Peptide name : B11

Source/Organism : Litopenaeus vannamei hemocyanin-derived peptide

Linear/Cyclic : Linear

Chirality : L

Peptide length: 15

C-terminal modification: Linear

N-terminal modification : Free

Non-natural peptide information:

Assay type : MTS assay

Assay time : 24-h

Activity : Decreased cell viability by 20% at 50 μg/mL

Cell line : HeLa

Cancer type : Cervical Cancer

Other activity : Antimicrobial

Amino acid composition bar chart :

Molecular mass : 1725.9882 Dalton

Aliphatic index : 1.3

Instability index : -35.9

Hydrophobicity (GRAVY) : 0.0467

Isoelectric point : 8.596

Charge (pH 7) : 0.8475

Aromaticity : 6.666

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

Hydrophobic/hydrophilic ratio : 1.1429

hydrophobic moment : 0.3424

Missing amino acid : C,E,F,L,M,N,P,Q,S,T,W

Most occurring amino acid : I

Most occurring amino acid frequency : 3

Least occurring amino acid : H

Least occurring amino acid frequency : 1

Secondary structure fraction (Helix, Turn, Sheet): (20, 20, 40)

SMILES Notation: CC[C@H](C)[C@H](NC(=O)[C@H](C)NC(=O)[C@H](CC(=O)O)NC(=O)[C@H](CCCNC(=N)N)NC(=O)[C@@H](NC(=O)[C@@H](N)CCCNC(=N)N)[C@@H](C)CC)C(=O)N[C@@H](C)C(=O)N[C@@H](Cc1c[nH]cn1)C(=O)NCC(=O)N[C@@H](Cc1ccc(O)cc1)C(=O)N[C@H](C(=O)N[C@H](C(=O)N[C@@H](CC(=O)O)C(=O)N[C@@H](CCCCN)C(=O)N[C@H](C(=O)O)C(C)C)C(C)C)[C@@H](C)CC

1 : Liu S, et al. A Litopenaeus vannamei Hemocyanin-Derived Antimicrobial Peptide (Peptide B11) Attenuates Cancer Cells' Proliferation. Molecules. 2018; 23:(unknown pages). doi: 10.3390/molecules23123202

Paper title : A Litopenaeus vannamei Hemocyanin-Derived Antimicrobial Peptide (Peptide B11) Attenuates Cancer Cells' Proliferation.

Doi : https://doi.org/10.3390/molecules23123202

Abstract : Antimicrobial peptides play important roles in the immune response to pathogens and tumor cells; for this reason, they are being exploited for therapeutic use. In this study, we describe a Litopenaeus vannamei hemocyanin-derived peptide, denoted B11, which shares similar features with other anticancer peptides and attenuates the proliferation of cancer cells. Cell viability assay revealed that B11 significantly inhibited the proliferation of human cervical (HeLa), human hepatocellular carcinoma (HepG2), and human esophageal cancer (EC109) cancer cell lines, but not normal liver cell lines (T-antigen-immortalized human liver epithelial (THLE) cells or THLE-3), by inducing morphological changes, nuclear condensation, and margination, features which are indicative of apoptosis. Besides, peptide B11-induced apoptosis was confirmed by isothiocyanate-labeled Annexin V/propidium iodide (Annexin V-FITC/PI) double staining of HeLa cells. Moreover, cell uptake studies, confocal microscopy, and Western blot analysis revealed that rhodamine-labeled B11 permeated HeLa cells and localized to the mitochondria, causing mitochondria dysfunction through lost mitochondrial membrane potential, which consequently triggered the induction of apoptosis. Increased expression levels of caspase-9, caspase-3, and Bax (Bcl-2-associated X) proteins, coupled with a decrease in Bcl-2 (B-cell lymphoma 2) protein, confirmed that peptide B11 induced apoptosis via the mitochondrial pathway. Thus, the hemocyanin-derived peptide, B11, inhibits the proliferation of cancer cells by causing mitochondrial dysfunction and inducing apoptotic cell death, for which reason it could be explored as an anticancer peptide.