Peptide name : Transactivator of transcript-DV1-Bcl-2, AT-DV1-BH3

Source/Organism : Transactivator of transcript-DV1-Bcl-2 TAT-DV1-BH5

Linear/Cyclic : Not found

Chirality : Not found

Peptide length: 23

C-terminal modification: Not found

N-terminal modification : Not found

Non-natural peptide information: None

Assay type : Cell viability assay, Transwell invasion assay

Assay time : 72h

Activity : Not specified

Cell line : HEK-293

Cancer type : Kidney cancer

Other activity : Not found

Amino acid composition bar chart :

Molecular mass : 2716.0824 Dalton

Aliphatic index : 0.213

Instability index : 127.239

Hydrophobicity (GRAVY) : -2.308

Isoelectric point : 12

Charge (pH 7) : 8.8453

Aromaticity : 0.043

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

Hydrophobic/hydrophilic ratio : 0.64285714

hydrophobic moment : -0.462

Missing amino acid : C,T,M,I,E,F,Y,N,V

Most occurring amino acid : R

Most occurring amino acid frequency : 7

Least occurring amino acid : Q

Least occurring amino acid frequency : 1

Secondary structure fraction (Helix, Turn, Sheet): (0.2, 0.3, 0.0)

SMILES Notation: CC(C)C[C@H](NC(=O)CNC(=O)CNC(=O)CNC(=O)CNC(=O)[C@H](CCCNC(=N)N)NC(=O)[C@H](CCCCN)NC(=O)[C@H](CCCCN)NC(=O)[C@H](CCCNC(=N)N)NC(=O)[C@H](CCCNC(=N)N)NC(=O)[C@H](CCC(N)=O)NC(=O)[C@H](CCCNC(=N)N)NC(=O)[C@H](CCCNC(=N)N)NC(=O)[C@@H](N)CCCNC(=N)N)C(=O)NCC(=O)N[C@@H](C)C(=O)N[C@@H](CO)C(=O)N[C@@H](Cc1c[nH]c2ccccc12)C(=O)N[C@@H](Cc1c[nH]cn1)C(=O)N[C@@H](CCCNC(=N)N)C(=O)N1CCC[C@H]1C(=O)N[C@@H](CC(=O)O)C(=O)N[C@@H](CCCCN)C(=O)O

1 : Liang AL, et al. Bifunctional fused polypeptide inhibits the growth and metastasis of breast cancer. Drug Des Devel Ther. 2015; 9:5671-86. doi: 10.2147/DDDT.S90082

Paper title : Bifunctional fused polypeptide inhibits the growth and metastasis of breast cancer.

Doi : https://doi.org/10.2147/DDDT.S90082

Abstract : Breast cancer is the most common cancer and the leading cause of cancer-related death among women worldwide, with urgent need to develop new therapeutics. Targeted therapy is a promising strategy for breast cancer therapy. Stromal-derived factor-1/CXC chemokine receptor 4 (CXCR4) has been implicated in the metastasis of breast cancer, which renders it to be therapeutic target. This study aimed to evaluate the anticancer effect of fused TAT- DV1-BH3 polypeptide, an antagonist of CXCR4, and investigate the underlying mechanism for the cancer cell-killing effect in the treatment of breast cancer in vitro and in vivo. This results in a potent inhibitory effect of fused TAT-DV1-BH3 polypeptide on tumor growth and metastasis in nude mice bearing established MDA-MB-231 tumors. Fused TAT-DV1-BH3 polypeptide inhibited the proliferation of MDA-MB-231 and MCF-7 cells but did not affect that of HEK-293 cells. The fused TAT-DV1-BH3 polypeptide colocalized with mitochondria and exhibited a proapoptotic effect through the regulation of caspase-9 and -3. Furthermore, the fused TAT-DV1-BH3 polypeptide suppressed the migration and invasion of the highly metastatic breast cancer cell line MDA-MB-231 in a concentration-dependent manner. Notably, the DV1-mediated inhibition of the stromal-derived factor-1/CXCR4 pathway contributed to the antimetastasis effect, evident from the reduction in the level of phosphoinositide 3 kinase and matrix metalloproteinase 9 in MDA-MB-231 cells. Collectively, these results indicate that the apoptosis-inducing effect and migration- and invasion-suppressing effect explain the tumor regression and metastasis inhibition in vivo, with the involvement of caspase- and CXCR4-mediated signaling pathway. The data suggest that the fused TAT-DV1-BH3 polypeptide is a promising agent for the treatment of breast cancer, and more studies are warranted to fully elucidate the therapeutic targets and molecular mechanism.