Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2016 Oct 11;6:34053. doi: 10.1038/srep34053

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright © 2016, The Author(s)

This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

PMC Copyright notice

Western blot analysis of expression level of apoptotic and anti-apoptotic proteins by MDA-MB-231 cells treated with CPMSNs (A–D). ER and mitochondrial membrane proteins along with p53 were found to be overexpressed in CPMSNs treated cells when compared to untreated cells. However, the expression of mitochondrial membrane protein Bcl-2 was found to be down regulated in treated cells, indicating the induction of mitochondrial dependant apoptosis. β-actin served as internal standard. (E) The schematic representation of molecular mechanisms involved in the induction of apoptosis in MDA-MB-231 cells while CPMSN targets the integrin receptors via interaction with cRGD to facilitate internalization of CPMSNs by cells. The intracellular acidic pH triggers rapid dissociation of nanocarrier resulting in discharge of TPT and QT drugs. The released drugs induce ER stress, activate p53 and promote loss of Δψm leading to apoptosis.