SNRPE is Associated with ERK/mTOR Signaling Activation and Reduced Autophagy to Promote Lung Adenocarcinoma Cell Proliferation.

Objective: To explore the effect of small nuclear ribonucleoprotein E (SNRPE) on proliferation and autophagy in lung adenocarcinoma (LUAD). Methods: SNRPE expression was measured in LUAD and para-cancerous tissues by immunohistochemical detection and in LUAD cell-lines by real-time fluorescence quantitative PCR (RT-qPCR) and Western blotting. Cell proliferation was evaluated by cell counting kit (CCK-8) and colony formation, cell cycle progression and apoptosis were assessed by flow cytometry. Extracellular signal-regulated kinase (ERK)/Mammalian target of rapamycin (mTOR) signaling and autophagy proteins, Microtubule-associated protein 1 light chain 3B (LC3B), Sequestosome-1 (P62) and Beclin1 were measured by Western blotting. The impact of SNRPE expression on tumor growth in vivo was assessed by an animal model of LUAD. Results: LUAD tissues showed high SNRPE expression and expression correlated with T stage. SNRPE knockdown in LUAD cells decreased proliferation, induced autophagy, trapped cells in G1 phase and inhibited the activation of ERK/mTOR signaling. Xenograft tumors with SNRPE knockdown showed reduced growth rate. Conclusion: SNRPE was expressed at high levels in LUAD cancer tissues. SNRPE knockdown inhibited LUAD cell proliferation and stimulated autophagy in vivo and in vitro. SNRPE may target the ERK/mTOR signaling pathway. These findings may expose a novel target for LUAD treatment. In this study, limitations include the relatively small clinical sample size, lack of autophagy flux assays, and absence of mechanistic rescue experiments, which warrant further studies.