南方医科大学学报杂志最新文献

{"title":"[Layered double hydroxide-loaded si-NEAT1 regulates paclitaxel resistance and tumor-associated macrophage polarization in breast cancer by targeting miR-133b/PD-L1].","authors":"Zhaojun Zhang, Qiong Wu, Miaomiao Xie, Ruyin Ye, Chenchen Geng, Jiwen Shi, Qingling Yang, Wenrui Wang, Yurong Shi","doi":"10.12122/j.issn.1673-4254.2025.08.16","DOIUrl":"10.12122/j.issn.1673-4254.2025.08.16","url":null,"abstract":"<p><strong>Objectives: </strong>To study the molecular mechanisms of LDH-loaded si-NEAT1 for regulating paclitaxel resistance and tumor-associated macrophage (TAM) polarization in breast cancer.</p><p><strong>Methods: </strong>qRT-PCR and Western blotting were used to detect the expression of lncRNA NEAT1, miR-133b, and PD-L1 in breast cancer SKBR3 cells and paclitaxel-resistant SKBR3 cells (SKBR3-PR). The effects of transfection with si-NEAT1 and miR-133b mimics on MRP, MCRP and PD-L1 expressions and cell proliferation, migration and apoptosis were investigated using qRT-PCR, Western blotting, scratch and Transwell assays, and flow cytometry. Rescue experiments were conducted using si-NEAT1 and miR-133b inhibitor. Human THP-1 macrophages were cultured in the presence of conditioned media (CM) derived from SKBR3 and SKBR3-PR cells with or with si-NEAT1 transfection for comparison of IL-4-induced macrophage polarization by detecting the surface markers. LDH@si-NEAT1 nanocarriers were constructed, and their effects on MRP, MCRP and PD-L1 expressions and cell behaviors of the tumor cells were examined. THP-1 cells were treated with the CM from LDH@si-NEAT1-treated tumor cells, and the changes in their polarization were assessed.</p><p><strong>Results: </strong>SKBR3-PR cells showered significantly upregulated NEAT1 and PD-L1 expressions and lowered miR-133b expression as compared with their parental cells. Transfection with si-NEAT1 and miR-133b mimics inhibited viability, promoted apoptosis and enhanced MRP and BCRP expressions in SKBR3-PR cells. NEAT1 knockdown obvious upregulated miR-133b and downregulated PD-L1, MRP and BCRP expressions. The CM from SKBR3-PR cells obviously promoted M2 polarization of THP-1 macrophages, which was significantly inhibited by CM from si-NEAT1-transfected cells. Treatment with LDH@si-NEAT1 effectively inhibited migration and invasion, promoted apoptosis, and reduced MRP, BCRP and PD-L1 expressions in the tumor cells. The CM from LDH@si-NEAT1-treated SKBR3-PR cells significantly downregulated Arg-1, CD163, IL-10, and PD-L1 and upregulated miR-133b expression in THP-1 macrophages.</p><p><strong>Conclusions: </strong>LDH@si-NEAT1 reduces paclitaxel resistance of breast cancer cells and inhibits TAM polarization by targeting the miR-133b/PD-L1 axis.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 8","pages":"1718-1731"},"PeriodicalIF":0.0,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12415571/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015901","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Electroacupuncture combined with rehabilitation training improves neurological function of mice with cerebral ischemia by promoting astrocyte transdifferentiation].","authors":"Dongning Tang, Yunyun Kang, Wenjie He, Qing Xia","doi":"10.12122/j.issn.1673-4254.2025.07.09","DOIUrl":"10.12122/j.issn.1673-4254.2025.07.09","url":null,"abstract":"<p><strong>Objectives: </strong>To explore the effects of acupuncture combined with rehabilitation training for promoting transdifferentiation of astrocytes into neurons in mice after cerebral ischemia.</p><p><strong>Methods: </strong>Male C57/BL6J mice were subjected to intracerebral microinjection of an adeno-associated virus carrying the GFAP promoter for NeuroD1 and Ngn2 overexpression in the astrocytes, followed 3 or 12 days later by electrocoagulation of the distal middle cerebral artery. After modeling, the mice were randomly divided into model group without interventions and intervention group treated with electroacupuncture at the acupoints Baihui (GV20), left Hegu (LI4), Neiguan (PC6), Zusanli (ST36), and Yanglingquan (GB34) 24 h after surgery. The mice in the intervention group were housed individually in cages with running wheels, and their activity was recorded every 24 h. Neurological function scores of the mice were assessed on the 1st, 14th, and 21st days after modeling. Transdifferentiation of astrocytes in the target brain regions was observed using double immunofluorescence staining.