Nucleosides, Nucleotides & Nucleic Acids最新文献

{"title":"Bioinformatics analysis of differentially expressed genes in hyperplastic scars using microarray data.","authors":"Jiayue Ding, Chun Xiang","doi":"10.1080/15257770.2025.2466427","DOIUrl":"10.1080/15257770.2025.2466427","url":null,"abstract":"<p><strong>Objective: </strong>Using DNA microarray technology, we compared the differences in mRNA expression profiles between human hypertrophic scars (HTS) and normal skin tissues. Analyzing the differential genes in bioinformatics, to explore the pathogenesis of HTS at the molecular level, and to provide new targets for clinical treatment of HTS.</p><p><strong>Methods: </strong>Three HTS samples and their adjacent normal skin samples were collected. The extraction of total RNA was performed for cDNA microarray analysis. The screening of differentially expressed genes was carried out by using Genespring 10.0 software, and cluster analysis was performed between HTS and normal skin groups within the group, and Gene Ontology (GO) and biological pathway analysis were performed for differentially expressed genes by using DAVID Bioinformatics Resources 6.7.</p><p><strong>Results: </strong>In the 3 HTS samples, 3832 mRNAs overlapped in 3 HTS samples with more than 2-fold changes, 1920 mRNAs with more than 2-fold up-regulation, 1912 mRNAs with more than 2-fold down-regulation, 18 mRNAs with more than 5-fold up-regulation, and 29 mRNAs with more than 5-fold down-regulation. The results of the GO analysis showed that CDKN1C, CDKN2A, CTNNA3, COL6A3, HOXB4 and other differentially expressed genes are closely related to biological processes such as cell cycle, cell proliferation, and cell adhesion. The kegg pathway enrichment analysis showed that TGF-β1, CDKN1C, CDKN2A, CDC14A, ITGB6, EGF and other differentially expressed genes are mainly involved in the formation of adhesion plaques, β transforming factor signaling pathways, cell cycle signaling pathways, P53 signaling pathways, and tumor-related signaling pathways.</p><p><strong>Conclusion: </strong>The mRNA expression profile of human HTS samples showed significant changes compared to normal skin samples. TGF-β1, SMAD2, SMAD7, BAX, IGF2, COL1A1, COL1A2, MMPs, CDC14A, ITGB6, EGF, CDKN1C, CDKN2A, CTNNA3, HOXA3 and other related genes involved in biological processes, molecular functions, signaling pathways may be closely related to the occurrence and development of hypertrophic scars.</p>","PeriodicalId":19343,"journal":{"name":"Nucleosides, Nucleotides & Nucleic Acids","volume":" ","pages":"379-391"},"PeriodicalIF":1.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143573348","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"miR-508-5p regulates macrophage polarization via targeting TSGA10 to promote malignant behavior in esophageal cancer cells.","authors":"Yuan Zhu, Zuojun Fu, Tianjiao Duan, Jing Wang, Lingjuan Zhang, Guisheng Liu, Xueyan Guo, Rong Zhang","doi":"10.1080/15257770.2025.2491561","DOIUrl":"10.1080/15257770.2025.2491561","url":null,"abstract":"<p><strong>Background: </strong>Esophageal cancer (EC) is among the deadliest malignancies in humans, with various miRNAs shown to regulate its progression by targeting distinct genes. miR-508-5p was identified as being linked to the malignant behavior of various tumors. Nevertheless, the precise role and mechanism of miR-508-5p in esophageal cancer (EC) remain ambiguous.</p><p><strong>Objective: </strong>This investigation focuses on the role and mechanism of the miR-508-5p/TSGA10 axis in the progression of EC.</p><p><strong>Methods: </strong>The expression of miR-508-5p and TSGA10 in EC cell lines was evaluated using quantitative Real-Time Polymerase Chain Reaction (qRT-PCR). Cell transfection techniques were used to knock down miR-508-5p and observe its effects on cell proliferation, migration, invasion, and apoptosis. A dual-luciferase reporter gene assay was conducted to verify the targeting relationship of miR-508-5p with TSGA10. Co-culture studies were undertaken to examine the regulatory effect of the miR-508-5p/TSGA10 axis on the polarization state of tumor-associated macrophages (TAMs) and the malignant behavior of EC cells.</p><p><strong>Results: </strong>The expression of miR-508-5p was significantly elevated in EC cells. Knocking down miR-508-5p curbed cell proliferation, migration, and invasion while promoting apoptosis. TSGA10 was validated as a primary target gene of miR-508-5p. miR-508-5p knockdown could inhibit the M2 polarization of TAMs by upregulating TSGA10, thereby suppressing the tumorigenic behavior of EC cells.