Peptide name : TT 1

Source/Organism : Venom base

Linear/Cyclic : Linear

Chirality : L

Peptide length: 11

C-terminal modification: Linear

N-terminal modification : Not found

Non-natural peptide information: None

Assay type : MTT assay

Assay time : 48h

Activity : IC50 : 3.87 ± 0.34 μg/ml

Cell line : TT

Cancer type : Thyroid cancer

Other activity : Not found

Amino acid composition bar chart :

Molecular mass : 1213.5527 Dalton

Aliphatic index : 1.681

Instability index : -21.781

Hydrophobicity (GRAVY) : 0.8364

Isoelectric point : 10.302

Charge (pH 7) : 2.7571

Aromaticity : 0

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

Hydrophobic/hydrophilic ratio : 1.2

hydrophobic moment : 0.6659

Missing amino acid : C,R,W,H,Q,P,M,E,F,S,D,Y,N,G

Most occurring amino acid : K

Most occurring amino acid frequency : 3

Least occurring amino acid : I

Least occurring amino acid frequency : 1

Secondary structure fraction (Helix, Turn, Sheet): (0.5, 0, 0.6)

SMILES Notation: CC[C@H](C)[C@H](NC(=O)[C@@H](N)CCCCN)C(=O)N[C@@H](CCCCN)C(=O)N[C@@H](C)C(=O)N[C@H](C(=O)N[C@@H](CC(C)C)C(=O)N[C@@H](CCCCN)C(=O)N[C@H](C(=O)N[C@@H](CC(C)C)C(=O)N[C@H](C(=O)N[C@H](C(=O)O)[C@@H](C)O)[C@@H](C)O)C(C)C)C(C)C

1 : Wan L, et al. TT-1, an analog of melittin, triggers apoptosis in human thyroid cancer TT cells via regulating caspase, Bcl-2 and Bax. Oncol Lett. 2018; 15:1271-1278. doi: 10.3892/ol.2017.7366

Paper title : TT-1, an analog of melittin, triggers apoptosis in human thyroid cancer TT cells via regulating caspase, Bcl-2 and Bax.

Doi : https://doi.org/10.3892/ol.2017.7366

Abstract : Melittin is a 26 amino acid residue antimicrobial peptide with known antitumor activity. In the present study, a novel peptide TT-1, derived from melittin and contained only 11 amino acids, was designed, and its antitumor effect was investigated. The present study is aimed to elucidate the effects and relative mechanisms of TT-1 on a human thyroid cancer cell line (TT) in vitro and in vivo. Cell viability assays, Annexin V/propidium iodide assays, western blotting and quantitative reverse transcription polymerase chain reaction were performed. Furthermore, a tumor-xenograft model was established to investigate the apoptotic mechanisms of TT-1 on TT cells. The results obtained indicated that TT-1 was able to suppress the proliferation of TT cells and exhibited low cytotoxicity to normal thyroid cells in vitro. The apoptotic rates of TT cells were also increased following TT-1 treatment. Additionally, TT-1 stimulated caspase-3, caspase-9 and Bax, and inhibited B-cell lymphoma 2 mRNA and protein expression. Finally, it was also demonstrated that TT-1 is able to markedly suppress tumor growth in a TT-bearing nude mouse model. In summary, TT-1 may inhibit the proliferation of TT cells by inducing apoptosis in vitro and in vivo, indicating that TT-1 may be a potential candidate for the treatment of thyroid cancer.