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已发表论文
SNRPE 与 ERK/mTOR 信号通路激活及自噬减少相关，可促进肺腺癌细胞增殖
Authors Yang J , Dai W, Ren B, Chen H, Dang X, Jiang L
Received 12 May 2025
Accepted for publication 7 November 2025
Published 15 November 2025 Volume 2025:18 Pages 1299—1312
DOI https://doi.org/10.2147/OTT.S539944
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 4
Editor who approved publication: Professor Yong Teng
Jun Yang,1,2 Wenchao Dai,1,2 Bi Ren,2 Hang Chen,1,2 Xin Dang,1,2 Li Jiang1
1Department of Respiratory and Critical Care Medicine, The Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan, People’s Republic of China; 2Department of Clinical Medicine, North Sichuan Medical College, Nanchong, Sichuan, People’s Republic of China
Correspondence: Li Jiang, Department of Respiratory and Critical Care Medicine, The Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan, People’s Republic of China, Email lanqilily@163.com
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.
Plain Language Summary: Lung adenocarcinoma is a common type of lung cancer that often grows quickly and is difficult to treat. In this study, we focused on a protein called SNRPE, which is found in high amounts in lung cancer tissues. Our experiments in cells and mice showed that lowering SNRPE levels slowed cancer cell growth and increased a cell-cleaning process called autophagy, likely linked to reduced activity in the ERK/mTOR signaling pathway. These findings, based on laboratory models, suggest SNRPE may contribute to lung cancer growth, but more research is needed to confirm these effects and explore SNRPE as a potential treatment target.
Keywords: lung adenocarcinoma, small nuclear ribonucleoprotein E, ERK/mTOR, LC3, P62 autophagy
1Department of Respiratory and Critical Care Medicine, The Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan, People’s Republic of China; 2Department of Clinical Medicine, North Sichuan Medical College, Nanchong, Sichuan, People’s Republic of China
Correspondence: Li Jiang, Department of Respiratory and Critical Care Medicine, The Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan, People’s Republic of China, Email lanqilily@163.com
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.
Plain Language Summary: Lung adenocarcinoma is a common type of lung cancer that often grows quickly and is difficult to treat. In this study, we focused on a protein called SNRPE, which is found in high amounts in lung cancer tissues. Our experiments in cells and mice showed that lowering SNRPE levels slowed cancer cell growth and increased a cell-cleaning process called autophagy, likely linked to reduced activity in the ERK/mTOR signaling pathway. These findings, based on laboratory models, suggest SNRPE may contribute to lung cancer growth, but more research is needed to confirm these effects and explore SNRPE as a potential treatment target.
Keywords: lung adenocarcinoma, small nuclear ribonucleoprotein E, ERK/mTOR, LC3, P62 autophagy