Peptide name : EGFR-related peptide

Source/Organism : EGFR-related peptide

Linear/Cyclic : Linear

Chirality : L

Peptide length: 4

C-terminal modification: Linear

N-terminal modification : Free

Non-natural peptide information: None

Assay type : MTT/MTS assay

Assay time : 48h

Activity : 30% Cell viability at 5 µg/ml

Cell line : PC-3

Cancer type : Prostate cancer

Other activity : Not found

Amino acid composition bar chart :

Molecular mass : 556.6159 Dalton

Aliphatic index : 0

Instability index : 198.85

Hydrophobicity (GRAVY) : -3.525

Isoelectric point : 9.6985

Charge (pH 7) : 0.8368

Aromaticity : 0

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

Hydrophobic/hydrophilic ratio : 0.33333333

hydrophobic moment : 0.1775

Missing amino acid : W,T,I,M,K,F,D,N,G,C,H,Q,S,Y,L,A,V

Most occurring amino acid : R

Most occurring amino acid frequency : 2

Least occurring amino acid : E

Least occurring amino acid frequency : 1

Secondary structure fraction (Helix, Turn, Sheet): (0.2, 0.2, 0)

SMILES Notation: N=C(N)NCCC[C@H](NC(=O)[C@@H](N)CCC(=O)O)C(=O)N[C@@H](CCCNC(=N)N)C(=O)N1CCC[C@H]1C(=O)O

1 : Marciniak DJ, et al. Epidermal growth factor receptor-related peptide inhibits growth of PC-3 prostate cancer cells. Mol Cancer Ther. 2004; 3:1615-21.

Paper title : Epidermal growth factor receptor-related peptide inhibits growth of PC-3 prostate cancer cells.

Doi : https://doi.org/Not available

Abstract : Interference with the activation of growth factor receptors, specifically epidermal growth factor receptor (EGFR), represents a promising strategy for the development of novel and selective anticancer therapies. We reported that EGFR-related peptide (ERRP), a recently isolated negative regulator of EGFR, could be a potential therapeutic agent for colorectal cancer. To determine whether ERRP could potentially be a therapeutic agent for prostate carcinoma, we examined the effect of recombinant ERRP on the growth of the prostate cancer cell line PC-3 in vitro. Events of the EGFR signal transduction pathways were also examined. ERRP caused a marked inhibition of cell growth in a dose- and time-dependent manner and also induced apoptosis. The latter was evidenced by increased number of apoptotic cells, activation of caspase-3, and cleavage of poly(ADP-ribose)polymerase. The transforming growth factor-alpha-induced stimulation of cell growth and activation of EGFR was also inhibited by ERRP. These changes were accompanied by a concomitant attenuation of activation of Akt and mitogen-activated protein kinases as well as basal and transforming growth factor-alpha-induced activation of nuclear factor-kappaB. Inhibition of EGFR activation by ERRP could be partly attributed to increased sequestration of EGFR ligands. In summary, our data show that ERRP inhibits the growth of prostate cancer cells by attenuating EGFR signaling processes. ERRP could potentially be an effective therapeutic agent for prostate cancer.