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. 2015 Jan 19;5:519. doi: 10.3389/fphys.2014.00519

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Copyright © 2015 Chernet, Fields and Levin.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Enhanced gap junctional communication (GJC) through connexin 26 (Cx26) overexpression increases tumor incidence. To determine the effect of GJC disruption on tumorigenesis, Cx26 and KRAS^G12D injections—aimed at enhancing GJC host-wide, within tumors, and away from tumors—were performed. Compared to KRAS^G12D-only injected embryos (treatment mode A), long-range and host-wide Cx26 treatment modes (C, D, F) show an increase in the number of embryos with tumor by 6.4 to 11.4%. However, treatments involving the expression of oncogene and Cx26 on the same side (treatment modes B and E), while non-significant, lower tumor incidence when compared to treatment modes A and F, respectively. ^*P < 0.05; t-test.