Researchers from University of Brown have found that by decreasing or blocking specific protein level, two different types of cancer cells could be suppressed to metastasize in mice. This protein is common in human and other animals. The imbalance of the protein contributes to cancer metastasis. This study was published in Cancer Research.

Chitinase 3-like-1(Chi3L1) is the prototypic mammalian CLP. It was originally discovered in mouse breast cancer cells. It is now known to be expressed by a variety of cells including macrophages, neutrophis, epithelial cells, smooth muscle cells and chondrocytes and is stimulated by a number of mediators including IL-12, IL-6, IL-1β, and IFNγ. The Chi3L1 is induced in cancers and portends a poor prognosis, but whether it contributes to cancer progression is unknown.

In this study, scientists hypothesized that host Chi3L1 plays an essential role in the pathogenesis of malignant melanoma and that interventions that alter the induction Chi3L1 decrease the metastatic spread of this tumor. To test this hypothesis they characterized the ability of B16-F10 melanoma cells to stimulate Chi3L1 in wild type mice and their ability to generate pulmonary metastasis in wild type(WT) mice and mice with null mutations of Chi3L1.

Their studies highlight a novel host pathway in which Sema7a stimulates the production of Chi3L1 by interacting with β1 integrin and inhibits Chi3L1 by interacting with Plexin C1. They also demonstrate that the host Sema7a- Chi3L1-IL-13Rα2 axis plays a critical role in the generation of a metastasis-permissive pulmonary microenvironment leading to melanoma lung metastasis.

Reference:

Ma B, Herzog E L, Lee C G, et al. Role of Chitinase 3-like-1 and Semaphorin 7A in Pulmonary Melanoma Metastasis[J]. Cancer research, 2014: canres. 3339.2013.