We discriminated the role of gap junctional communication and phenotypic constitution of tumour cells in determining their responsiveness to apigenin. Effects of apigenin on intercellular communication and proliferation of two lines of carcinoma cells, uncoupled HeLa cells and their coupled Cx43-transfected counterparts, were analysed and compared with the responses of highly coupled BICR/M1Rk cells. Dye transfer analyses demonstrated that apigenin decreases the degree of coupling in Cx43-coupled populations of HeLa cells but does not affect BICR/M1Rk cells.
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