{"title":"下调SMPDL3B抑制肺腺癌细胞的增殖、迁移和侵袭","authors":"Jae Woong Koh, Seon-Joo Park","doi":"10.21873/anticanres.17688","DOIUrl":null,"url":null,"abstract":"<p><strong>Background/aim: </strong>Sphingomyelin phosphodiesterase acid-like 3B (SMPDL3B) is an enzyme involved in lipid metabolism and cellular signaling. SMPDL3B expression is up-regulated in several cancers, suggesting its potential as a novel prognostic biomarker and therapeutic target for cancer treatment. However, its role in lung cancer remains unclear. In this study, we evaluated the biological role of SMPDL3B in lung cancer.</p><p><strong>Materials and methods: </strong>SMPDL3B expression in lung adenocarcinoma (LUAD) tissues and cells was validated using quantitative real-time PCR and western blotting. To determine the role of SMPDL3B in LUAD cells, a small interfering RNA targeting SMPDL3B was used to suppress intracellular gene expression. Cell proliferation was performed using MTT and colony formation assays, and transwell assays with or without Matrigel were used to evaluate the role of SMPDL3B in LUAD cells migration and invasion.</p><p><strong>Results: </strong>SMPDL3B was overexpressed in LUAD tissues and cells. Knockdown of SMPLD3B significantly inhibited cell proliferation by regulating cell cycle progression and also prevented the migration and invasion of LUAD cells.</p><p><strong>Conclusion: </strong>SMPDL3B plays a role in LUAD, suggesting its potential as a therapeutic target for selective and personalized lung cancer treatment.</p>","PeriodicalId":8072,"journal":{"name":"Anticancer research","volume":"45 8","pages":"3275-3286"},"PeriodicalIF":1.7000,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Down-regulation of SMPDL3B Inhibits the Proliferation, Migration, and Invasion of Lung Adenocarcinoma Cells.\",\"authors\":\"Jae Woong Koh, Seon-Joo Park\",\"doi\":\"10.21873/anticanres.17688\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background/aim: </strong>Sphingomyelin phosphodiesterase acid-like 3B (SMPDL3B) is an enzyme involved in lipid metabolism and cellular signaling. SMPDL3B expression is up-regulated in several cancers, suggesting its potential as a novel prognostic biomarker and therapeutic target for cancer treatment. However, its role in lung cancer remains unclear. In this study, we evaluated the biological role of SMPDL3B in lung cancer.</p><p><strong>Materials and methods: </strong>SMPDL3B expression in lung adenocarcinoma (LUAD) tissues and cells was validated using quantitative real-time PCR and western blotting. To determine the role of SMPDL3B in LUAD cells, a small interfering RNA targeting SMPDL3B was used to suppress intracellular gene expression. Cell proliferation was performed using MTT and colony formation assays, and transwell assays with or without Matrigel were used to evaluate the role of SMPDL3B in LUAD cells migration and invasion.</p><p><strong>Results: </strong>SMPDL3B was overexpressed in LUAD tissues and cells. Knockdown of SMPLD3B significantly inhibited cell proliferation by regulating cell cycle progression and also prevented the migration and invasion of LUAD cells.</p><p><strong>Conclusion: </strong>SMPDL3B plays a role in LUAD, suggesting its potential as a therapeutic target for selective and personalized lung cancer treatment.</p>\",\"PeriodicalId\":8072,\"journal\":{\"name\":\"Anticancer research\",\"volume\":\"45 8\",\"pages\":\"3275-3286\"},\"PeriodicalIF\":1.7000,\"publicationDate\":\"2025-08-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Anticancer research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.21873/anticanres.17688\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"ONCOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Anticancer research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.21873/anticanres.17688","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"ONCOLOGY","Score":null,"Total":0}
Down-regulation of SMPDL3B Inhibits the Proliferation, Migration, and Invasion of Lung Adenocarcinoma Cells.
Background/aim: Sphingomyelin phosphodiesterase acid-like 3B (SMPDL3B) is an enzyme involved in lipid metabolism and cellular signaling. SMPDL3B expression is up-regulated in several cancers, suggesting its potential as a novel prognostic biomarker and therapeutic target for cancer treatment. However, its role in lung cancer remains unclear. In this study, we evaluated the biological role of SMPDL3B in lung cancer.
Materials and methods: SMPDL3B expression in lung adenocarcinoma (LUAD) tissues and cells was validated using quantitative real-time PCR and western blotting. To determine the role of SMPDL3B in LUAD cells, a small interfering RNA targeting SMPDL3B was used to suppress intracellular gene expression. Cell proliferation was performed using MTT and colony formation assays, and transwell assays with or without Matrigel were used to evaluate the role of SMPDL3B in LUAD cells migration and invasion.
Results: SMPDL3B was overexpressed in LUAD tissues and cells. Knockdown of SMPLD3B significantly inhibited cell proliferation by regulating cell cycle progression and also prevented the migration and invasion of LUAD cells.
Conclusion: SMPDL3B plays a role in LUAD, suggesting its potential as a therapeutic target for selective and personalized lung cancer treatment.
期刊介绍：
ANTICANCER RESEARCH is an independent international peer-reviewed journal devoted to the rapid publication of high quality original articles and reviews on all aspects of experimental and clinical oncology. Prompt evaluation of all submitted articles in confidence and rapid publication within 1-2 months of acceptance are guaranteed.
ANTICANCER RESEARCH was established in 1981 and is published monthly (bimonthly until the end of 2008). Each annual volume contains twelve issues and index. Each issue may be divided into three parts (A: Reviews, B: Experimental studies, and C: Clinical and Epidemiological studies).
Special issues, presenting the proceedings of meetings or groups of papers on topics of significant progress, will also be included in each volume. There is no limitation to the number of pages per issue.
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