Lung cancer is the most common
malignancy and cause of
cancer deaths worldwide, owing to the dismal prognosis for most affected patients.
Phosphatase and
tensin homolog deleted in chromosome 10 (PTEN) acts as a powerful tumor suppressor gene and even partial reduction of its levels increases
cancer susceptibility. While the most validated anti-oncogenic duty of PTEN is the negative regulation of the PI3K/mTOR/Akt oncogenic signaling pathway, further
tumor suppressor functions, such as chromosomal integrity and DNA repair have been reported.
PTEN protein loss is a frequent event in
lung cancer, but genetic alterations are not equally detected. It has been demonstrated that its expression is regulated at multiple genetic and epigenetic levels and deeper delineation of these mechanisms might provide fertile ground for upgrading
lung cancer therapeutics. Today, PTEN expression is usually determined by immunohistochemistry and low
protein levels have been associated with decreased survival in
lung cancer. Moreover, available data involve PTEN mutations and loss of activity with resistance to targeted treatments and
immunotherapy. This review discusses the current knowledge about PTEN status in
lung cancer, highlighting the prevalence of its alterations in the disease, the regulatory mechanisms and the implications of PTEN on available treatment options.