Abstract
Abstract : Previous research from this laboratory indicated that: (1) the expression of Tropomyosin-1 (TM1), a microfilament-associated protein, is abolished from many human breast carcinoma cells, and; (2) that TM1 is suppressor of the malignant transformation. These data led to the hypothesis that TM1 plays an important role in mammary carcinogenesis. Therefore, we investigated whether TM1 could serve as a biomarker of breast cancer, and TM1 could function as a suppressor of the malignant growth of breast cancer cells. Initial experiments with a TM1-specific antibody suggested that TM1 expression may be absent in the breast tumors (Objective 1). We demonstrated that restoration of TM1 expression is adequate to suppress the malignant growth phenotype of MCF-7 cells, indicating that TM1 is a suppressor of the transformed growth (Objective 2). The reverse experiment, i.e., antisense-suppression of TM1 expression in normal mammary epithelial cells is in progress. MCF10A cells were transduced with TM1 antisense cDNA and those clones are being evaluated (Objective 3). To assess the structure-function relationship of tumor suppression by TM1, chimeras of TM1 and TM2 (which is not a tumor suppressor) are being constructed. These chimeras will be transfected into MCF-7 cells (Objective 4).
Published Version
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