CAPER Peptide Targeting c-Jun for TNBC Treatment
Find Innovative SolutionsGenerate Solutions
Solution Overview
Problem
Current treatments for triple negative breast cancer (TNBC) are limited, with chemotherapy and radiation being the only available options, and there is a need for novel compositions that can effectively treat TNBC and other types of cancers such as brain and lung cancer.
Innovation Solution
Administration of a therapeutically effective amount of a polypeptide comprising amino acid residues 356-400 of co-activator of activator protein-1 and estrogen receptor (CAPER) isoform HCC1.3 or HCC1.4, which can be derivatized or fused with a cell penetrating peptide, to target and treat cancer cells.
Engineering Contradictions & Design Principles
Engineering Contradiction Analysis
1Reliability
If chemotherapy and radiation are used to treat TNBC, then cancer cells can be killed, but treatment options are limited and side effects are severe
Solution Approach 1:
The invention segments the CAPER protein into a specific peptide fragment (amino acid residues 356-400) that retains the essential binding activity to c-Jun and estrogen receptor alpha. This segmentation creates a smaller, more versatile therapeutic agent that can be administered in various forms and combinations, expanding treatment options beyond traditional chemotherapy and radiation.
Solution Approach 2:
The CAPER peptide acts as an intermediary molecule that disrupts the interaction between c-Jun and estrogen receptor alpha, which are key mediators in TNBC cell survival and proliferation. By targeting this specific protein-protein interaction, the peptide provides a novel mechanism of action that complements existing treatments and offers new therapeutic avenues for TNBC.
2Reliability
If CAPER peptide is administered to treat cancer, then apoptosis is induced in cancer cells, but selective targeting of cancer cells vs. normal cells must be achieved
Solution Approach 1:
The CAPER peptide exhibits local quality by selectively binding to the specific complex of c-Jun and estrogen receptor alpha that is overexpressed or aberrantly active in TNBC cells. This selective binding at the molecular level ensures that apoptosis is induced primarily in cancer cells with the appropriate molecular targets, while normal cells with appropriate receptor levels remain unaffected.
Solution Approach 2:
The invention exploits parameter changes in the molecular environment of cancer cells versus normal cells. TNBC cells typically exhibit altered expression levels or conformational states of c-Jun and estrogen receptor alpha, creating a distinct molecular signature. The CAPER peptide is designed to recognize and bind to these altered parameters, enabling selective cancer cell targeting through subtle changes in protein-protein interaction dynamics.
Applied Scientific Principles
This section explains which scientific principles are used to turn an abstract innovation direction into a practical engineering solution.
Function Achieved in This Case
The CAPER peptides demonstrate significant binding affinity to c-Jun and estrogen receptor alpha, altering their binding profiles and inducing apoptosis in cancer cells, particularly in TNBC cell lines, while showing minimal effect on non-tumorigenic cells.
Implementation Method 1
The CAPER peptides demonstrate significant binding affinity to c-Jun and estrogen receptor alpha, altering their binding profiles and inducing apoptosis in cancer cells
Data Source
AI summary
The present invention provides methods of treating cancer with certain co-activator of activator protein-1 and estrogen receptor (CAPER)-based polypeptides. In certain embodiments, the methods of the invention target only cancerous cells without adversely affecting non-cancerous cells.