An All-dAmino Acid Peptide Model of α1(IV)531−543 from Type IV Collagen Binds the α3β1Integrin and Mediates Tumor Cell Adhesion, Spreading, and Motility†

Biochemistry ◽  
1997 ◽  
Vol 36 (49) ◽  
pp. 15404-15410 ◽  
Author(s):  
Changfen Li ◽  
James B. McCarthy ◽  
Leo T. Furcht ◽  
Gregg B. Fields
Keyword(s):  
Cell Adhesion ◽  
Tumor Cell ◽  
Type Iv Collagen ◽  
Tumor Cell Adhesion ◽  
Type Iv

scholarly journals Characterization of a synthetic peptide from type IV collagen that promotes melanoma cell adhesion, spreading, and motility.

1990 ◽  
Vol 111 (1) ◽  
pp. 261-270 ◽  
Author(s):  
M K Chelberg ◽  
J B McCarthy ◽  
A P Skubitz ◽  
L T Furcht ◽  
E C Tsilibary
Keyword(s):  
Cell Adhesion ◽  
Tumor Cell ◽  
Melanoma Cell ◽  
Cell Invasion ◽  
Synthetic Peptide ◽  
Type Iv Collagen ◽  
Cell Types ◽  
Tumor Cell Invasion ◽  
Type Iv

The adhesion and motility of tumor cells on basement membranes is a central consideration in tumor cell invasion and metastasis. Basement membrane type IV collagen directly promotes the adhesion and migration of various tumor cell types in vitro. Our previous studies demonstrated that tumor cells adhered and spread on surfaces coated with intact type IV collagen or either of the two major enzymatically purified domains of this protein. Only one of these major domains, the pepsin-generated major triple helical fragment, also supported tumor cell motility in vitro, implicating the involvement of the major triple helical region in type IV collagen-mediated tumor cell invasion in vivo. The present studies extend our previous observations using a synthetic peptide approach. A peptide, designated IV-H1, was derived from a continuous collagenous region of the major triple helical domain of the human alpha 1(IV) chain. This peptide, which has the sequence GVKGDKGNPGWPGAP, directly supported the adhesion, spreading, and motility of the highly metastatic K1735 M4 murine melanoma cell line, as well as the adhesion and spreading of other cell types, in a concentration-dependent manner in vitro. Furthermore, excess soluble peptide IV-H1, or polyclonal antibodies directed against peptide IV-H1, inhibited type IV collagen-mediated melanoma cell adhesion, spreading, and motility, but had no effect on these cellular responses to type I collagen. The full complement of cell adhesion, spreading, and motility promoting activities was dependent upon the preservation of the three prolyl residues in the peptide IV-H1 sequence. These studies indicate that peptide IV-H1 represents a cell-specific adhesion, spreading, and motility promoting domain that is active within the type IV collagen molecule.

scholarly journals CD44/chondroitin sulfate proteoglycan and alpha 2 beta 1 integrin mediate human melanoma cell migration on type IV collagen and invasion of basement membranes.

1996 ◽  
Vol 7 (3) ◽  
pp. 383-396 ◽  
Author(s):  
J R Knutson ◽  
J Iida ◽  
G B Fields ◽  
J B McCarthy
Keyword(s):  
Cell Migration ◽  
Cell Adhesion ◽  
Cell Surface ◽  
Tumor Cell ◽  
Melanoma Cell ◽  
Cell Invasion ◽  
Type Iv Collagen ◽  
Human Melanoma ◽  
Type Iv ◽  
Beta 1 Integrin

