Abstract

TGF beta1 suppressed the colony forming ability of human lung carcinoma cell line, A549 cells in a dose-dependent manner. Accompanying these changes, the levels of the expression of high-molecular weight tropomyosin (TM) isoforms, especially TM1 and TM2, were significantly increased in the TGF beta1-treated A549 cells in a dose-dependent manner. When A549 cells were treated with TGF beta1 (2.5 pM) and EGF (1 nM) simultaneously, anchorage-independent growth of A549 cells was restored. In these cells, the expression of high-molecular weight TM decreased. The results suggest that the levels of the expression of high-molecular weight TM may be involved in antagonistic effects of EGF and TGF beta1 on the anchorage-independent growth of A549 cells.

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