Figure 2.

Selective disruption of gap junctional communication (GJC) reduced tumor incidence. To determine the effect of GJC disruption on tumorigenesis, H7 and KRAS^G12D injections—aimed at disrupting GJC host-wide, within tumors, and away from tumors—were performed. Compared to KRAS^G12D-only injected embryos (treatment mode A), treatment modes B and D showed significant decrease in % embryos with tumor by 6.6 and 5.8%, respectively, implying that H7 contralateral to the oncogene has no effect if there is H7 ipselateral to the oncogene. Contralateral H7 only (treatment mode C) significantly reduces the % embryos with tumor by 15.8%. Doubling the level of oncogene injected along with host-wide introduction of H7 (treatment mode F) does not affect tumor incidence when compared to oncogene-only (one side) injected embryos (treatment mode A), but is able to counter the 9.9% increase in tumor incidence resulting from excess oncogene introduced (treatment mode G) down to the tumor incidence level of one-side oncogene injection. Similarly, tumor incidence from the excess oncogene introduction can be reduced by H7 introduction to either side of the embryo (treatment mode E). ^*P < 0.05, ^**P < 0.001; t-test.