</p><p><strong>Conclusion: </strong>miR-508-5p promotes the M2 polarization of TAMs and enhances the malignant behavior of EC cells by inhibiting TSGA10.</p>","PeriodicalId":19343,"journal":{"name":"Nucleosides, Nucleotides & Nucleic Acids","volume":" ","pages":"453-467"},"PeriodicalIF":1.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144012717","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bacteriophage-based gene delivery: a novel approach for targeted breast cancer therapy.","authors":"Dilpreet Singh","doi":"10.1080/15257770.2025.2500042","DOIUrl":"10.1080/15257770.2025.2500042","url":null,"abstract":"<p><p>Bacteriophage-based gene delivery systems are emerging as a promising alternative to traditional viral and non-viral vectors for targeted gene therapy in breast cancer. Their unique structural adaptability, low immunogenicity, and cost-effective production make them ideal candidates for precision medicine applications. Unlike conventional gene delivery platforms, bioengineered bacteriophages can be functionalized with tumor-specific ligands, modified for PEGylation to enhance circulation stability, and integrated with CRISPR/Cas9 gene-editing systems for precise genomic modifications. Additionally, bacteriophage vectors can be utilized in combination therapy, amplifying the effectiveness of chemotherapy and immunotherapy in breast cancer treatment. This mini-review discusses the bioengineering strategies used to enhance bacteriophage-based gene delivery, including surface modifications for tumor targeting, ligand-receptor binding for cellular uptake, and controlled genetic cargo release. We further examine <i>in vitro</i> and <i>in vivo</i> studies that demonstrate the potential of bacteriophage vectors in tumor suppression, gene expression efficiency, and immunomodulation. Furthermore, we explore the challenges and future directions of integrating bacteriophage-mediated gene therapy into clinical applications, addressing key issues such as systemic circulation half-life, off-target effects, and immune system interactions.</p>","PeriodicalId":19343,"journal":{"name":"Nucleosides, Nucleotides & Nucleic Acids","volume":" ","pages":"407-425"},"PeriodicalIF":1.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144032570","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LINC00365 serves as a prognostic biomarker for thyroid cancer and regulates cell proliferation, migration and invasion by targeting miR-485-5p.","authors":"Henghua Xiao, Manlong Long, Jun Yang, Qiong Luo, Lingli Hu, Fang Chen","doi":"10.1080/15257770.2025.2522350","DOIUrl":"10.1080/15257770.2025.2522350","url":null,"abstract":"<p><p>Thyroid cancer (TC) is the most prevalent form of malignancy within the endocrine system globally, and its incidence has been increasing significantly in recent years. The aim of this study was to explore the clinical role of LINC00365 in TC, and to analyze the regulatory mechanism between LINC00365 and miR-485-5p and its specific impact on TC. This study included 135 TC patients. The levels of LINC00365 in TC tissues and cells were detected by RT-qPCR. The impact of LINC00365 on TC prognosis was investigated using Kaplan-Meier curve and multivariate Cox regression analysis. Furthermore, the impact of LINC00365 on TC cell proliferation was examined <i>via</i> CCK-8 assay, while transwell assays were utilized to evaluate changes in migration and invasion capabilities. The regulatory interaction between LINC00365 and miR-485-5p was confirmed through dual-luciferase reporter assay. The expression of LINC00365 was upregulated in TC tissues and cells, and its high expression was closely related to the poor prognosis of TC patients. Kaplan-Meier curve revealed a notable correlation between elevated LINC00365 expression levels and reduced survival outcomes and multivariate Cox regression analysis revealed that elevated LINC00365 expression levels served as an independent prognostic indicator, significantly associated with adverse clinical outcomes in TC patients. In addition, LINC00365 negatively regulated the expression level of miR-485-5p. Inhibiting LINC00365 may suppress the proliferation, migration and invasion abilities of TC cells. LINC00365 may be a potential prognostic indicator for TC, and LINC00365 may promote tumor growth and metastasis of TC by inhibiting miR-485-5p expression.