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Role of SWI/SNF chromatin remodeling genes in lung cancer development
Beatriz Monterde1, Ignacio Varela1
1Instituto de Biomedicina y Biotecnología de Cantabria, Universidad de Cantabria-CSIC, Santander, Spain.
Abstract:
SWI/SNF family of chromatin remodeling complexes uses the energy of ATP to change the structure of DNA, playing key roles in DNA regulation and repair. It is estimated that up to 25% of all human cancers contain alterations in SWI/SNF, although the precise molecular mechanisms for their involvement in tumor progression are largely unknown. Despite the improvements achieved in the last decades on our knowledge of lung cancer molecular biology, it remains the major cause of cancer-related deaths worldwide and it is in urgent need for new therapeutic alternatives. We and others have described recurrent alterations in different SWI/SNF genes in nearly 20% of lung cancer patients, some of them with a significant association with worse prognosis, indicating an important role of SWI/SNF in this fatal disease. These alterations might be therapeutically exploited, as it has been shown in cellular and animal models with the use of EGFR inhibitors, DNA-damaging agents and several immunotherapy approaches. Therefore, a better knowledge of the molecular mechanisms regulated by SWI/SNF alterations in lung cancer might be translated into a therapeutic improvement of this frequently lethal disease. In this review, we summarize all the evidence of SWI/SNF alterations in lung cancer, the current knowledge about the potential mechanisms involved in their tumorigenic role, as well as the results that support a potential exploitation of these alterations to improve the treatment of lung cancer patients.
Insights
Alterations in SWI/SNF chromatin remodeling complexes are common in lung cancer, impacting prognosis. Understanding these SWI/SNF changes may reveal new therapeutic strategies for this deadly disease.
Area of Science:
- Molecular Biology
- Cancer Research
- Genetics
Background:
- SWI/SNF chromatin remodeling complexes are crucial for DNA regulation and repair.
- Alterations in SWI/SNF genes are found in up to 25% of human cancers, including nearly 20% of lung cancers.
- Lung cancer remains a leading cause of cancer-related mortality, necessitating novel therapeutic approaches.
Purpose of the Study:
- To review the evidence of SWI/SNF alterations in lung cancer.
- To explore the molecular mechanisms underlying the role of SWI/SNF in lung tumorigenesis.
- To discuss the therapeutic potential of targeting SWI/SNF alterations in lung cancer treatment.
Main Methods:
- Literature review of studies on SWI/SNF alterations in lung cancer.
- Analysis of existing data on the association between SWI/SNF mutations and lung cancer prognosis.
- Synthesis of current knowledge on SWI/SNF's role in DNA repair, regulation, and cancer progression.
Main Results:
- Recurrent alterations in SWI/SNF genes are observed in a significant subset of lung cancer patients.
- These alterations are associated with worse prognosis in some cases, highlighting SWI/SNF's oncogenic role.
- Preclinical models suggest that SWI/SNF alterations can be therapeutically exploited using various treatment strategies.
Conclusions:
- SWI/SNF alterations play a significant role in lung cancer development and progression.
- Further understanding of SWI/SNF's molecular mechanisms in lung cancer is critical for therapeutic advancement.
- Targeting SWI/SNF alterations offers a promising avenue for improving lung cancer treatment outcomes.
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