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. Author manuscript; available in PMC: 2020 Jan 1.
Published in final edited form as: Cancer Res. 2018 Nov 2;79(1):196–208. doi: 10.1158/0008-5472.CAN-18-1615

Figure 6. Restoration of Cx43 gap junction suppresses motility in HEC-1A endometrial cancer cells.

Figure 6.

A, Labelling of Cx43 in intracellular pools was evident for EME6/7t and Ishikawa, and weekly observed in HEC-1A, with surface labeling of plaques between cells most evident in EME6/7t cells (white arrows). DAC treatment induces Cx43 gap junction plaque formation in Ishikawa and HEC-1A cells, although these were less organized in the Ishikawa cells. B-C, Restoration of Cx43 in HEC-1A cells by expression vector transduction was performed (B). This Cx43 induction resulted in decreased cellular migration of HEC-1A cells, with limited effects on proliferation (C). D-E, In complementary experiments, Knockdown of Cx43 by siRNA in EME6/7t cells, as demonstrated by immunofluorescence (D), led to enhanced cellular migration in scratch assays, with no effect on proliferation (E). Also, treating EME6/7t cells with the Cx43 gap junction specific peptide inhibitor, gap27, led to enhanced migration in a dose-dependent manner, with a limited effect on proliferation (F).