</p><p><strong>Results: </strong>Compared with those in the model group, the mice receiving eletroacupuncture and rehabilitation training showed significant improvement of neurological deficits at 14 and 21 days after modeling. The GFAP promoter of the AAV2/5 vector specifically labeled the local astrocytes, and compared with that that in the model group, the number of AAV-positive cells colabeled with the neuronal marker DCX significantly increased after 14 days of electroacupuncture and rehabilitation intervention, and the number of AAV-positive cells colabeled with the neuronal marker NeuN significantly increased after 21 days of intervention.</p><p><strong>Conclusions: </strong>In mice with cerebral ischemia, electroacupuncture and rehabilitation training can promote transdifferentiation of astrocytes into neurons in the ischemic brain region, and the efficiency of transdifferentiation is positively correlated with the improvement of motor function.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 7","pages":"1434-1441"},"PeriodicalIF":0.0,"publicationDate":"2025-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12268914/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144649952","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[High PRELID1 expression promotes epithelial-mesenchymal transition in gastric cancer cells and is associated with poor prognosis].","authors":"Xuan Wu, Jiamin Fang, Weiwei Han, Lin Chen, Jing Sun, Qili Jin","doi":"10.12122/j.issn.1673-4254.2025.07.21","DOIUrl":"10.12122/j.issn.1673-4254.2025.07.21","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the correlation of PRELID1 with gastric cancer (GC) progression, prognosis, and epithelial-mesenchymal transition (EMT) and the underlying mechanisms.</p><p><strong>Methods: </strong>We analyzed the data of 115 patients undergoing radical gastrectomy for GC in our hospital between February, 2018 and March, 2023 to explore the correlation of PRELID1 expression level in GC tissues with tumor progression and patient prognosis. In cultured GC cells, the effects of lentivirus-mediated overexpression or interference of PRELID1 were observed on cell migration, invasion and EMT.</p><p><strong>Results: </strong>Immunohistochemical staining revealed significantly higher PRELID1 expression in GC tissues (<i>P</i><0.001), whose expression level was positively correlated with CEA ≥5 ng/mL (<i>P</i>=0.007), CA199 ≥37 U/mL (<i>P</i>=0.007), G_3-4 stages (<i>P</i>=0.001), T_3-4 stages (<i>P</i>=0.001), and N_2-3 stages (<i>P</i>=0.020). Univariate and Cox multifactorial analysis showed that high PRELID1 level was an independent risk factor affecting 5-year survival of GC patients (<i>P</i>=0.001). In cultured GC cells, PRELID1 overexpression obviously promoted cell proliferation, migration, invasion, and the expressions of MMP2 and MMP9, and interference of PRELID1 produced the opposite changes. PRELID1 overexpression also increased the expressions of N-cadherin and vimentin and reduced the expression of E-cadherin. Mechanistic analyses showed that up-regulation of PRELID1 increased the expression of p-PI3K, p-AKT, and p-mTOR in GC cells, whereas its interference caused the opposite changes; the application of 740 Y-P, a PI3K/AKT pathway activator, significantly enhanced the migration, invasion, and EMT of GC cells with PRELID1 knockdown.</p><p><strong>Conclusions: </strong>PRELID1 is highly expressed in GC and affects prognosis of the patients, and its high expression promotes migration, invasion and epithelial mesenchymal transition of GC cells possibly by activating the PI3K/AKT/mTOR pathway.