Growth-suppressing activity of the transfected Cx26 on BICR-M1Rk breast cancer cell line.

There are accumulating evidences suggesting that connexin (Cx), a gap junction channel-forming protein, acts as a growth suppressor in various cancer cells, and this effect is attributed to the gap junction-mediated intercellular communication (GJIC). In order to characterize the relationship between the growth-arresting activity of Cx26 and its cytoplasmic localizations after expression, we linked a nuclear export signal (NES) sequence to Cx26 cDNA before transfecting into a rat breast cancer cell line. A confocal fluorescent microscopic observation revealed that the insertion of NES minimized the nuclear expression of Cx26, and increased its cytoplasmic expression, including plasma membrane junctions.

Inhibitory effect of bisphenol A on gap junctional intercellular communication in an epithelial cell line of rat mammary tissue.

An endocrine disruptor, bisphenol-A (BPA), has been reported to have several short-term actions in various cells and tissues. However, the mechanisms of these actions have not been fully elucidated. In order to assess the effect of BPA on the intercellular communication mediated by gap junctions, we conducted the present study in the rat epithelium-derived BICR-M1Rk cell-line, in which connexin 43 (Cx43) is a major gap junction channel-forming protein.

Mutations induced by 1,3-butadiene metabolites, butadiene diolepoxide, and 1,2,3,4-diepoxybutane at the Hprt locus in CHO-K1 cells.

Butadiene (BD) is an important industrial chemical that is classified as a probable human carcinogen. Butadiene diolepoxide (BDE) and 1,2,3,4-diepoxybutane (DEB) are metabolites of carcinogenic BD and contain the DNA-reactive one and two epoxides, respectively. In this study, the mutation frequencies and mutation spectra that are induced by BDE and DEB have been investigated at the hprt locus in CHO-K1 cells.

Growth inhibition by connexin26 expression in cultured rodent tumor cells.

The Connexin (Cx) gene family acts as a tumor suppressor. However, it is unclear whether the tumor-suppressing activity acquired by Cx gene transfection is mainly due to the recovery of the gap junction-mediated intercellular communication (GJIC) or to other unknown mechanisms. In order to elucidate the mechanism of the Cx-induced tumor-suppressing activity, we transfected Cx26 cDNA into a rodent mammary tumor cell-line (BICR-M1Rk) in which Cx43 had been normally expressed and a typical pattern of GJIC had been observed.