B7‑H3 promotes the epithelial‑mesenchymal transition of NSCLC by targeting SIRT1 through the PI3K/AKT pathway

• DOI: 10.3892/mmr.2022.12595
• Publication Date: 2022-02-09T17:16:30Z
• Authors: Haixiu Liao; Meng Ding; Nannan Zhou; Ying Yang; Liwen Chen
• Keywords: LY294002; Sirtuin 1

Epithelial‑mesenchymal transition (EMT) is a key step in cancer metastasis. B7‑H3, co‑signaling molecule associated with poor prognosis of non‑small cell lung (NSCLC), promotes the metastasis NSCLC by activating EMT process. However, its underlying mechanism remains poorly understood. In present study, it was shown that CRISPR/Cas9‑mediated B7‑H3 deletion downregulated expression class III histone deacetylase, sirtuin‑1 (SIRT1), A549 cells. Accordingly, SIRT1 silencing resulted markedly decreased migration and invasion Both gene‑edited SIRT1‑silenced cells were typically characterized an increased epithelial marker E‑cadherin, downregulation mesenchymal markers N‑cadherin vimentin, as compared mock‑edited scrambled negative small interfering RNA control, respectively. It further demonstrated ablation significantly phosphorylated AKT/protein kinase B expression, substantially suppressed PI3K‑specific inhibitor, LY294002. Taken together, findings study revealed B7‑H3‑induced signaling upregulates via PI3K/AKT pathway to promote activation NSCLC.