Non-small cell lung cancer

Non-small cell lung cancer

HDAC11 a novel treatment for lung cancer

Non-small cell lung cancer (NSCLC) has seen an exponential rise in survival rates in the last decade due to new targeted therapy choices they now have. Nonetheless, lung cancer stands at the leading position in cancer-related mortality, with a death toll of around 154,000 per year in the United States. The concerns pertaining to the new targeted treatments is that either the patients fail to respond to them or develop drug resistance. Researchers belonging to Moffitt Cancer Center are working on identifying alternative strategies to treat this disease. Their recent study explains a novel therapeutic approach for NSCLC by targeting histone deacetylase HDAC11.

Histone deacetylases (HDACs) are proteins responsible for regulating gene expression and activity of genes by modifying proteins and DNA compaction. HDACs are typically deregulated in some types of cancer, and certain drugs that inhibit the proteins have been approved for inclusion in the treatment of the same. The role of HDAC11, the most recent HDAC to be identified, in cancer remains unknown. Moffitt researchers performed preclinical studies designed to recognize the role of HDAC11 in NSCLC. They observed that patients with NSCLS showed high levels of HDAC11, and these levels are associated with poor survival.

The researchers then focused on cancer stem cells (CSCs), which have been found to play a role in tumor development and progression and are significantly resistant to chemotherapy and targeted drug therapies. Srikumar Chellappan, Ph.D., Chair, Department of Tumor Biology, Moffitt, and his team discovered that HDAC11 is present in high levels in CSCs and is linked to the expression of Sox2, the gene vital for self-renewal of CSCs.

When the team targeted HDAC11 in NSCLC with specific inhibitors, the researchers saw the ability of CSCs to go through self renewal and observed that the expression of Sox2 was considerably reduced. The research findings indicate a novel therapeutic strategy to stop CSCs’ self-renewal and obstruct the progression of NSCLC.

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