Tumor cell invasion of basement membranes (BM) represents one of the critical steps in the metastatic process. Tumor cell recognition of individual BM matrix components may involve individual cell adhesion receptors, such as integrins or cell surface proteoglycans, or may involve a coordinate action of both types of receptors. In this study, we have focused on the identification of a cell surface CD44/chondroitin sulfate proteoglycan (CSPG) and alpha 2 beta 1 integrin on human melanoma cells that are both directly involved in the in vitro invasion of reconstituted BM via a type IV collagen-dependent mechanism. Interfering with cell surface expression of human melanoma CSPG with either p-nitro-phenyl-beta-D-xylopyranoside treatment or anti-CD44 monoclonal antibody (mAb) preincubation (mAb) preincubation inhibits melanoma cell invasion through reconstituted BM. These treatments also strongly inhibit melanoma cell migration on type IV collagen, however, they are ineffective at inhibiting cell adhesion to type IV collagen. Purified melanoma cell surface CD44/CSPG, or purified chondroitin sulfate, bind to type IV collagen affinity columns, consistent with a role for CD44/CSPG-type IV collagen interactions in mediating tumor cell invasion. In contrast, melanoma cell migration on laminin (LM) does not involve CD44/CSPG, nor does CD44/CSPG bind to LM, suggesting that CD44/CSPG-type IV collagen interactions are specific in nature. Additionally, anti-alpha 2 and anti-beta 1 integrin mAbs are capable of blocking melanoma cell invasion of reconstituted BM. Both of these anti-integrin mAbs inhibit melanoma cell adhesion and migration on type IV collagen, whereas only anti-beta 1 mAb inhibits cell adhesion to LM. Collectively, these results indicate that melanoma cell adhesion to type IV collagen is an important consideration in invasion of reconstituted BM in vitro, and suggest that CD44/CSPG and alpha 2 beta 1 integrin may collaborate to promote human melanoma cell adhesion, migration, and invasion in vivo.

Platelet and Shear Rate Promote Tumor Cell Adhesion to Human Endothelial Extracellular Matrix - Absence of a Role for Platelet Cyclooxygenase

1989 ◽  
Vol 61 (03) ◽  
pp. 485-489 ◽  
Author(s):  
Eva Bastida ◽  
Lourdes Almirall ◽  
Antonio Ordinas
Keyword(s):  
Cell Adhesion ◽  
Shear Rate ◽  
Tumor Cell ◽  
Umbilical Vein ◽  
Blood Platelets ◽  
Flow Conditions ◽  
Tumor Cell Adhesion ◽  
Rate Dependent ◽  
Static Conditions

SummaryBlood platelets are thought to be involved in certain aspects of malignant dissemination. To study the role of platelets in tumor cell adherence to vascular endothelium we performed studies under static and flow conditions, measuring tumor cell adhesion in the absence or presence of platelets. We used highly metastatic human adenocarcinoma cells of the lung, cultured human umbilical vein endothelial cells (ECs) and extracellular matrices (ECM) prepared from confluent EC monolayers. Our results indicated that under static conditions platelets do not significantly increase tumor cell adhesion to either intact ECs or to exposed ECM. Conversely, the studies performed under flow conditions using the flat chamber perfusion system indicated that the presence of 2 × 105 pl/μl in the perfusate significantly increased the number of tumor cells adhered to ECM, and that this effect was shear rate dependent. The maximal values of tumor cell adhesion were obtained, in presence of platelets, at a shear rate of 1,300 sec-1. Furthermore, our results with ASA-treated platelets suggest that the role of platelets in enhancing tumor cell adhesion to ECM is independent of the activation of the platelet cyclooxygenase pathway.

scholarly journals Tailored chitosan/hyaluronan coatings for tumor cell adhesion: Effects of topography, charge density and surface composition

2019 ◽  
Vol 486 ◽  
pp. 508-518 ◽  
Author(s):  
J.B.M. Rocha Neto ◽  
T.B. Taketa ◽  
R.A. Bataglioli ◽  
S.B. Pimentel ◽  
D.M. Santos ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Tumor Cell ◽  
Charge Density ◽  
Surface Composition ◽  
Tumor Cell Adhesion

scholarly journals Tubulointerstitial nephritis antigen interacts with laminin and type IV collagen and promotes cell adhesion.

1994 ◽  
Vol 269 (3) ◽  
pp. 1654-1659 ◽  
Author(s):  
T.A. Kalfa ◽  
J.D. Thull ◽  
R.J. Butkowski ◽  
A.S. Charonis
Keyword(s):  
Cell Adhesion ◽  
Type Iv Collagen ◽  
Tubulointerstitial Nephritis ◽  
Type Iv

scholarly journals Raf-1 activation in gastrointestinal carcinoid cells decreases tumor cell adhesion

2007 ◽  
Vol 193 (3) ◽  
pp. 331-335 ◽  
Author(s):  
David Yü Greenblatt ◽  
Muthusamy Kunnimalaiyaan ◽  
Herbert Chen
Keyword(s):  
Cell Adhesion ◽  
Tumor Cell ◽  
Tumor Cell Adhesion ◽  
Gastrointestinal Carcinoid
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