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Exploiting ING2 Epigenetic Modulation as a Therapeutic Opportunity for Non-Small Cell Lung Cancer
Alice Blondel1, Amine Benberghout2, Rémy Pedeux3
1INSERM U1242, Chemistry Oncogenesis Stress and Signaling, CLCC Eugène Marquis, 35033 Rennes, France. alice.blondel@univ-rennes1.fr.
Abstract:
Non-small cell lung cancer (NSCLC) has been the leading cause of cancer-related death worldwide, over the last few decades. Survival remains extremely poor in the metastatic setting and, consequently, innovative therapeutic strategies are urgently needed. Inhibitor of Growth Gene 2 (ING2) is a core component of the mSin3A/Histone deacetylases complex (HDAC), which controls the chromatin acetylation status and modulates gene transcription. This gene has been characterized as a tumor suppressor gene and its status in cancer has been scarcely explored. In this review, we focused on ING2 and other mSin3A/HDAC member statuses in NSCLC. Taking advantage of existing public databases and known pharmacological properties of HDAC inhibitors, finally, we proposed a therapeutic model based on an ING2 biomarker-guided strategy.
Insights
Non-small cell lung cancer (NSCLC) survival is poor. This review explores the tumor suppressor Inhibitor of Growth Gene 2 (ING2) in NSCLC, proposing an ING2 biomarker strategy for novel therapies.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Genetics
Background:
- Non-small cell lung cancer (NSCLC) remains a leading cause of cancer mortality globally.
- Poor survival rates in metastatic NSCLC necessitate innovative therapeutic approaches.
- The Inhibitor of Growth Gene 2 (ING2) functions within the mSin3A/Histone deacetylases (HDAC) complex, regulating gene transcription.
Purpose of the Study:
- To review the role and status of ING2 and other mSin3A/HDAC members in NSCLC.
- To explore the therapeutic potential of targeting the mSin3A/HDAC complex in NSCLC.
- To propose a novel therapeutic strategy for NSCLC guided by ING2 as a biomarker.
Main Methods:
- Literature review of existing public databases focusing on ING2 and mSin3A/HDAC members in NSCLC.
- Analysis of known pharmacological properties of HDAC inhibitors.
- Development of a conceptual therapeutic model.
Main Results:
- The status of ING2 in cancer, particularly NSCLC, has been underexplored.
- The mSin3A/HDAC complex plays a significant role in NSCLC pathogenesis.
- HDAC inhibitors represent a potential therapeutic avenue.
Conclusions:
- ING2 is a potential tumor suppressor gene in NSCLC with underexplored clinical relevance.
- A therapeutic strategy leveraging ING2 as a biomarker could guide the use of HDAC inhibitors for NSCLC treatment.
- Further research into ING2's function and modulation is warranted for clinical application.
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