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 7","pages":"1535-1542"},"PeriodicalIF":0.0,"publicationDate":"2025-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12268903/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144649956","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Live combined <i>Bacillus subtilis</i> and <i>Enterococcus faecium</i> improves glucose and lipid metabolism in type 2 diabetic mice with circadian rhythm disruption via the SCFAs/GPR43/GLP-1 pathway].","authors":"Ruimin Han, Manke Zhao, Junfang Yuan, Zhenhong Shi, Zhen Wang, Defeng Wang","doi":"10.12122/j.issn.1673-4254.2025.07.15","DOIUrl":"10.12122/j.issn.1673-4254.2025.07.15","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the effects of live combined <i>Bacillus subtilis</i> and <i>Enterococcus faecium</i> (LCBE) on glucose and lipid metabolism in mice with type 2 diabetes mellitus (T2DM) and circadian rhythm disorder (CRD) and explore the possible mechanisms.</p><p><strong>Methods: </strong>KM mice were randomized into normal diet (ND) group (<i>n</i>=8), high-fat diet (HFD) group (<i>n</i>=8), and rhythm-intervention with HFD group (<i>n</i>=16). After 8 weeks of feeding, the mice were given an intraperitoneal injection of streptozotocin (100 mg/kg) to induce T2DM. The mice in CRD-T2DM group were further randomized into two equal groups for treatment with LCBE (225 mg/kg) or saline by gavage; the mice in ND and HFD groups also received saline gavage for 8 weeks. Blood glucose level of the mice was measured using a glucometer, and serum levels of Bmal1, PER2, insulin, C-peptide and lipids were determined with ELISA. Colon morphology and hepatic lipid metabolism of the mice were examined using HE staining and Oil Red O staining, respectively, and fecal short-chain fatty acids (SCFAs) was detected using LC-MS; GPR43 and GLP-1 expression levels were analyzed using RT-qPCR and Western blotting.</p><p><strong>Results: </strong>Compared with those in CRD-T2DM group, the LCBE-treated mice exhibited significant body weight loss, lowered levels of PER2, insulin, C-peptide, total cholesterol (TC) and LDL-C, and increased levels of Bmal1 and HDL-C levels. LCBE treatment significantly increased SCFAs, upregulated GPR43 and GLP-1 expressions at both the mRNA and protein levels, and improved hepatic steatosis and colon histology.</p><p><strong>Conclusions: </strong>LCBE ameliorates lipid metabolism disorder in CRD-T2DM mice by reducing body weight and improving lipid profiles and circadian regulators possibly via the SCFAs/GPR43/GLP-1 pathway.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 7","pages":"1490-1497"},"PeriodicalIF":0.0,"publicationDate":"2025-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12268902/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144649958","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[The peptide toxin components and nucleotide metabolites in <i>Macrothele raveni</i> venom synergistically inhibit cancer cell proliferation by activating the pro-apoptotic pathways].","authors":"Ting Xie, Yunyun Wang, Ting Guo, Chunhua Yuan","doi":"10.12122/j.issn.1673-4254.2025.07.12","DOIUrl":"10.12122/j.issn.1673-4254.2025.07.12","url":null,"abstract":"<p><strong>Objectives: </strong>To evaluate the inhibitory effect of <i>Macrothele raveni</i> crude venom against proliferation of different cancer cells and identify the active components in the venom.</p><p><strong>Methods: </strong>Different cancer cell lines were treated with different concentrations of <i>Macrothele raveni</i> venom for 48 h, and cell proliferation and the half-maximal inhibitory concentrations (IC₅₀) of the venom were assessed with CCK-8 assay. The apoptosis rate of breast cancer MCF7 cells following the treatment was analyzed with flow cytometry, and the changes in cellular caspase-8 and caspase-9 expressions were detected. The crude venom was separated into protein, peptide, and small-molecule compound fractions using gel filtration chromatography and high-performance liquid chromatography (HPLC). The protein and peptide components were identified using proteomics analysis, and small-molecule compounds were structurally characterized using nuclear magnetic resonance (NMR), mass spectrometry (MS), and HPLC.