dbACP: A Comprehensive Database of Anti-Cancer Peptides

dbacp06322

General Description

Peptide name : TP3

Source/Organism : Not found

Linear/Cyclic : Linear

Chirality : L

Sequence Information

Sequence : FIHHIIGGLFSVGKHIHSLIHGH

Peptide length: 23

C-terminal modification: Linear

N-terminal modification : Not found

Non-natural peptide information: None

Activity Information

Assay type : MTT assay

Assay time : 24h

Activity : 10.02 ± 1.10 μM

Cell line : MG63

Cancer type : Bone cancer

Other activity : Anti-microbial activity

Physicochemical Properties

Amino acid composition bar chart :

Molecular mass : 2556.965 Dalton

Aliphatic index : 1.313

Instability index : 57.3435

Hydrophobicity (GRAVY) : 0.5913

Isoelectric point : 8.79

Charge (pH 7) : 1.2821

Aromaticity : 0.087

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

Hydrophobic/hydrophilic ratio : 1.55555555

hydrophobic moment : 0.6271

Missing amino acid : C,R,W,Q,T,P,M,E,D,Y,N,A

Most occurring amino acid : H

Most occurring amino acid frequency : 6

Least occurring amino acid : V

Least occurring amino acid frequency : 1

Structural Information

3D structure :

Secondary structure fraction (Helix, Turn, Sheet): (0.1, 0.2, 0.4)

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

Secondary Structure :

Method Prediction
GOR EEEEEETCEEEETHHEEEEEETC
Chou-Fasman (CF) EEEEEEEEEEEEECEEEEEECCC
Neural Network (NN) EEEEEECCEEECCCCEEEEECCC
Joint/Consensus EEEEEECCEEEECCCEEEEECCC

Molecular Descriptors and ADMET Properties

Molecular Descriptors: Click here to download

ADMET Properties: Click here to download

Cross Referencing databases

Pubmed Id : 32492449

Uniprot : Not available

PDB : Not available

CancerPPD : Not available

ApIAPDB : Not available

CancerPPD2 ID : Not available

Reference

1 : Yuan CH, et al. The antimicrobial peptide tilapia piscidin 3 induces mitochondria-modulated intrinsic apoptosis of osteosarcoma cells. Biochem Pharmacol. 2020; 178:114064. doi: 10.1016/j.bcp.2020.114064

Literature

Paper title : The antimicrobial peptide tilapia piscidin 3 induces mitochondria-modulated intrinsic apoptosis of osteosarcoma cells.

Doi : https://doi.org/10.1016/j.bcp.2020.114064

Abstract : Osteosarcoma (OS) is the most common solid tumor of the bone that most often affects adolescents. The introduction of chemotherapy for the treatment of OS has largely improved the survival rates of patients with localized tumors. However, the 5-year survival rate of OS patients with relapsed or metastatic disease is only 10 to 20%. In this study, the antimicrobial peptide tilapia piscidin 3 (TP3), isolated from Nile tilapia (Oreochromis niloticus), was treated to OS MG63 cells. Our findings showed that TP3 concentration as low as 1 μM induced significant inhibition of cell viability and increased DNA fragmentation, as determined by the MTT and TUNEL assays, respectively. The protein expression levels of cleaved caspases 3/9 were increased. An in situ live-cell time-lapse video and cell tomographic microscopy images showed cellular blebbing, shrinkage, nuclear fragmentation, and chromatin condensation, with the formation of beaded apoptopodia. Moreover, there were significant increase in the production of TP3-induced mitochondrial and cellular reactive oxygen species (ROS), as well as down-regulated mitochondrial oxygen consumption and extracellular acidification rates. Additionally, TP3 enhanced mitochondrial fission, whereas fusion was attenuated. Furthermore, after administration of the mitochondria targeted antioxidant mitoTempo, TP3-induced ROS oxidant levels and alterations in cleaved caspases 3/9 expression were rescued. TP3 promoted mitochondria-modulated intrinsic apoptosis through the induction of ROS production, activation of caspases 3/9, and the down-regulation of mitochondrial oxygen consumption and extracellular acidification rates, suggesting that TP3 has potential as an innovative alternative for OS treatment.