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. 2019 Sep 5;8(9):1391. doi: 10.3390/jcm8091391

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© 2019 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

PMC Copyright notice

The oncogenic role of the α7-nicotinic acetylcholine receptor (α7-nAChR) is mediated in part by JAK2 activation. (A) Visualization of the molecular connectivity network among the α7-nAChR, JAK2, STAT3, SOX2, OCT4A (POU5F1), Survivin (BIRC5), Bcl-xL (BCL2L1), MCL-1, MMP2, MMP9, RhoA, and ROCK1 using STRING version 10.5. (B) Differential expressions of the α7-nAChR and JAK2 in hepatocellular carcinoma (HCC) specimens compared to non-tumor liver specimens in the GSE14323 dataset. (C) Representative images of α7-nAChR and JAK2 expression levels in HCC tissues of different TMN stages showing mild expression in stage I, moderate expression in stage II, and high expression in stage III, compared to no expression in non-tumor liver (NL) tissues. The original magnification is indicated; bar = 100 μm. (D) Photo-images showing the differential expression of JAK2 in HCC specimens from a current smoker compared to non-tumor liver specimens from a non-smoker. (E) Dot and whisker plots showing that the α7-nAChR and JAK2 are upregulated in tumor compared to non-tumor liver tissues. * p < 0.05. (F) Graph showing the positive correlation between the α7-nAChR and JAK2 in patients with HCC.