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Introduction:

Forkhead box protein P2 (FOXP2) is a protein that, in humans, is encoded by the FOXP2 gene, also known as CAGH44, SPCH1 or TNRC10, and is required for proper development of speech and language.[3] FOXP2 is a transcription factor, meaning that it encodes for a regulatory protein. Regulatory proteins help control the synthesis of others protein in cells. The FOXP2 gene is shared with many vertebrates, where it generally plays a role in communication (for instance, the development of bird song).

FOXP2 and Implications in Cancer
For generations, FOXP2 has been widely accepted and recognized as a "language gene", however, new evidence may allow for the addition of "oncogene" to its designations. A “proto-oncogene” is a gene that, under normal circumstances, helps cells grow. However, if a proto-oncogene becomes mutated, it can become an “oncogene”. Oncogenes cause uncontrolled cell growth which can lead to cancer. A group of researchers at Beth Israel Deaconess Medical Center found an unexpected and surprising link between the dysregulation of the FOXP2 gene and clinically advanced breast cancers.

Several FOXP family transcription factors play a role in the initiation and progression of cancer but not until recently was FOXP2, specifically, investigated. Much of the research concerning FOXP2 investigates its role in neuronal tissue, however FOXP2 is also expressed in numerous other cell types, including the lung, heart, and central nervous system. Researchers have found FOXP2 primarily acts as a repressor, or inhibitor of protein synthesis, and plays a role in both, oncogenesis, and cancer progression. The gene has been found to be implicated in various cancer cell types including breast cancer, liver cancer, and gastric cancers, all in which FOXP2 is down regulated. In other words, the gene is less active than normal in various cancers, hinting at a possible protective mechanism of the gene against certain kinds of cancer. On the other hand, the gene has been found to be over-expressed in multiple myelomas, several lymphomas, and neuroblastomas. These findings suggest that abnormal FOXP2 levels may be the result of either mutated proto-oncogenes or deficient tumor suppressor genes, depending on the cell and cancer type. Gaining the most attention by researchers right now is the role that FOXP2 may play in the malignancy, or cancer causing, and metastasis, or spreading, of breast cancer specifically.

Researchers have recently looked into the mechanism by which FOXP2 can become cancer-causing. It was found that FOXP2 expression was significantly lower in breast cancer cells as opposed to normal, healthy breast tissues. In terms of phenotype, or observable traits due to gene changes, FOXP2 gene expression was correlated with poorer prognoses; with lower FOXP2 expression, there were lower relapse-free survival rates for patients. In other words, FOXP2 may play a role in the recurrence and relapse of breast cancers.

Other researchers noted that the human FOXP2 locus is located within a region of chromosomes 7 that is surrounded by numerous recombination hotspots. These fragile recombination hotspots are regions of DNA that are particularly susceptible to mutations. In other words, the surrounding bases to the FOXP2 gene are prone to chromosomal instability and therefore chromosomal rearrangements. Chromosomal instability (CIN) refers to persistently high rates of either partial or whole chromosomal deletions or duplications. CIN has been frequently connected to cancer or tumor cell progression. This susceptibility of the FOXP2 locus to mutations thus may lead to rearrangements and cause tumor-genesis and cancer progression.