Related Experiment Video
Updated: Jun 6, 2025
A Flow Cytometry-Based Cell Surface Protein Binding Assay for Assessing Selectivity and Specificity of an Anticancer Aptamer
Published on: September 13, 2022
Anti-EGFR aptamer exhibits direct anti-cancer effects in NSCLC cells harboring EGFR L858R mutations
Brian J Thomas1,2, Sania Z Awan3, Trupti Joshi2,3,4
1Department of Molecular Microbiology and Immunology, University of Missouri School of Medicine, Columbia, MO, USA.
Abstract:
Non-small cell lung cancer (NSCLC) adenocarcinoma (LUAD) is a leading cause of death worldwide. Activating mutations in the tyrosine kinase domain of the oncogene epidermal growth factor receptor (EGFR) are responsible for ~10-50% of all LUAD cases. Although tyrosine kinase inhibitors (TKIs) have been effective in prolonging patient survival and quality of life, acquired resistance and disease progression are inevitable, presenting a clear unmet need for alternative or adjuvant therapeutics. Here we show that an anti-EGFR aptamer (EGFRapt) decreases viability and tumor growth of LUAD cell lines harboring the L858R ± T790M mutation in EGFR. Additionally, we elucidate the mechanism by which EGFRapt exerts these effects by monitoring cellular processes associated with kinase-dependent and kinase-independent mechanisms. Overall, these data establish that EGFRapt has direct anti-cancer activity in mutant EGFR positive LUAD via targetable mechanisms that are independent of existing approaches, and they provide a foundation for further development of nucleic acid-based therapies that target EGFR.
Insights
An anti-epidermal growth factor receptor (EGFR) aptamer demonstrates anti-cancer activity against non-small cell lung cancer (NSCLC) with EGFR mutations. This novel nucleic acid therapy offers a potential new treatment avenue independent of current approaches.
Area of Science:
- Oncology
- Molecular Biology
- Biotechnology
Background:
- Non-small cell lung cancer (NSCLC) adenocarcinoma (LUAD) is a major global health concern.
- Activating mutations in epidermal growth factor receptor (EGFR) drive approximately 10-50% of LUAD cases.
- Existing tyrosine kinase inhibitors (TKIs) face challenges with acquired resistance and disease progression.
Purpose of the Study:
- To investigate the anti-cancer effects of an anti-EGFR aptamer (EGFRapt) in LUAD.
- To elucidate the mechanisms underlying EGFRapt's anti-tumor activity.
- To establish EGFRapt as a potential therapeutic agent for mutant EGFR-positive LUAD.
Main Methods:
- Utilized LUAD cell lines with L858R ± T790M mutations in EGFR.
- Administered an anti-EGFR aptamer (EGFRapt).
- Monitored cellular processes to determine kinase-dependent and independent mechanisms.
Main Results:
- EGFRapt significantly decreased viability and tumor growth in LUAD cell lines.
- The study elucidated the specific cellular mechanisms of EGFRapt action.
- EGFRapt demonstrated direct anti-cancer activity through targetable, kinase-independent pathways.
Conclusions:
- EGFRapt exhibits direct anti-cancer activity in mutant EGFR-positive LUAD.
- The therapeutic mechanisms are independent of current TKI approaches.
- These findings support the development of nucleic acid-based therapies targeting EGFR.
More Related Videos
09:38Establishment and Characterization of Three Afatinib-resistant Lung Adenocarcinoma PC-9 Cell Lines Developed with Increasing Doses of Afatinib
Published on: June 26, 2019
09:38Establishing Dual Resistance to EGFR-TKI and MET-TKI in Lung Adenocarcinoma Cells In Vitro with a 2-step Dose-escalation Procedure
Published on: August 11, 2017
Related Concept Videos
02:57Targeted Cancer Therapies
There are several types of targeted therapies against...
02:38Mitogens and the Cell Cycle