BIRC5: A novel therapeutic target for lung cancer stem cells and glioma stem cells

Baculoviral inhibitor of apoptosis repeat containing 5 (BIRC5) is also known as survivin. BIRC5, a member of the apoptosis inhibitor (IAP) family, negatively regulates apoptosis or programmed cell death by inhibiting caspase activation. Due to these properties, overexpression of BIRC5 enables specific survival and division associated with cancer malignancies. In addition, BIRC5 is highly expressed in stem cells, but not present at all in terminally differentiated cells. On this basis, there is speculation that BIRC5 may be involved in the regulation of cancer stem cells (CSCs), but few study results have been reported. In addition, the molecular mechanisms of BIRC5 regulation are not yet well understood. Through the present study, it was confirmed that BIRC5 is a key factor regulating CSCs and epithelial to mesenchymal transition (EMT). BIRC5 was simultaneously overexpressed in lung cancer stem cells (LCSCs) and glioma stem cells (GSCs), and when the expression was suppressed, the characteristics of CSCs disappeared. In addition, plasminogen activator inhibitor-1 (PAI-1), a secreted factor regulated by BIRC5, is involved in signaling mechanisms that regulate cancer stem cells and EMT, and PAI-1 forms an autocrine chain. Based on these results, BIRC5 is proposed as a novel therapeutic target protein for LCSCs and GSCs.

Automated summary

BIRC5, also known as survivin, is a protein that negatively regulates apoptosis by inhibiting caspase activation. Its overexpression enables cancer cells to survive and divide. BIRC5 is highly expressed in stem cells and may be involved in the regulation of cancer stem cells (CSCs). The study shows that BIRC5 is a key factor in CSCs and epithelial to mesenchymal transition (EMT) regulation, and it regulates the secretion of plasminogen activator inhibitor-1 (PAI-1), which is involved in signaling mechanisms regulating CSCs and EMT.