Abstract
Glioblastoma (GBM) is the most common adult neural malignancy and the deadliest. The standard of care is optimal, safe, cytoreductive surgery followed by combined radiation therapy and alkylating chemotherapy with temozolomide. Recurrence is common and therapeutic options in the recurrent setting are limited. The dismal prognosis of GBM has led to novel treatments being a serious roadblock in the field, with most new treatments failing to show efficacy. Targeted therapies have shown some success in many cancers, but GBM remains one of the most difficult to treat, especially in recurrence. New chemotherapeutic directions need to be explored, possibly expanding the targeted chemotherapy spectrum in previously unforeseen ways. In this perspective paper, we will explain why AVIL, an actin-binding protein recently found to be overexpressed in GBM and a driving force for GBM, could prove versatile in the fight against cancer. By looking at AVIL and its potential to regulate FOXM1 and LIN28B, we will be able to highlight a way to improve outcomes for GBM patients who normally have very little hope.
Highlights
Glioblastoma multiforme (GBM) is the grade IV astrocytoma
AVIL is heavily overexpressed in almost 100% of GBMs, while the gene products are virtually non-existent in normal brain tissue [34]
Our lab found that when silencing AVIL in A172 GBM cells (IDH wild-type/P53 wildtype), there was a dramatic reduction in cell movement in a wound-healing assay [34]
Summary
Glioblastoma multiforme (GBM) is the grade IV astrocytoma. As one of the most common and malignant adult neural malignancy, it affects approximately 14,000 people in the United States per year [1,2,3,4]. Advillin may be a relatively cancer-specific cytoskeletal protein that sits at the crossroads of the two therapeutic philosophies: broad range cytotoxic agents that target machinery required for division and a cancer-specific targeted therapy that limits toxicities in normal cells. In this manuscript we will give a brief overview of AVIL and its functions, a summary of the known family members and their proto-oncogenic roles, roles of downstream targets of AVIL and their specific functions in GBM, and look at AVIL functions involved in GBM dissemination and immune system evasion. We will speculate the therapeutic potential of targeting AVIL in GBM
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