</p>","PeriodicalId":19343,"journal":{"name":"Nucleosides, Nucleotides & Nucleic Acids","volume":" ","pages":"802-815"},"PeriodicalIF":1.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144497558","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Upregulation of miR-1266-5p serves as a prognostic biomarker of triple-negative breast cancer and facilitates tumor cell proliferation, migration and invasion.","authors":"Linmei Lin, Wanqi Lin, Yi Zheng","doi":"10.1080/15257770.2025.2551833","DOIUrl":"10.1080/15257770.2025.2551833","url":null,"abstract":"<p><strong>Background: </strong>Triple-negative breast cancer (TNBC) is an aggressive subtype characterized by a poor prognosis. MicroRNAs (miRNAs) play a crucial regulatory role in tumorigenesis, but the specific function and mechanism of miR-1266-5p in TNBC remain unclear.</p><p><strong>Methods: </strong>This study included 118 TNBC patients, from whom both tumor and adjacent normal tissues were collected. The expression of miR-1266-5p was determined, and its association with clinicopathological features and patient prognosis was evaluated. Functional experiments were conducted using TNBC cell lines (MDA-MB-231, MDA-MB-468), assessing the impact of miR-1266-5p on cellular processes. Bioinformatics tools and dual-luciferase reporter assays were employed to identify and validate the target gene of miR-1266-5p.</p><p><strong>Results: </strong>miR-1266-5p was upregulated in TNBC tissues and cells (<i>p</i> < 0.05), and its high expression was associated with lymph node metastasis, higher histological grade, and advanced TNM stage. Kaplan-Meier analysis revealed that patients with high miR-1266-5p expression had shorter overall survival, and it was an independent prognostic factor. Functional experiments demonstrated that overexpression of miR-1266-5p significantly promoted TNBC cell proliferation, migration, and invasion (<i>p</i> < 0.05), while knockdown suppressed these phenotypes. Bioinformatics analysis and dual-luciferase assays identified MKRN1 as a direct target of miR-1266-5p.</p><p><strong>Conclusion: </strong>miR-1266-5p promotes tumor progression in TNBC by targeting MKRN1. Its high expression correlates with poor patient outcomes, suggesting that it may serve as a promising biomarker for prognosis and a potential therapeutic target in TNBC.</p>","PeriodicalId":19343,"journal":{"name":"Nucleosides, Nucleotides & Nucleic Acids","volume":" ","pages":"954-966"},"PeriodicalIF":1.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145138124","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"miR-34c-3p targets FOXO3 to promote pancreatic carcinoma progression.","authors":"Zhenxiong Xie, Lin Ji, Fang Wu, Hui Cao","doi":"10.1080/15257770.2025.2537167","DOIUrl":"10.1080/15257770.2025.2537167","url":null,"abstract":"<p><p>MicroRNAs (miRNAs) have been a popular subject of tumor research including pancreatic carcinoma (PC). MicroRNA-34c-3p (miR-34c-3p) is a member of miR-34c cluster, which is strongly associated with tumorigenesis. Nonetheless, miR-34c-3p has not been explored in PC. MiR-34c-3p was taken as a target to explore its current clinical significance and related molecular mechanisms in PC. Real-time quantitative polymerase chain reaction (RT-qPCR) was employed to monitor miR-34c-3p and FOXO3 level in tissues and PC cells. Dual-Luciferase reporter assay was utilized to verifying the relationship between miR-34c-3p and FOXO3. Cell Counting Kit-8 (CCK-8) and Transwell assay were applied to detect cell proliferation, migration and invasion. MiR-34c-3p was markedly elevated in PC tissues and closely related with lymph node metastasis, post-treatment nodal margin category and degree of differentiation. MiR-34c-3p upregulation could predict poorer prognosis and higher risk of PC patients. In PC cells, overexpression of miR-34c-3p enhanced cell proliferation, migration and invasion. Moreover, miR-34c-3p negatively regulated FOXO3 to promote cellular processes. High level of miR-34c-3p is a poor prognostic factor for PC patients and miR-34c-3p promotes tumor progression by negatively regulating FOXO3.</p>","PeriodicalId":19343,"journal":{"name":"Nucleosides, Nucleotides & Nucleic Acids","volume":" ","pages":"927-939"},"PeriodicalIF":1.