Peptide name : LK-L1C/K6W/L8C

Source/Organism : Not found

Linear/Cyclic : Linear

Chirality : L

Peptide length: 16

C-terminal modification: Linear

N-terminal modification : Not found

Non-natural peptide information: None

Assay type : MTS assay

Assay time : 1h

Activity : Not found

Cell line : HeLa

Cancer type : Not specified

Other activity : Not found

Amino acid composition bar chart :

Molecular mass : 1858.4473 Dalton

Aliphatic index : 1.525

Instability index : 10.6625

Hydrophobicity (GRAVY) : 0.55

Isoelectric point : 9.9043

Charge (pH 7) : 4.7353

Aromaticity : 0.062

Molar extinction coefficient (cysteine, cystine): (5500, 5625)

Hydrophobic/hydrophilic ratio : 2.2

hydrophobic moment : 1.2789

Missing amino acid : R,H,Q,T,P,M,I,E,F,S,D,Y,N,V

Most occurring amino acid : L

Most occurring amino acid frequency : 6

Least occurring amino acid : W

Least occurring amino acid frequency : 1

Secondary structure fraction (Helix, Turn, Sheet): (0.7, 0.0, 0.4)

SMILES Notation: CC(C)C[C@H](NC(=O)[C@H](CCCCN)NC(=O)[C@H](CC(C)C)NC(=O)[C@H](CC(C)C)NC(=O)[C@H](CCCCN)NC(=O)[C@H](CCCCN)NC(=O)[C@H](CS)NC(=O)[C@H](CC(C)C)NC(=O)[C@H](Cc1c[nH]c2ccccc12)NC(=O)[C@H](CC(C)C)NC(=O)[C@H](CC(C)C)NC(=O)[C@H](CCCCN)NC(=O)[C@H](CCCCN)NC(=O)[C@@H](N)CS)C(=O)N[C@@H](C)C(=O)NCC(=O)O

1 : Kim S, et al. An Amphiphilic Peptide Induces Apoptosis Through the miR29b-p53 Pathway in Cancer Cells. Mol Ther Nucleic Acids. 2016; 5:e330. doi: 10.1038/mtna.2016.45

Paper title : An Amphiphilic Peptide Induces Apoptosis Through the miR29b-p53 Pathway in Cancer Cells.

Doi : https://doi.org/10.1038/mtna.2016.45

Abstract : Peptides have been in the limelight, as therapeutic agents for cancer treatment through various applications due to their high target selectivity and exceptional ability to penetrate the cell membrane. Recent studies have revealed that synthesized peptides bind to hairpin structures of RNA that affect their activities such as changing the efficacy of microRNA maturation. MicroRNA-mediated p53 activation by the microRNA-29 (miR29) family is one of the most important regulatory pathways in cancer therapeutics. By targeting the suppressors of p53, a tumor suppressor protein, miR29 induces apoptosis of cancer cells through p53 stabilization. Here, we identify a novel synthesized amphiphilic peptide, LK-L1C/K6W/L8C, which enhances expression of miR29b and promotes p53 activity. In the presence of LK-L1C/K6W/L8C, pre-miR29b preferentially forms a complex with the Dicer protein through interaction of LK-L1C/K6W/L8C with the terminal loop region of pre-miR29b, leading to an increase in Dicer processing. Furthermore, LK-L1C/K6W/L8C stimulates apoptosis by improving p53 stability in miR29-inducible HeLa and MCF7 cells. Collectively, our study shows that a peptide can directly influence the miR29b-mediated p53 activation pathway in cancer cells. Therefore, our findings provide the basis for a new, potentially promising peptide-based drug for cancer therapy.