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. 2022 May 16;10(5):e004113. doi: 10.1136/jitc-2021-004113

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© Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See http://creativecommons.org/licenses/by-nc/4.0/.

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SNORA38B activated the AKT/mTOR and its downstream effectors. (A) Gene set enrichment analysis of gene sets including SNORA38B high and SNORA38B low in NSCLC. (B) Western blotting analysis of AKT/mTOR and its downstream effectors in A549 cells transfected with SNORA38B KO, SNORA38B OE or their counterparts. (C) Rescue experiment using SNORA38B KO and SNORA38B OE in A549 cell was conducted to detect the regulation of AKT/mTOR and its downstream effectors by SNORA38B. Assays were conducted in triple. AKT, protein kinase B; FDR, false discovery rate; KO, knockout; mTOR, mammalian target of rapamycin; NES, normalized enrichment score; OE, overexpress; SNORNA, small nucleolar RNA.