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. 2021 Jul 15;15:17534666211028072. doi: 10.1177/17534666211028072

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© The Author(s), 2021

This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Figure 2. — CASC2 overexpression alleviated CSE-induced apoptosis and inflammation in 16HBE cells. (a) The levels of CASC2 decreased gradually in 16HBE cells as the CSE concentration increased, and the CASC2 levels were significantly suppressed at 2% and 4% CSE concentration. **p < 0.01; ***p < 0.001. (b) The levels of CASC2 decreased gradually in the cell culture medium as the CSE concentration increased, and the CASC2 levels were significantly suppressed at 2% and 4% CSE concentration. **p < 0.01; ***p < 0.001. (c) CASC2 was significantly upregulated in both cells and cell culture medium by pcDNA-CASC2 transfection. ***p < 0.001, compared with control group; ^###p < 0.001 compared with CSE group. (d) and (e) CASC2 overexpression significantly promoted cell viability, while it inhibited CSE-induced cell apoptosis. ***p < 0.001, compared with control group; ^###p < 0.001 compared with CSE group. (f) CSE promoted the release of IL-6, IL-8, IL-1β, and TNF-α in 16HBE cells, which was reversed by CASC2 overexpression. ***p < 0.001, compared with the control group; ^###p < 0.001 compared with CSE group. Differences between groups were compared using one-way analysis of variance.

CASC2, cancer susceptibility candidate 2; CSE, cigarette smoke extract; pcDNA, plasmid cloning DNA.