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. 2017 Oct 2;38(6):3309–3318. doi: 10.3892/or.2017.6014

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Copyright: © Zhang et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 3. — Knockdown of α7nAChR decreases nicotine-stimulated vimentin expression in xenograft tumors in nude mice. (A) In the sections from xenograft tumors composed of Ctrl-shRNA H1299 cells, the expression of α7nAChR was greatly increased in the group stimulated with nicotine compared with the group treated with saline. Concomitant with the upregulation of α7nAChR, the expression of vimentin was markedly increased. When α7nAChR was knocked down, the expression of vimentin was subsequently attenuated, even under stimulation with nicotine. Sections were scanned at a magnification of ×10. (a-h) Representative areas scanned at a magnification of ×20. (B) Vimentin quantitation in sections taken from tumors consisting of Ctrl shRNA or KDα7nAChR-shRNA H1299 cells. In the Ctrl-shRNA groups, vimentin increased markedly following nicotine stimulation compared with the untreated group. In the KDα7nAChR-shRNA group, the expression of vimentin after nicotine stimulation remained considerably lower than that in the Ctrl-shRNA group. (C) Quantitation of α7nAChR expression in Ctrl shRNA and KDα7nAChR-shRNA H1299 cell xenograft sections. Compared with the untreated group, the expression of α7nAChR in sections from Ctrl-shRNA tumors was strongly increased following nicotine stimulation. In the sections consisting of cells transfected with KDα7nAChR shRNA, the expression of α7nAChR was markedly attenuated, regardless of nicotine stimulation, when compared with the sections derived from cells transfected with Ctrl shRNA with or without nicotine stimulation. α7nAChR; α7 nicotinic acetylcholine receptor.