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. 2023 Jun 22;14(22):2093–2104. doi: 10.1111/1759-7714.14989

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© 2023 The Authors. Thoracic Cancer published by China Lung Oncology Group and John Wiley & Sons Australia, Ltd.

This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ 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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AHNAK2 interacts with RUVBL1 and causes G1/S phase cell cycle arrest in A549 cells. (a) The Co‐immunoprecipitation (Co‐IP) assay demonstrated the specific interactions between AHNAK2 and RUVBL1. Cell cycle analysis. (bi) A549 cells treated with Ctrl‐AHNAK2 and Ctrl‐RUVBL1. (bii) A549 cells with lower expression of AHNAK2 showed cell cycle arrest at the G1/S phase. (biii) H1975 cells with lower expression of RUVBL1 showed cell cycle arrest at the G1/S phase. (biv) H1975 cells treated with sh‐AHNAK2 and si‐RUVBL1 showed cell cycle arrest at the G1/S phase more significantly. (bv) The G1/S cell cycle arrest deteriorated when both AHNAK2 and RUVBL1 were suppressed in sequence. (c) Gene set enrichment analysis (GSEA) revealed that samples with higher AHNAK2 expression exhibited higher pathway activity of “mitotic cell cycle” as compared to lower samples in TCGA datasets.