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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 3. — CASC2 functions as a ceRNA of miR-18a-5p. (a) The complementary sequence between miR-18a-5p and CASC2 3′-UTR. (b) The luciferase activity of different groups. ***p < 0.001, compared with control group. (c) CSE treatment significantly increased the level of miR-18a-5p, while overexpression of CASC2 led to the reduction of miR-18a-5p expression. ***p < 0.001, compared with control group; ^###p < 0.001, compared with CSE group). (d) Serum miR-18a-5p level in COPD patients. *p < 0.05, ***p < 0.001. (e) Serum miR-18a-5p expression showed a negative association with the level of CASC2. Differences between groups were compared using one-way analysis of variance.

CASC2, cancer susceptibility candidate 2; ceRNA, endogenous competitive RNA; COPD, chronic obstructive pulmonary disease; CSE, cigarette smoke extract; lncRNA, long non-coding RNA; Mut, mutant type; NC, negative control; pcDNA, plasmid cloning DNA; Wt, wild type.