# Nano-Enabled Fluorescence Switching: A Novel Strategy for PDGFRβ Detection and TKI Therapy Monitoring

## TL;DR

A new nanoprobe detects PDGFRβ levels in cancer cells, helping monitor treatment response and resistance to tyrosine kinase inhibitors.

## Contribution

A novel fluorescence-switching nanoprobe enables real-time PDGFRβ detection and TKI therapy monitoring.

## Key findings

- The nanoprobe Cy3-Gint4.T@BPNSs uses fluorescence quenching and recovery to detect PDGFRβ expression.
- Fluorescence intensity correlates with PDGFRβ levels, aiding tumor diagnosis and treatment guidance.
- Dynamic PDGFRβ changes during TKI therapy correlate with fluorescence variations, linking to resistance mechanisms.

## Abstract

Determining platelet-derived growth factor receptor β (PDGFRβ) expression in biological specimens is pivotal for cancer diagnosis, drug development, and therapeutic monitoring. After tyrosine kinase inhibitor (TKI) therapy, altered PDGFRβ expression may correlate with treatment resistance mechanisms. Real-time, accurate detection of PDGFRβ levels pre- and post-TKI treatment holds substantial clinical value, as it enables therapeutic efficacy evaluation, resistance prediction, and timely regimen adjustment. However, the current repertoire of real-time technologies for precise PDGFRβ monitoring remains highly limited. Herein, we present a novel nanoprobe (Cy3-Gint4.T@BPNSs) for PDGFRβ detection based on a fluorescence quenching–recovery mechanism. Cy3-Gint4.T is a cyanine 3 (Cy3)-labeled aptamer with high specificity and strong selective binding affinity for PDGFRβ. Black phosphorus nanosheets (BPNSs) adsorb Cy3-Gint4.T via van der Waals forces to quench its fluorescence. Upon targeting PDGFRβ on cancer cells, the aptamer–receptor interaction outcompetes Cy3-Gint4.T’s binding to BPNSs, triggering its release and subsequent fluorescence restoration. Notably, the restored fluorescence intensity shows a direct correlation with cellular PDGFRβ expression, highlighting the nanoprobe’s potential for guiding tumor diagnosis and treatment. Critically, our data confirm that dynamic PDGFRβ expression changes induced by specific TKI therapies exhibit a proportional relationship with corresponding fluorescence intensity variations. This finding further supports an association between PDGFRβ expression dynamics and TKI resistance mechanisms, facilitating precise PDGFRβ monitoring and individualized therapeutic guidance.