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. 2015 Mar 5;10(3):e0118845. doi: 10.1371/journal.pone.0118845

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© 2015 Zhang et al

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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Fig 5 — NNK promoted the expression of p-ERK1/2, cyclin-D1, Bcl-2, and VEGF, and decreased the expression of Bax in KYSE410 (A) and HET-1A (B) cells. Knockdown of beta-adrenoceptors decreased the expression of p-ERK1/2, cyclin D1, Bcl-2, and VEGF, and increased the expression of Bax. More importantly, down-regulation of both beta1- and beta2-adrenoceptors before treatment with NNK reversed the NNK-associated protein expression, and beta2-adrenoceptors showed a more significant effect. Beta-actin served as an endogenous control. Independent experiments were repeated three times. Negative is representative of nonspecific control siRNA for beta-adrenoceptors.