Highlights HDACs are dysregulated in various malignancies and in some inflammatory lung diseases. HDAC inhibitors are emerging as a successful epigenetic therapy by exploiting pathophysiology of tumor microenvironment. HDAC inhibitors can activate multiple antitumor pathway which results in the destruction of transformed cells. Nanocarrier-based HDACi delivery is a huge step forward in improving the targeted delivery of HDAC inhibitors.

Members of the signal transducer and activator of transcription (STAT) protein family are intracellular transcription factors that facilitate several facets of cellular immunity, proliferation, apoptosis, and differentiation. They are principally stimulated by membrane receptor-associated Janus kinases. Dysregulation of this pathway is often detected in primary tumors and hints at augmented angiogenesis, which enriches tumors persistence and immunosuppression. STAT proteins play indispensable roles in cytokine signaling and T helper (Th) cell differentiation. Among STAT proteins, STAT1 plays a vital role in interferon signaling, which initiates the expression of genes encoding proteins with antitumor and apoptotic roles. STAT1 signaling is essential for Th1 cell differentiation. Several studies have also shown the role of STAT1 as a tumor suppressor in breast cancer, which is the most common intrusive malignancy and the second most common cause of cancer death in women. Herein, we review the intricate STAT1-mediated molecular mechanisms associated with Th cell differentiation and anti-tumor function in breast cancer.

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Highlights Some common epigenetic regulations exist between coronary artery disease (CAD) and non-small cell lung cancer (NSCLC). VEGFA and AIMP1 both are up-regulated/ down-regulated in a similar pattern in both CAD and NSCLC. Several DNA damage-repair factors (e.g., BRCA1, ERCC1, XPF, RAD51 etc.) and R-loops are involved in CAD and NSCLC.

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