The grim prognosis of
lung cancer, that has an overall 10-15% survival at 5 years, remains in the US the leading cause of
cancer mortality, provides a compelling rationale for studying the molecular basis of this
malignancy. Surmising the common, general association with smoking,
lung cancers differ at the microscopic, anatomical, epidemiological and clinical level and harbor complex genetic and epigenetic alterations. Currently,
lung cancer is divided into
small cell lung carcinoma (SCLC) and
non small cell lung carcinoma (NSCLC) for the purpose of clinical management. (NSCLC) constitutes 80-85% of
lung cancers and is further divided into histological subtypes such as
adenocarcinoma,
squamous cell carcinoma, and
large cell carcinoma, etc. The ultimate goal for
lung cancer research is to develop a strategy to block the
tumor progression and improve the prognosis of
lung cancer. This goal can realistically be achieved only when the biological complexity of this disease is taken into account. To this end, identification and understanding of molecular markers that are mechanistically involved in
tumor progression is needed. Our recent studies suggest histological subtype-dependent distinct correlations between the expression and/or subcellular localization of
tumor suppressive
maspin with the progression and prognosis of NSCLC.
Maspin is an epithelial specific member of the
serine protease inhibitor (
serpin) superfamily but recently identified as an endogenous inhibitor of
histone deacetylase 1 (HDAC1). This novel biochemical activity coincides with a consensus emerged recently from the evidence that nuclear
maspin confers better differentiated epithelial phenotypes, decreased
tumor angiogenesis, increased
tumor sensitivity to drug-induced apoptosis, and a more favorable prognosis. In the current review, we discuss the evidence that
maspin may be a marker that stratifies the progression and prognosis of different subtypes of NSCLC.