</p><p><strong>Results: </strong>The crude venom exhibited strong concentration-dependent inhibitory effects on proliferation of MCF7 cells and nasopharyngeal carcinoma SUNE1 and HONE1 cells (IC₅₀ of 2.14±0.29, 1.57±0.14, and 2.85±0.15 µg/mL, respectively), with less potent inhibitory effects in gastric cancer HGC27 cells and colorectal cancer SW620 cells (IC₅₀ of 3.02±0.27 and 3.02±0.28 µg/mL, respectively). The crude venom significantly promoted MCF7 cell apoptosis likely <i>via</i> the caspase 8 signaling pathway. The protein fraction from the crude venom showed a weak inhibitory effect in MCF7 cells, whereas the peptide fraction exhibited a much stronger inhibitory effect (IC₅₀ of 6.41±0.31 µg/mL). The peptides in the peptide fraction, with relative molecular mass around 10 000, were homologous to those found in <i>Macrothele gigas</i> venom. The small-molecule fraction consisted mainly of nucleotide metabolites without obvious inhibitory effects in MCF7 cells, but its combination with the peptide fraction showed significantly enhanced inhibitory activity. C<b>onclusion</b> The inhibitory effects of <i>Macrothele raveni</i> venom, which vary significantly across different cancer cell lines, are attributed primarily to its peptide components, which may act synergistically with the nucleotide metabolites.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 7","pages":"1460-1470"},"PeriodicalIF":0.0,"publicationDate":"2025-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12268906/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144649965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[The TGF‑β/miR-23a-3p/IRF1 axis mediates immune escape of hepatocellular carcinoma by inhibiting major histocompatibility complex class I].","authors":"Ying Yu, Li Tu, Yang Liu, Xueyi Song, Qianqian Shao, Xiaolong Tang","doi":"10.12122/j.issn.1673-4254.2025.07.06","DOIUrl":"10.12122/j.issn.1673-4254.2025.07.06","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the mechanism by which transforming growth factor‑β (TGF‑β) regulates major histocompatibility complex class I (MHC-I) expression in hepatocellular carcinoma (HCC) cells and its role in immune evasion of HCC.</p><p><strong>Methods: </strong>HCC cells treated with TGF‑β alone or in combination with SB-431542 (a TGF-β type I receptor inhibitor) were examined for changes in MHC-I expression using RT-qPCR and Western blotting. A RNA interference experiment was used to explore the role of miR-23a-3p/IRF1 signaling in TGF‑β‑mediated regulation of MHC-I. HCC cells with different treatments were co-cultured with human peripheral blood mononuclear cells (PBMCs), and the changes in HCC cell proliferation was assessed using CCK-8 and colony formation assays. T-cell cytotoxicity in the co-culture systems was assessed with lactate dehydrogenase (LDH) release and JC-1 mitochondrial membrane potential assays, and T-cell activation was evaluated by flow cytometric analysis of CD69 cells and ELISA for TNF-α secretion.</p><p><strong>Results: </strong>TGF‑β treatment significantly suppressed MHC-I expression in HCC cells and reduced T-cell activation, leading to increased tumor cell proliferation and decreased HCC cell death in the co-culture systems. Mechanistically, TGF-β upregulated miR-23a-3p, which directly targeted IRF1 to inhibit MHC-I transcription. Overexpression of miR-23a-3p phenocopied TGF‑β‑induced suppression of IRF1 and MHC-I.</p><p><strong>Conclusions: </strong>We reveal a novel immune escape mechanism of HCC, in which TGF‑β attenuates T cell-mediated antitumor immunity by suppressing MHC-I expression through the miR-23a-3p/IRF1 signaling axis.