Peptide name : LJP-2

Source/Organism : Laminaria japonica

Linear/Cyclic : Linear

Chirality : L

Peptide length: 6

C-terminal modification: Linear

N-terminal modification : Free

Non-natural peptide information:

Assay type : MTT assay

Assay time : 48-h

Activity : IC50 = 0.62 ± 0.05 mM

Cell line : H-22

Cancer type : Liver Cancer

Other activity : Anticancer

Amino acid composition bar chart :

Molecular mass : 807.8527 Dalton

Aliphatic index : 0.65

Instability index : 35.2333

Hydrophobicity (GRAVY) : -1.3

Isoelectric point : 5.9824

Charge (pH 7) : -1.0627

Aromaticity : 16.66

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

Hydrophobic/hydrophilic ratio : 0.5

hydrophobic moment : 1.2473

Missing amino acid : A,C,D,F,G,I,K,M,N,P,Q,R,T,V,Y

Most occurring amino acid : H

Most occurring amino acid frequency : 2

Least occurring amino acid : L

Least occurring amino acid frequency : 1

Secondary structure fraction (Helix, Turn, Sheet): (33., 16., 33.)

SMILES Notation: CC(C)C[C@H](N)C(=O)N[C@@H](Cc1c[nH]c2ccccc12)C(=O)N[C@@H](CCC(=O)O)C(=O)N[C@@H](Cc1c[nH]cn1)C(=O)N[C@@H](CO)C(=O)N[C@@H](Cc1c[nH]cn1)C(=O)O

1 : Wu Y, et al. Laminaria japonica Peptides Suppress Liver Cancer by Inducing Apoptosis: Possible Signaling Pathways and Mechanism. Mar Drugs. 2022; 20:(unknown pages). doi: 10.3390/md20110704

Paper title : Laminaria japonica Peptides Suppress Liver Cancer by Inducing Apoptosis: Possible Signaling Pathways and Mechanism.

Doi : https://doi.org/10.3390/md20110704

Abstract : The anticancer properties of Laminaria japonica peptides (LJPs) have never been studied. Here, we extracted LJPs from fresh seaweed and explored their anti-liver cancer activity (in vivo and in vitro). LJPs were isolated/purified by HPLC-ESI-MS. HepG2 cell apoptosis and cell cycle were evaluated. MTT assays were used to examine the cytotoxicity of LJPs. Caspase activation of caspases 3 and 9, cleaved caspases 3 and 9, and cleaved PARP was examined by Western blotting. The PI3K/AKT pathway and the phosphorylation states of MAPKs (p38 and JNK) were examined. We found that the LJP-1 peptide had the most antiproliferative activity in H22 cells in vitro. LJP-1 blocked H22 cells in the G0/G1 phase, accompanied by inhibition of cyclin expression. LJP-1 induced apoptosis through caspase activation and regulation of the ASK1/MAPK pathway. Concurrent in vivo studies demonstrated that LJP-1 significantly inhibited tumor growth and induced tumor cell apoptosis/necrosis. In conclusion, LJPs, particularly LJP-1, exert strong inhibitory effects on liver cancer growth in vivo and in vitro. LJP-1 induces HCC cell apoptosis through the caspase-dependent pathway and G0/G1 arrest. LJP-1 induces caspase-dependent apoptosis, in part by inhibiting PI3K, MAPK signaling pathways, and cell cycle proteins. LJP-1 has the potential to be a novel candidate for human liver cancer therapeutics.