Peptide name : P7

Source/Organism : Not found

Linear/Cyclic : Linear

Chirality : L

Peptide length: 11

C-terminal modification: Linear

N-terminal modification : Free

Non-natural peptide information: None

Assay type : WST-1 assay

Assay time : 48h

Activity : IC50 : 1 µM

Cell line : B16-F10

Cancer type : Skin cancer

Other activity : Not found

Amino acid composition bar chart :

Molecular mass : 1013.1455 Dalton

Aliphatic index : 1.154

Instability index : 61.1636

Hydrophobicity (GRAVY) : 0.4909

Isoelectric point : 5.955

Charge (pH 7) : -0.0415

Aromaticity : 0

Molar extinction coefficient (cysteine, cystine): (0, 0)

Hydrophobic/hydrophilic ratio : 2.66666666

hydrophobic moment : -0.704

Missing amino acid : C,R,W,H,M,I,E,K,F,D,Y,N,V

Most occurring amino acid : L

Most occurring amino acid frequency : 3

Least occurring amino acid : P

Least occurring amino acid frequency : 1

Secondary structure fraction (Helix, Turn, Sheet): (0.3, 0.4, 0.3)

SMILES Notation: CC(C)C[C@H](NC(=O)[C@@H]1CCCN1)C(=O)N[C@@H](CC(C)C)C(=O)N[C@@H](CCC(N)=O)C(=O)N[C@@H](C)C(=O)N[C@H](C(=O)N[C@@H](CC(C)C)C(=O)NCC(=O)NCC(=O)NCC(=O)N[C@@H](CO)C(=O)O)[C@@H](C)O

1 : Yu Y, et al. The FGF2-binding peptide P7 inhibits melanoma growth in vitro and in vivo. J Cancer Res Clin Oncol. 2012; 138:1321-8. doi: 10.1007/s00432-012-1201-7

Paper title : The FGF2-binding peptide P7 inhibits melanoma growth in vitro and in vivo.

Doi : https://doi.org/10.1007/s00432-012-1201-7

Abstract : PURPOSE: Melanoma is a malignant tumor and causes majority of deaths related to skin cancer. Fibroblast growth factor 2 (FGF2) greatly contributes to melanoma growth and progress. In this paper, we attempt to evaluate the therapeutic potential of FGF2-binding peptide (named P7) using as a potent FGF2 antagonist via exploration of its antitumor effect on melanoma in vitro and in vivo. METHODS: Cell viability was measured by WST-1. Cell cycle progression was determined by propidium iodide staining and flow cytometry. Western blotting was carried out to detect the activation of Erk1/2, P38, Akt, and MEK, and the expression of apoptosis-associated proteins. The influence of P7 on FGF2 internalization was assessed by separation of nuclear and cytoplasmic protein fractions followed by Western blotting. Female C57BL/6 mice bearing xenograft melanoma were established and used to evaluate the antitumor effect of P7 in vivo. RESULTS: In this study, we first proved that P7 peptides significantly inhibited proliferation of FGF2-induced melanoma cell line B16-F10. Further investigations revealed that the mechanisms of P7 peptides inhibiting cell proliferation of melanoma cells stimulated with FGF2 in vitro involved cell cycle arrest at the G0/G1 phase, blockade of the activation of Erk1/2, P38, and Akt cascades, and inhibition of FGF2 internalization. Finally, treatment of P7 peptides in a murine melanoma model resulted in significant inhibition of tumor growth and angiogenesis in vivo, which was associated with blockade of mitogen-activated protein kinase signal activation, and suppression of the expressions of anti-apoptotic Bcl-2 protein and angiogenic factor in the melanoma tumors. CONCLUSIONS: The FGF2-binding peptide with potent antiproliferation and anti-angiogenic activity may have therapeutic potential in melanoma.