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HERO ID
2751547
Reference Type
Technical Report
Title
Mechanism of Abnormal Cell-Extracellular Matrix Interactions in Human Breast Cancer
Author(s)
Chen, HM
Year
1997
Report Number
NTIS/03002907
Volume
GRA and I
Issue
GRA and I
Abstract
Differential display was exploited to analyze expression patterns of premalignant (S2) and tumor (T4) cells, two sublines of a unique human breast cancer progression HMT3522 series, to identify candidate genes participating in the final-stage tumorigenic conversion in breast cancer. Message levels of a novel gene AZ-i was significantly lower in T4 than in S2 cells cultured either on plastic or in 3-D matrix system. Az-i was abundantly present in nonmalignant counterpart S 1 and human breast luminal epithelial cells. In contrast, expression of this gene was drastically repressed in ten human breast epithelial cancer lines. Modulation of Az-i gene expression by phenotypic alteration of tumor cells was examined in a reversion system described recently in our laboratory. Briefly, when T4 cells were cultured in the presence of inhibitory % 1 -integrin antibody in a 3-D system, they reverted morphologically to S 1-like cells. They formed acini while re-assembled a basement membrane, reorganized cytoskeleton network, suppressed cyclin Di and were growth arrested. Interestingly, AZ-i gene was up-regulated in the reverted T4 cells to a level reminiscent of that seen in the S I cells. Based on the sequence homology with coiled-coil domain of several structural proteins, i.e., myosin heavy chain and desmoplakin I and II, Az-i may play a role in organization of cytoskeletal architecture.
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