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
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.