Yameng Liu, Yue Zhao, Jingjing Zhang, Xiao Wu, Yumei Li, Ke Tang, Zhengquan Han
{"title":"OPN3通过调控TGF-β信号通路促进三阴性乳腺癌细胞的增殖、迁移和侵袭。","authors":"Yameng Liu, Yue Zhao, Jingjing Zhang, Xiao Wu, Yumei Li, Ke Tang, Zhengquan Han","doi":"10.21037/tcr-24-1374","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong><i>Opsin3</i> (<i>OPN3</i>) belongs to the guanine nucleotide-binding protein-coupled receptor superfamily, implicated in several pathological mechanisms that contribute to tumor development and resistance to treatment. This study examined <i>OPN3</i> expression in triple-negative breast cancer (TNBC) tissues and its function in TNBC cell propagation, invasion, and migration.</p><p><strong>Methods: </strong>The study analyzed OPN3 expression in TNBC patients and its diagnostic value using immunohistochemistry (IHC) staining and The Cancer Genome Atlas (TCGA) data. To evaluate the impact of <i>OPN3</i> on the growth, invasion, and migration of TNBC cells, both <i>in</i> <i>vitro</i> and <i>in</i> <i>vivo</i> experiments were carried out. The biological mechanisms of <i>OPN3</i>-induced cell migration and invasion were evaluated <i>via</i> quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting (WB) analyses.</p><p><strong>Results: </strong>In this study, <i>OPN3</i> upregulation in TNBC tissues was found to be correlated with decreased overall survival (OS) and progression-free survival (PFS) rates. The propagation, invasion, and migration of BT-549 cells were promoted and apoptosis was reduced after <i>OPN3</i> overexpression. It was silenced in BT-549 cells, which resulted in the opposite effects. Further, the transforming growth factor-beta (TGF-β)/SMAD2 signaling pathway was stimulated and the epithelial-mesenchymal transition (EMT) was modulated by <i>OPN3</i> overexpression in BT-549 cells.</p><p><strong>Conclusions: </strong>The findings revealed that <i>OPN3</i> is involved in the stimulation of the TGF-β/SMAD2 signaling pathway, which promotes the growth, migration, and dissemination of TNBC cells. Moreover, <i>OPN3</i> can serve as a diagnostic biomarker and a treatment target for TNBC.</p>","PeriodicalId":23216,"journal":{"name":"Translational cancer research","volume":"14 2","pages":"1141-1156"},"PeriodicalIF":1.5000,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11912049/pdf/","citationCount":"0","resultStr":"{\"title\":\"<i>OPN3</i> enhances the proliferation, migration, and invasion of triple-negative breast cancer cells via the regulation of the TGF-β signaling pathway.\",\"authors\":\"Yameng Liu, Yue Zhao, Jingjing Zhang, Xiao Wu, Yumei Li, Ke Tang, Zhengquan Han\",\"doi\":\"10.21037/tcr-24-1374\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong><i>Opsin3</i> (<i>OPN3</i>) belongs to the guanine nucleotide-binding protein-coupled receptor superfamily, implicated in several pathological mechanisms that contribute to tumor development and resistance to treatment. This study examined <i>OPN3</i> expression in triple-negative breast cancer (TNBC) tissues and its function in TNBC cell propagation, invasion, and migration.</p><p><strong>Methods: </strong>The study analyzed OPN3 expression in TNBC patients and its diagnostic value using immunohistochemistry (IHC) staining and The Cancer Genome Atlas (TCGA) data. To evaluate the impact of <i>OPN3</i> on the growth, invasion, and migration of TNBC cells, both <i>in</i> <i>vitro</i> and <i>in</i> <i>vivo</i> experiments were carried out. The biological mechanisms of <i>OPN3</i>-induced cell migration and invasion were evaluated <i>via</i> quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting (WB) analyses.</p><p><strong>Results: </strong>In this study, <i>OPN3</i> upregulation in TNBC tissues was found to be correlated with decreased overall survival (OS) and progression-free survival (PFS) rates. The propagation, invasion, and migration of BT-549 cells were promoted and apoptosis was reduced after <i>OPN3</i> overexpression. It was silenced in BT-549 cells, which resulted in the opposite effects. Further, the transforming growth factor-beta (TGF-β)/SMAD2 signaling pathway was stimulated and the epithelial-mesenchymal transition (EMT) was modulated by <i>OPN3</i> overexpression in BT-549 cells.</p><p><strong>Conclusions: </strong>The findings revealed that <i>OPN3</i> is involved in the stimulation of the TGF-β/SMAD2 signaling pathway, which promotes the growth, migration, and dissemination of TNBC cells. Moreover, <i>OPN3</i> can serve as a diagnostic biomarker and a treatment target for TNBC.</p>\",\"PeriodicalId\":23216,\"journal\":{\"name\":\"Translational cancer research\",\"volume\":\"14 2\",\"pages\":\"1141-1156\"},\"PeriodicalIF\":1.5000,\"publicationDate\":\"2025-02-28\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11912049/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Translational cancer research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.21037/tcr-24-1374\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/2/26 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q4\",\"JCRName\":\"ONCOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Translational cancer research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.21037/tcr-24-1374","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/2/26 0:00:00","PubModel":"Epub","JCR":"Q4","JCRName":"ONCOLOGY","Score":null,"Total":0}
OPN3 enhances the proliferation, migration, and invasion of triple-negative breast cancer cells via the regulation of the TGF-β signaling pathway.
Background: Opsin3 (OPN3) belongs to the guanine nucleotide-binding protein-coupled receptor superfamily, implicated in several pathological mechanisms that contribute to tumor development and resistance to treatment. This study examined OPN3 expression in triple-negative breast cancer (TNBC) tissues and its function in TNBC cell propagation, invasion, and migration.
Methods: The study analyzed OPN3 expression in TNBC patients and its diagnostic value using immunohistochemistry (IHC) staining and The Cancer Genome Atlas (TCGA) data. To evaluate the impact of OPN3 on the growth, invasion, and migration of TNBC cells, both invitro and invivo experiments were carried out. The biological mechanisms of OPN3-induced cell migration and invasion were evaluated via quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting (WB) analyses.
Results: In this study, OPN3 upregulation in TNBC tissues was found to be correlated with decreased overall survival (OS) and progression-free survival (PFS) rates. The propagation, invasion, and migration of BT-549 cells were promoted and apoptosis was reduced after OPN3 overexpression. It was silenced in BT-549 cells, which resulted in the opposite effects. Further, the transforming growth factor-beta (TGF-β)/SMAD2 signaling pathway was stimulated and the epithelial-mesenchymal transition (EMT) was modulated by OPN3 overexpression in BT-549 cells.
Conclusions: The findings revealed that OPN3 is involved in the stimulation of the TGF-β/SMAD2 signaling pathway, which promotes the growth, migration, and dissemination of TNBC cells. Moreover, OPN3 can serve as a diagnostic biomarker and a treatment target for TNBC.
期刊介绍：
Translational Cancer Research (Transl Cancer Res TCR; Print ISSN: 2218-676X; Online ISSN 2219-6803; http://tcr.amegroups.com/) is an Open Access, peer-reviewed journal, indexed in Science Citation Index Expanded (SCIE). TCR publishes laboratory studies of novel therapeutic interventions as well as clinical trials which evaluate new treatment paradigms for cancer; results of novel research investigations which bridge the laboratory and clinical settings including risk assessment, cellular and molecular characterization, prevention, detection, diagnosis and treatment of human cancers with the overall goal of improving the clinical care of cancer patients. The focus of TCR is original, peer-reviewed, science-based research that successfully advances clinical medicine toward the goal of improving patients'' quality of life. The editors and an international advisory group of scientists and clinician-scientists as well as other experts will hold TCR articles to the high-quality standards. We accept Original Articles as well as Review Articles, Editorials and Brief Articles.
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