Abstract
Simple SummaryIn this article we have highlighted the possible role of nuclear maspin in identification of tumor cells “on the point of budding” and the epithelial mesenchymal transition phenomenon of these cells, along with a deep exploration of the maspin-molecular mediated mechanisms in colorectal cancer.In this review the authors aimed to emphasize the practical value of nuclear expression of the mammary serine protease inhibitor (maspin), also known as serpin B5 protein, in colorectal carcinoma (CRC), from pre-malignant disorders to carcinogenesis and metastasis. As the role of maspin is controversial and not yet understood, the present update highlights the latest data revealed by literature which were filtrated through the daily experience of the authors, which was gained at microscopic examination of maspin expression in CRCs and other tumors for daily diagnosis. Data regarding the subcellular localization of maspin, in correlation with the microsatellite status, grade of tumor dedifferentiation, and epithelial-mesenchymal transition (EMT) phenomenon of the tumor buds were presented with details. An original observation refers to the maspin capacity to mark the tumor cells which are “at the point of budding” that were previously considered as having “hybrid EMT phenotype”. It refers to the transitional status of tumor cell that is between “epithelial status” and “mesenchymal status”. The second original hypothesis highlights the possible role of maspin in dysregulating the intestinal microbiota, in patients with idiopathic inflammatory bowel diseases (IBD) and inducing IBD-related CRC. The dynamic process of budding and EMT of tumor buds, possible mediated by maspin, needs further investigation and validation in many human CRC samples. The histological and molecular data reveal that synthesis of maspin-based therapeutics might represent a novel individualized therapeutic strategy for patients with CRC.
Highlights
Introduction published maps and institutional affilPersonalized health care in cancer tends to be based on histological and molecular classification of solid cancers and should be realized using standardized and reproducible biomarkers [1]
We proved that loss of maspin might be induced by TP53 gene mutations in exon 7 whereas wild-type p53 was hypothesized to be responsible by restoration of the nuclear maspin expression and further decreasing of the metastatic potential [20]
The first results of our team were published in 2013, and we proposed a system of quantification of maspin subcellular expression, which was further certified in other papers elaborated with our Ph.D. students [2,6]
Summary
Being known as the serpin B5 or peptidase inhibitor 5, maspin is an unsusual non-inhibitory member of the the serine protease inhibitor (serpin) superfamily [4,5]. Maspin acts as a pro-apoptotic protein with role in implantation of the embryos into the uterine wall, embryonic development, cell adhesion, and oxidative stress response [7,9,13]. It can inhibit the urokinase plasminogen activator (uPA) and tissue plasminogen activator and modulate the mammary gland morphogenesis during pregnancy; high maspin expression was associated with low milk production [7]. Maspin is overexpressed in the hyperplastic epidermis [15]
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