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144732431","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting c-Myc with antisense oligonucleotides to induce apoptosis in tumor cells.","authors":"Yuemei Ye, Yanhui Wang, Zhaoyun Zong, Shiyu Chen","doi":"10.1080/15257770.2025.2542835","DOIUrl":"10.1080/15257770.2025.2542835","url":null,"abstract":"<p><p>Transcription factors (TFs) play a crucial role in tumorigenesis by driving oncogene expression in key signaling pathways. However, their small size and flat surfaces make them challenging targets for small-molecule inhibitors, while macromolecular therapies struggle to cross the cell membrane. Modulating TF activity at the genetic level offers a promising alternative. Antisense oligonucleotides (ASOs), which regulate protein expression by targeting mRNA, have emerged as effective therapeutics for previously undruggable proteins, including TFs. Over the past two decades, ASO therapeutics have advanced significantly, demonstrating long-lasting efficacy by promoting mRNA degradation. c-Myc, a key regulator of oncogene expression, drives cancer cell growth and proliferation but remains undruggable due to its nuclear localization and dynamic structure. In this study, we utilized our ASO development platform to design ASOs targeting c-Myc. Our sequence optimization algorithm achieved high accuracy, with one of three designed ASOs successfully silencing c-Myc. <i>Ex vivo</i> validation showed that ASO3 inhibited A549 cell growth with an IC₅₀ of 152.5 nM. At the molecular level, ASO3 significantly reduced both c-Myc mRNA and protein expression. Functional assays, including trypan blue exclusion assay and CCK-8, confirmed that ASO3 decreased cell viability, suppressed proliferation, and induced apoptosis. These findings highlight ASO3's therapeutic potential and support further investigation as an anti-cancer agent targeting c-Myc.</p>","PeriodicalId":19343,"journal":{"name":"Nucleosides, Nucleotides & Nucleic Acids","volume":" ","pages":"1030-1053"},"PeriodicalIF":1.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144822145","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Selective serotonin reuptake inhibitors modulate adenylate homeostasis and redox status in human endothelial cells.","authors":"Jakub Jarczewski, Patryk T Mucha, Sylwester Dumała, Marta Tomczyk","doi":"10.1080/15257770.2026.2699383","DOIUrl":"10.1080/15257770.2026.2699383","url":null,"abstract":"<p><p>Major depressive disorder is increasingly prevalent, and selective serotonin reuptake inhibitors (SSRIs) remain first-line pharmacotherapy. Beyond their canonical neuronal mechanism, attention has turned to potential off-target effects in peripheral tissues. Because serotonergic transport and receptor pathways have been described in vascular endothelial models, SSRIs could directly modulate vascular pathways. Thus, this study investigated the effects of 24-h exposure to selected SSRIs, including sertraline, fluoxetine, and paroxetine, on bioenergetics, redox status, extracellular purine handling, and endothelial activation markers in human microvascular endothelial cells (HMEC-1). SSRI exposure did not change total intracellular adenosine triphosphate (ATP), but consistently reduced adenosine diphosphate (ADP), resulting in higher ATP/ADP ratios and increased adenylate energy charge. Sertraline and fluoxetine reduced nicotinamide adenine dinucleotide (NADH) and basal reactive oxygen species (ROS) formation, whereas the NADH/NAD⁺ ratio was reduced after paroxetine and fluoxetine treatment. In the extracellular purine profiling, sertraline uniquely accelerated the degradation of ATP and adenosine monophosphate (AMP). Assessment of adhesion molecules by immunocytochemistry indicated divergent effects on endothelial activation markers, with fluoxetine decreasing intercellular adhesion molecule-1 (ICAM-1) and paroxetine increasing vascular cell adhesion molecule-1 (VCAM-1). Collectively, these findings suggest that SSRIs can modulate endothelial energy/redox balance and purinergic signaling in a compound-dependent manner and support further validation in primary and multicellular vascular models.</p>","PeriodicalId":19343,"journal":{"name":"Nucleosides, Nucleotides & Nucleic Acids","volume":" ","pages":"1191-1202"},"PeriodicalIF":1.