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Utilizing Functional Genomics Screening to Identify Potentially Novel Drug Targets in Cancer Cell Spheroid Cultures

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Targeting SWI/SNF Complexes in Cancer: Pharmacological Approaches and Implications.

Megan R Dreier¹, Jasmine Walia¹, Ivana L de la Serna¹

¹Department of Cell and Cancer Biology, University of Toledo College of Medicine and Life Sciences, 3000 Arlington Ave, Toledo 43614, OH, USA.

|February 23, 2024

Summary

This summary is machine-generated.

Targeting SWI/SNF complexes, crucial for DNA repair and transcription, shows promise in cancer therapy. Novel PROTACs degrade specific subunits, advancing drug development from preclinical to clinical trials.

Keywords:

DNA damage PROTACs SWI/SNF chromatin-remodeling complexes allosteric ATPAse inhibitors bromodomain inhibitors cancer epigenetics transcription

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Area of Science:

Biochemistry
Molecular Biology
Cancer Therapeutics

Background:

SWI/SNF enzymes are ATP-dependent chromatin remodelers with vital roles in DNA replication, repair, and transcription.
Dysregulation of SWI/SNF complexes, including sub-complexes like cBAF, ncBAF, and PBAF, is implicated in various cancers.
SWI/SNF complexes are attractive targets for cancer drug development due to their critical functions.

Purpose of the Study:

To review current therapeutic strategies targeting SWI/SNF complexes in cancer.
To highlight the development and potential of pharmacological agents, including PROTACs, for cancer treatment.
To assess the progression of SWI/SNF-targeting agents from preclinical research to clinical trials.

Main Methods:

Review of existing literature on SWI/SNF complex function and therapeutic targeting.
Analysis of pharmacological agents, including catalytic subunit inhibitors and bromodomain binders.
Examination of Proteolysis-targeting chimeras (PROTACs) designed for SWI/SNF subunit degradation.

Main Results:

Inhibitors targeting catalytic subunits (SMARCA4/2) and bromodomains are key strategies.
PROTACs enhance SWI/SNF inhibition by promoting targeted subunit degradation.
Preclinical studies demonstrate significant therapeutic potential across diverse cancer types.

Conclusions:

Targeting SWI/SNF complexes represents a promising avenue for cancer therapy.
PROTAC technology offers an advanced approach for modulating SWI/SNF function.
Several SWI/SNF-targeting agents are advancing into clinical trials, indicating therapeutic progress.