Coadministration of kla peptide with HPRP-A1 to enhance anticancer activity

The apoptosis-inducing peptide kla (KLAKLAK)2 possesses the ability to disrupt mitochondrial membranes and induce cancer cell apoptosis, but this peptide has a poor eukaryotic cell-penetrating potential. Thus, it requires the assistance of other peptides for effective translocation at micromolar concentrations. In this study, breast and lung cancer cells were treated by kla peptide co-administrated with membrane-active anticancer peptide HPRP-A1. HPRP-A1 assisted kla to enter cancer cells and localized on mitochondrial membranes to result in cytochrome C releasing and mitochondrial depolarization which ultimately induced apoptosis.The apoptosis rate was up to 65%and 45% on MCF-7 and A549 cell lines, respectively, induced by HPRP-A1 coadministration with kla group. The breast cancer model was constructed in mice, and the anticancer peptides were injected to observe the changes in cancer volume, andimmunohistochemical analysis was performed on the tissues and organs after the drug was administered. Both the weight and volume of tumor tissue were remarkable lower in HPRP-A1 with kla group compared with thosepeptidealonggroups. The results showed that the combined drug group effectively inhibited the growth of cancer and did not cause toxic damage to normal tissues, as well as exhibited significantly improvement on peptide anticancer activity in vitro and in vivo.

Medienart:

E-Artikel

Erscheinungsjahr:

2019

Erschienen:

2019

Enthalten in:

Zur Gesamtaufnahme - volume:14

Enthalten in:

PloS one - 14(2019), 11 vom: 08., Seite e0223738

Sprache:

Englisch

Beteiligte Personen:

Hao, Wenjing [VerfasserIn]
Hu, Cuihua [VerfasserIn]
Huang, Yibing [VerfasserIn]
Chen, Yuxin [VerfasserIn]

Links:

Volltext

Themen:

Antineoplastic Agents
Intercellular Signaling Peptides and Proteins
Journal Article
KLA peptide
Peptides
Research Support, Non-U.S. Gov't

Anmerkungen:

Date Completed 16.03.2020

Date Revised 19.10.2023

published: Electronic-eCollection

Citation Status MEDLINE

doi:

10.1371/journal.pone.0223738

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM303068930