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148422382","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel Nilotinib derivative N-12 inhibits the proliferation and migration of colon cancer cells through the EMT signaling pathway.","authors":"Zirui Jiang, Xiaoqing Ye, Mengwei Song, Yue Qiao, Wenhao Cheng, Dan Wang, Xingyu Zhang, Xiuming Li, Xudong Yu, Xiujun Wang, Jing Ji, Yi Mou","doi":"10.1080/15257770.2025.2473437","DOIUrl":"10.1080/15257770.2025.2473437","url":null,"abstract":"<p><p>Colon cancer ranks among the prevalent malignancies globally, and its proclivity for metastasis significantly contributes to the adverse prognostic outcomes observed in patients. The epithelial-mesenchymal transition (EMT) represents a critical biological process through which tumor cells gain migratory and invasive capabilities. Nilotinib is a selective inhibitor of tyrosine kinases, commonly utilized in the treatment of chronic myeloid leukemia. Prior investigations have demonstrated that the Nilotinib derivative, N-12, exhibits significant antitumor properties. The objective of this study is to elucidate the inhibitory effects of N-12 on the progression of EMT in colon cancer cells. So, the human colon cancer cell line HCT116 and SW480 were selected for experimentation. Initially, assessments of cell proliferation, migration and invasion were conducted utilizing MTT, colony formation, Edu and Transwell assays. Subsequently, the chick embryo chorioallantoic membrane model was employed to evaluate tumor size and its impact on angiogenesis in vivo. Thereafter, HCT116 cells treated with N-12 underwent RNA sequencing for analysis. Finally, the expression levels of EMT markers in colon cancer cells were determined by Western blot analysis. The results showed that N-12 significantly curtails the proliferation, migration, and invasion of colon cancer cells, and concurrently impedes tumor growth in vivo by influencing angiogenesis within the chick embryo chorioallantoic membrane. Furthermore, RNA sequencing and Western blot analyses have elucidated that the antitumor efficacy of N-12 is attributable to the inhibition of the EMT signaling pathway. These results underscore the therapeutic potential of N-12 in the management of colon cancer and delineate its mechanism of action.</p>","PeriodicalId":19343,"journal":{"name":"Nucleosides, Nucleotides & Nucleic Acids","volume":" ","pages":"64-87"},"PeriodicalIF":1.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143542812","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LncRNA PGM5-AS1 inhibits the progression of breast cancer by inhibiting miR-182-5p.","authors":"Yonghui Zhang, Mingxi Chen, Xuan Zheng, Kejia Li, Zhi Li, Xuelian Li","doi":"10.1080/15257770.2025.2498642","DOIUrl":"10.1080/15257770.2025.2498642","url":null,"abstract":"<p><p>LncRNAs serve as crucial regulators in the survival and proliferation of tumors. This study is dedicated to exploring the functional significance of lncRNA PGM5-AS1 in breast cancer (BRCA). First, the expression level of PGM5-AS1 in BRCA patients and its diagnostic ability for BRCA were analyzed by RT-qPCR and Receiver Operating Characteristic curve. Subsequently, LnCAR database was used to preliminarily explore the relationship between PGM5-AS1 and prognosis. Moreover, we investigated the effects PGM5-AS1 on proliferation, apoptosis, and migration of BRCA cells by MTT assay, flow cytometry, and Transwell assay. More importantly, the regulation effect of PGM5-AS1 on the downstream target miR-182-5p was verified by dual luciferase reporting experiment, and the role of miR-182-5p was further explored <i>in vitro</i> experiments. PGM5-AS1 is significantly decreased in both BRCA patients and BRCA cell lines. In the diagnosis of BRCA, the sensitivity and specificity of PGM5-AS1 were 81.5% and 78.5%. Furthermore, lower levels of PGM5-AS1 are associated with a poor prognosis for affected patients. <i>In vitro</i> studies demonstrate that the upregulation of PGM5-AS1 confers a protective effect against BRCA, markedly inhibiting the viability and migratory capacity of tumor cells. More importantly, overexpression of PGM5-AS1 inhibited the high expression of miR-182-5p in tumor cells. In fact, inhibition of miR-182-5p is detrimental to the proliferation and migration of BRCA cells <i>in vitro</i>. lncRNA PGM5-AS1 has potential as a diagnostic marker for BRCA and acts as an inhibitor in BRCA. It inhibits tumor proliferation and metastasis by targeting miR-182-5p.</p>","PeriodicalId":19343,"journal":{"name":"Nucleosides, Nucleotides & Nucleic Acids","volume":" ","pages":"468-481"},"PeriodicalIF":1.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144013236","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}