉ cytoskeleton ͉ mecanotransduction ͉ microfabrication ͉ pattern formation T he spatial organization of cells, and their migration, are essential for a wide variety of biological processes, including tissue formation, morphogenetic processes (1), responses to wounds, and inflammation (2) or tumor metastasis (3). Cells are subjected to chemical and physical signals from their neighbors (4), from the surrounding fluid (5), and from the extracellular matrix (ECM) (6), and they integrate these various cues to react in an appropriate way.…”

mentioning

confidence: 99%

Rigidity-driven growth and migration of epithelial cells on microstructured anisotropic substrates

Saez

Ghibaudo

Buguin

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

353

306

View full text Add to dashboard Cite

The physical properties of the cellular environment are involved in regulating the formation and maintenance of tissues. In particular, substrate rigidity appears to be a key factor dictating cell response on culture surfaces. Here we study the behavior of epithelial cells cultured on microfabricated substrates engineered to exhibit an anisotropic stiffness. The substrate consists of a dense array of micropillars of oval cross-section, so that one direction is made stiffer than the other. We demonstrate how such an anisotropic rigidity can induce directional epithelial growth and guide cell migration along the direction of greatest rigidity. Regions of high tractional stress and large cellular deformations within the sheets of cells are concentrated at the edges, in particular at the two poles of the islands along their long axis, in correlation with the orientation of actin stress fibers and focal adhesions. By inducing scattering activity of epithelial cells, we show that isolated cells also migrate along the direction of greatest stiffness. Taken together, these findings show that the mechanical interactions of cells with their microenvironment can be tuned to engineer particular tissue properties.cell migration ͉ cytoskeleton ͉ mecanotransduction ͉ microfabrication ͉ pattern formation

show abstract

Molecular mediators of interactions with extracellular matrix components in metastasis and angiogenesis

Cited by 144 publications

References 0 publications

Dominant-negative CREB inhibits tumor growth and metastasis of human melanoma cells

Dominant-negative CREB inhibits tumor growth and metastasis of human melanoma cells

Ninjurin1, a target of p53, regulates p53 expression and p53-dependent cell survival, senescence, and radiation-induced mortality

Rigidity-driven growth and migration of epithelial cells on microstructured anisotropic substrates

Contact Info

Product

Resources

About