The protein galectin-7, which leads to cell death, is expressed in and plays a metastatic role in various types of cancer. To determine the role of galectin-7 in breast cancer, Demers et al investigated galectin-7 expression and function in breast cancer cells. Galectin-7 was highly expressed in two pre-clinical models of breast cancer, and high galectin-7 expression levels increased the metastatic potential of these tumor cells. In humans, high expression levels of galectin-7 were restricted to high-grade tumors and were associated with metastasis. Taken together, these data implicate galectin-7 as both a breast cancer differentiation marker and a potential therapeutic target for metastatic breast cancer.
Dr. St.-Pierre and colleagues "believe that lower survival rates and increased metastases in mice injected with breast cancer cells overexpressing galectin-7 are related to the ability of galectin-7 to protect from apoptosis, as previously shown in the case of galectin-3. - Further studies regarding the role of galectin-7 in resistance to apoptosis are currently under investigation."
Demers M, Rose AAN, Grosset A-A, Biron-Pain K, Gaboury L, Siegel PM, St-Pierre Y: Overexpression of galectin-7, a myoepithelial cell marker, enhances spontaneous metastasis of breast cancer cells. Am J Pathol 2010, 3023-3031
Low Caveolin-1 Expression Contributes to Lung Disease
Dr. Craig Henke and colleagues at the University of Minnesota, Minneapolis, MN propose that low levels of caveolin-1 contribute to the over-proliferation of fibroblasts in lung disease. These results are presented in the June 2010 issue of The American Journal of Pathology.
Idiopathic pulmonary fibrosis (IPF) is a form of lung disease characterized by lung fibrosis, or development of excessive connective tissue resulting in lung damage, of unknown origin. Low levels of PTEN (phosphatase and tensin homolog), a molecule that prevents cells from growing and dividing too rapidly, have been implicated in the over-proliferation of fibroblasts following tissue injury. However, the molecular mechanisms underlying the low expression of PTEN in lung fibroblasts in IPF remain to be determined.
Xia et al hypothesized that caveolin-1, a molecule involved in cell signaling and intake of external molecules that is decreased in fibroblasts in IPF patients, may be responsible for the levels of PTEN expression in these cells. They correlated low levels of caveolin-1 and PTEN expression and demonstrated that overexpression of caveolin-1 restored PTEN expression in IPF fibroblasts. Indeed, PTEN interacted with caveolin-1 through its caveolin-1 binding sequence. Decreased caveolin-1 expression therefore facilitates the over-proliferation of fibroblasts in IPF.
Dr. Henke's group "demonstrate[s] that in IPF fibroblasts, a lack of caveolin-1 expression in the plasma membrane reduces membrane-associated PTEN levels and activity. - This confers IPF fibroblasts with a phenotype characterized by the ability to circumvent the proliferation-suppressive properties of polymerized type I collagen."
Source: American Journal of Pathology