Proteomic Level Changes on Treatment in MCF-7/DDP Breast Cancer Drug- Resistant Cells.

ABSTRACT:

Background

LCL161, a SMAC'S small molecule mimetic, can bind to a variety of IAPs and activate Caspases. We found that on its own, LCL161induces apoptosis of drug-resistant breast cancer cells by binding to a variety of IAPs and activating Caspases. However, when LCL161 is used in combination with Caspase Inhibitors (CI), its capacity to induce apoptosis of breast cancer cells is enhanced.

Objective

To carry out proteomic and bioinformatics analysis of LCL161 in combination with CI. We aim to identify the key proteins and mechanisms of breast cancer drug-resistant apoptosis, thereby aiding in the breast cancer drug resistance treatment and identification of drug targeting markers.

Methods

Cell culture experiments were carried out to explore the effect of LCL161 combin

SUBMITTER: Jin G 

PROVIDER: S-EPMC7403652 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature