{"title":"LncRNA HCP5通过miR-526b/PBX3轴促进胃癌的进展。","authors":"Guang-Chuan Mu, Xue-Yu Zeng, Chao-Zhen Hu","doi":"10.62347/IOYF4383","DOIUrl":null,"url":null,"abstract":"<p><strong>Objectives: </strong>To investigate whether LncRNA HLA complex P5 (HCP5) promotes gastric cancer (GC) via the miR-526b/Pre-B Cell Leukemia Homeobox 3 (PBX3) pathway.</p><p><strong>Methods: </strong>Thirteen paired GC and adjacent non-tumorous tissues, along with NCI-N87 GC cells, were analyzed. HCP5 expression levels were measured, and its impact on cell viability, proliferation, and migration were evaluated. Dual-luciferase reporter assays were performed to confirm the direct interactions among HCP5, miR-526b, and PBX3. The effects of HCP5 overexpression or silencing on miR-526b and PBX3 expression were analyzed. A miR-526b mimic was transfected for functional rescue.</p><p><strong>Results: </strong>HCP5 was significantly upregulated, while miR-526b was downregulated in GC tissues. Dual-luciferase assays confirmed the direct binding of HCP5 to miR-526b and of miR-526b to PBX3. In NCI-N87 cells, HCP5 overexpression downregulated miR-526b and upregulated PBX3 expression, whereas silencing HCP5 showed the opposite effects. Moreover, HCP5 overexpression decreased Bax and increased Bcl-2 levels, which was reversed by miR-526b mimic transfection. Functionally, HCP5 enhanced GC cell viability and migration, both of which were suppressed by miR-526b. HCP5 promoted cell proliferation, as evidenced by a reduced proportion of cells in the G0/G1 phase, which was reversed by miR-526b.</p><p><strong>Conclusions: </strong>HCP5 acts as an oncogenic lncRNA in GC by promoting cell viability, migration, and proliferation via the miR-526b/PBX3 axis. Targeting the HCP5/miR-526b/PBX3 axis may represent a promising therapeutic strategy for GC.</p>","PeriodicalId":7731,"journal":{"name":"American journal of translational research","volume":"17 7","pages":"5602-5613"},"PeriodicalIF":1.6000,"publicationDate":"2025-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12351625/pdf/","citationCount":"0","resultStr":"{\"title\":\"LncRNA HCP5 promotes the progression of gastric cancer through the miR-526b/PBX3 axis.\",\"authors\":\"Guang-Chuan Mu, Xue-Yu Zeng, Chao-Zhen Hu\",\"doi\":\"10.62347/IOYF4383\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objectives: </strong>To investigate whether LncRNA HLA complex P5 (HCP5) promotes gastric cancer (GC) via the miR-526b/Pre-B Cell Leukemia Homeobox 3 (PBX3) pathway.</p><p><strong>Methods: </strong>Thirteen paired GC and adjacent non-tumorous tissues, along with NCI-N87 GC cells, were analyzed. HCP5 expression levels were measured, and its impact on cell viability, proliferation, and migration were evaluated. Dual-luciferase reporter assays were performed to confirm the direct interactions among HCP5, miR-526b, and PBX3. The effects of HCP5 overexpression or silencing on miR-526b and PBX3 expression were analyzed. A miR-526b mimic was transfected for functional rescue.</p><p><strong>Results: </strong>HCP5 was significantly upregulated, while miR-526b was downregulated in GC tissues. Dual-luciferase assays confirmed the direct binding of HCP5 to miR-526b and of miR-526b to PBX3. In NCI-N87 cells, HCP5 overexpression downregulated miR-526b and upregulated PBX3 expression, whereas silencing HCP5 showed the opposite effects. Moreover, HCP5 overexpression decreased Bax and increased Bcl-2 levels, which was reversed by miR-526b mimic transfection. Functionally, HCP5 enhanced GC cell viability and migration, both of which were suppressed by miR-526b. HCP5 promoted cell proliferation, as evidenced by a reduced proportion of cells in the G0/G1 phase, which was reversed by miR-526b.</p><p><strong>Conclusions: </strong>HCP5 acts as an oncogenic lncRNA in GC by promoting cell viability, migration, and proliferation via the miR-526b/PBX3 axis. Targeting the HCP5/miR-526b/PBX3 axis may represent a promising therapeutic strategy for GC.</p>\",\"PeriodicalId\":7731,\"journal\":{\"name\":\"American journal of translational research\",\"volume\":\"17 7\",\"pages\":\"5602-5613\"},\"PeriodicalIF\":1.6000,\"publicationDate\":\"2025-07-25\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12351625/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"American journal of translational research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.62347/IOYF4383\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q3\",\"JCRName\":\"MEDICINE, RESEARCH & EXPERIMENTAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"American journal of translational research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.62347/IOYF4383","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q3","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
LncRNA HCP5 promotes the progression of gastric cancer through the miR-526b/PBX3 axis.
Objectives: To investigate whether LncRNA HLA complex P5 (HCP5) promotes gastric cancer (GC) via the miR-526b/Pre-B Cell Leukemia Homeobox 3 (PBX3) pathway.
Methods: Thirteen paired GC and adjacent non-tumorous tissues, along with NCI-N87 GC cells, were analyzed. HCP5 expression levels were measured, and its impact on cell viability, proliferation, and migration were evaluated. Dual-luciferase reporter assays were performed to confirm the direct interactions among HCP5, miR-526b, and PBX3. The effects of HCP5 overexpression or silencing on miR-526b and PBX3 expression were analyzed. A miR-526b mimic was transfected for functional rescue.
Results: HCP5 was significantly upregulated, while miR-526b was downregulated in GC tissues. Dual-luciferase assays confirmed the direct binding of HCP5 to miR-526b and of miR-526b to PBX3. In NCI-N87 cells, HCP5 overexpression downregulated miR-526b and upregulated PBX3 expression, whereas silencing HCP5 showed the opposite effects. Moreover, HCP5 overexpression decreased Bax and increased Bcl-2 levels, which was reversed by miR-526b mimic transfection. Functionally, HCP5 enhanced GC cell viability and migration, both of which were suppressed by miR-526b. HCP5 promoted cell proliferation, as evidenced by a reduced proportion of cells in the G0/G1 phase, which was reversed by miR-526b.
Conclusions: HCP5 acts as an oncogenic lncRNA in GC by promoting cell viability, migration, and proliferation via the miR-526b/PBX3 axis. Targeting the HCP5/miR-526b/PBX3 axis may represent a promising therapeutic strategy for GC.