Maspin is a member of the serpin family of protease inhibitors and was originally thought to be a tumor suppressor due to its ability to inhibit invasion, motility, and metastasis of mammary tumors [
16]. However, loss of maspin expression in several cancers, such as pancreatic, colorectal and ovarian cancer, is not commonly observed due to a lack of maspin expression in the corresponding normal tissue. The most compelling data regarding the clinical significance of maspin in cancer progression and metastasis emerged from survival studies of cancer patients. Although the original studies revealed an association between reduced maspin expression and cancer progression and worse prognosis, it has been demonstrated that this correlation was far more complex than originally suspected. Factors contributing to this complexity include the differences in cancer type (e.g. adenocarcinoma vs squamous cell carcinoma), cut-off values of positive criteria, antibodies used, methods of detection, and subcellular maspin distribution. The subcellular localization of maspin is predominantly cytoplasmic; however, maspin exerts its effect in the nucleus at the level of gene and chromatin regulation, and is released only as a consequence of cell damage or necrosis [
17],[
18]. Goulet
et al. demonstrated that nuclear localization of maspin was essential for its inhibition of tumor growth and metastasis [
19]. Sood
et al. reported that nuclear maspin staining was associated with increased survival, whereas cytoplasmic maspin staining was associated with a poor outcome in ovarian carcinoma [
20]. Additionally, Marioni
et al. reported that nuclear maspin expression was associated with a lower recurrence rate and a longer disease-free interval after surgery for squamous cell carcinoma of the larynx [
21]. We have also reported that cytoplasmic maspin expression was associated with an aggressive phenotype and poor prognosis of patients with breast cancer [
8]-[
10], colorectal cancer [
11], and endometrioid endometrial carcinoma [
12]. On the other hand, there have been few reports investigating maspin expression in non-epithelial tissue [
22], and only two reports have described the expression of maspin in STS. Kim
et al. reported a case of metastatic leiomyosarcoma from a uterus showing expression of maspin in addition to several types of growth factors, angiogenic factors, and proliferative markers in the metastatic tumor cells by immunohistochemistry and immunoblot detection [
14]. Although they did not describe the subcellular localization of maspin expression, they revealed that the maspin protein was more intensely expressed in the metastatic tumor compared to the primary uterine leiomyosarcoma. In the present study, we observed the expression of maspin in 56.4% of leiomyosarcomas. These results highlight the need for further studies on the use of maspin expression as a prognostic indicator in leiomyosarcomas. Fitzgerald
et al. reported that chondrosarcoma cells exhibited upregulated maspin mRNA expression in addition to decreased DNA methylation of the maspin gene [
15]. They also demonstrated that the upregulation of maspin mRNA may either play an important role in malignant progression, or simply be a biomarker of tumor progression. Their findings may support our present results that expression of maspin is correlated with the poor prognosis of patients with STS, although chondrosarcomas were not investigated in our study.