Peptide name : LvHemB1

Source/Organism : hemocyanin of Litopenaeus vannamei

Linear/Cyclic : Linear

Chirality : L

Peptide length: 15

C-terminal modification: Linear

N-terminal modification : Amidation

Non-natural peptide information:

Assay type : MTS assay

Assay time : 24-h

Activity : 65.1% apoptotic cells at 50 μg/mL

Cell line : HeLa

Cancer type : Cervical cancer

Other activity : Antimicrobial

Amino acid composition bar chart :

Molecular mass : 1865.1381 Dalton

Aliphatic index : 1.233

Instability index : 22.3867

Hydrophobicity (GRAVY) : -0.1

Isoelectric point : 8.5042

Charge (pH 7) : 0.8454

Aromaticity : 20

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

Hydrophobic/hydrophilic ratio : 0.875

hydrophobic moment : -0.178

Missing amino acid : A,C,E,M,P,Q,S,T,W

Most occurring amino acid : N

Most occurring amino acid frequency : 2

Least occurring amino acid : D

Least occurring amino acid frequency : 1

Secondary structure fraction (Helix, Turn, Sheet): (20, 26., 53.)

SMILES Notation: CC[C@H](C)[C@H](NC(=O)[C@H](CCCCN)NC(=O)[C@H](Cc1c[nH]cn1)NC(=O)[C@H](CC(C)C)NC(=O)[C@H](CC(C)C)NC(=O)[C@H](Cc1ccccc1)NC(=O)[C@H](CC(N)=O)NC(=O)[C@@H](NC(=O)[C@@H](N)CC(=O)O)C(C)C)C(=O)N[C@@H](Cc1ccc(O)cc1)C(=O)NCC(=O)N[C@@H](CC(N)=O)C(=O)N[C@H](C(=O)N[C@@H](CCCNC(=N)N)C(=O)N[C@@H](Cc1ccc(O)cc1)C(=O)O)[C@@H](C)CC

1 : Liu S, et al. LvHemB1, a novel cationic antimicrobial peptide derived from the hemocyanin of Litopenaeus vannamei, induces cancer cell death by targeting mitochondrial voltage-dependent anion channel 1. Cell Biol Toxicol. 2022; 38:87-110. doi: 10.1007/s10565-021-09588-y

Paper title : LvHemB1, a novel cationic antimicrobial peptide derived from the hemocyanin of Litopenaeus vannamei, induces cancer cell death by targeting mitochondrial voltage-dependent anion channel 1.

Doi : https://doi.org/10.1007/s10565-021-09588-y

Abstract : Current cancer treatment regimens such as chemotherapy and traditional chemical drugs have adverse side effects including the appearance of drug-resistant tumor cells. For these reasons, it is imperative to find novel therapeutic agents that overcome these factors. To this end, we explored a cationic antimicrobial peptide derived from Litopenaeus vannamei hemocyanin (designated LvHemB1) that induces cancer cell death, but sparing normal cells. LvHemB1 inhibits the proliferation of human cervical (HeLa), esophageal (EC109), hepatocellular (HepG2), and bladder (EJ) cancer cell lines, but had no significant effect on normal liver cell lines (T-antigen-immortalized human liver epithelial (THLE-3) cells). In addition to its antiproliferative effects, LvHemB1 induced apoptosis, by permeating cells and targeting mitochondrial voltage-dependent anion channel 1 (VDAC1). Colocalization studies revealed the localization of LvHemB1 in mitochondria, while molecular docking and pull-down analyses confirmed LvHemB1-VDAC1 interaction. Moreover, LvHemB1 causes loss in mitochondrial membrane potential and increases levels of reactive oxygen species (ROS) and apoptotic proteins (caspase-9, caspase-3, and Bax (Bcl-2-associated X)), which results in mitochondrial-mediated apoptosis. Thus, peptide LvHemB1 has the potential of being used as an anticancer agent due to its antiproliferation effect and targeting to VDAC1 to cause mitochondrial dysfunction in cancer cells, as well as its ability to induce apoptosis by increasing ROS levels, and the expression of proapoptotic proteins.