Related Experiment Video
Updated: Oct 16, 2025

Implementation of In Vitro Drug Resistance Assays: Maximizing the Potential for Uncovering Clinically Relevant Resistance Mechanisms
Published on: December 9, 2015
The implications of ABCC3 in cancer drug resistance: can we use it as a therapeutic target?
Adriana Ramírez-Cosmes1, Edilburga Reyes-Jiménez1, Cecilia Zertuche-Martínez1
1Laboratorio Fibrosis y Cáncer, Facultad de Medicina y Cirugía, Universidad Autónoma "Benito Juárez" de Oaxaca Oaxaca, Oax, México.
Abstract:
Drug resistance is one of the main causes of chemotherapy failure. Although several factors are involved in cancer drug resistant, the exporter pumps overexpression that mediates the drugs flow to outside the cells and reduces both the drugs intracellular concentration and effectiveness, has been one of the most important challenges. Overexpression of ABCC3, a member of the ABCC subfamily, has been strongly associated to the resistance to multiple drugs. ABCC3 has been found highly expressed in different types of cancers and is associated with poor prognosis and resistance to treatments. In this review, we summarize the molecular mechanisms involved in cancer drug resistance and discuss the current knowledge about the structure, function and role of ABCC3 in drug resistance, as well as, the expression status of ABCC3 in different types of cancer. We also provide evidences that place ABCC3 as a potential therapeutic target for improving the cancer treatment by focusing on the need of developing more effective cancer therapies to target ABCC3 in translational researches.
Insights
Drug resistance in cancer is a major challenge, often caused by efflux pumps like ABCC3. Targeting ABCC3 offers a promising strategy to overcome multidrug resistance and improve chemotherapy effectiveness.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Drug resistance significantly contributes to chemotherapy failure.
- Overexpression of efflux pumps, such as ABCC3, reduces intracellular drug concentration and efficacy.
- ABCC3 is implicated in multidrug resistance and is highly expressed in various cancers, correlating with poor prognosis.
Purpose of the Study:
- To review the molecular mechanisms of cancer drug resistance.
- To discuss the structure, function, and role of ABCC3 in mediating drug resistance.
- To examine the expression patterns of ABCC3 across different cancer types.
Main Methods:
- Literature review of molecular mechanisms in cancer drug resistance.
- Analysis of existing research on ABCC3 structure and function.
- Compilation of data on ABCC3 expression in various cancers.
Main Results:
- ABCC3 overexpression is a key factor in multidrug resistance.
- High ABCC3 expression is linked to poor treatment outcomes in multiple cancer types.
- ABCC3's role in drug efflux is a significant challenge in cancer therapy.
Conclusions:
- ABCC3 is a critical mediator of cancer multidrug resistance.
- Targeting ABCC3 presents a potential therapeutic strategy for enhancing cancer treatment.
- Further translational research is needed to develop effective ABCC3-targeted therapies.
More Related Videos
08:59Looking for Driver Pathways of Acquired Resistance to Targeted Therapy: Drug Resistant Subclone Generation and Sensitivity Restoring by Gene Knock-down
Published on: December 11, 2017
13:19Quantifying Antibody-Dependent Cellular Cytotoxicity in a Tumor Spheroid Model: Application for Drug Discovery
Published on: April 26, 2024
Related Concept Videos
Targeted Cancer Therapies
There are several types of targeted therapies against...
Treatment Resistant Cancers
Combination Therapies and Personalized Medicine
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...
ABC Transporters: Exporter
ABC Transporters: Importer
In bacteria, based on the number of transmembrane helices and the chemical nature of their substrates, the ABC importers can be divided into three types:
Inhibition of Cdk Activity