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 7","pages":"1397-1408"},"PeriodicalIF":0.0,"publicationDate":"2025-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12268904/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144649966","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Therapeutic mechanism of hederagenin, an active component in <i>Guizhi Fuling</i> Pellets, against cervical cancer in nude mice].","authors":"Yinfu Zhu, Yiran Li, Yi Wang, Yinger Huang, Kunxiang Gong, Wenbo Hao, Lingling Sun","doi":"10.12122/j.issn.1673-4254.2025.07.08","DOIUrl":"10.12122/j.issn.1673-4254.2025.07.08","url":null,"abstract":"<p><strong>Objectives: </strong>To explore the therapeutic mechanism of <i>Guizhi Fuling</i> (GZFL) Pellets against cervical cancer.</p><p><strong>Methods: </strong>Publicly available databases were used to identify the targets of GZFL Pellets and cervical cancer to construct the protein-protein interaction (PPI) network, followed by GO biological process and KEGG pathway enrichment analysis of the hub genes. The \"Traditional Chinese Medicine-Active Ingredients-Targets-Pathways\" network for GZFL Pellets in cervical cancer treatment was generated using Cytoscape v10.0.0, and molecular docking of the drug and potential targets was performed to predict the specific targets of active components in <i>Guizhi Fuling</i> Pellets. The inhibitory effects of hederagenin, an active ingredient in GZFL Pellets, was tested in cultured cervical cancer cells and in nude mice bearing cervical cancer xenografts.</p><p><strong>Results: </strong>GZFL Pellets contain 338 active components targeting 247 action sites. A total of 10127 cervical cancer-related targets were obtained, and among them 195 were identified as potential therapeutic targets of GZFL Pellets for cervical cancer treatment, including the key targets of GABRA1, PTK2, JAK2, HTR3A, GSR, and IL-17. Molecular docking study showed low binding energies of the active components such as hederagenin, campesterol, and stigmasterol for protein-molecule interaction. GO enrichment analysis suggested that GZFL Pellets inhibited cervical cancer primarily by regulating responses to steroid hormones, oxidative stress, and lipopolysaccharides. Among the active components of GZFL Pellets, hederagenin was found to inhibit cervical cancer cells <i>in vitro</i> and significantly reduced STAT3 phosphorylation level in the cancer cells. In nude mice bearing cervical cancer xenografts, hederagenin effectively inhibited tumor growth rate without causing obvious adverse effects.</p><p><strong>Conclusions: </strong>GZFL Pellets inhibit cervical cancer cell growth through its multiple active components that target different pathways. Among these components, hederagenin inhibits tumor cell growth possibly by directly binding to JAK2 protein to inhibit STAT3 phosphorylation.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 7","pages":"1423-1433"},"PeriodicalIF":0.0,"publicationDate":"2025-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12268911/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144649967","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[LncRNA SNHG15 promotes proliferation, migration and invasion of lung adenocarcinoma cells by regulating COX6B1 through sponge adsorption of miR-30b-3p].","authors":"Xiuying Gong, Shunfu Hou, Miaomiao Zhao, Xiaona Wang, Zhihan Zhang, Qinghua Liu, Chonggao Yin, Hongli Li","doi":"10.12122/j.issn.1673-4254.2025.07.16","DOIUrl":"10.12122/j.issn.1673-4254.2025.07.16","url":null,"abstract":"<p><strong>Objectives: </strong>To explore the molecular mechanism by which lncRNA SNHG15 regulates proliferation, invasion and migration of lung adenocarcinoma cells.</p><p><strong>Methods: </strong>The lncRNA microarray chip dataset GSE196584 and LncBase were used to predict the lncRNAs that interact with miR-30b-3p, and their association with patient prognosis were investigated using online databases, after which lncRNA nucleolar RNA host gene 15 (SNHG15) was selected for further analysis. The subcellular localization of lncRNA SNHG15 and its expression levels in normal human lung epithelial cells and lung adenocarcinoma cell lines were detected using fluorescence in situ hybridization and qRT-PCR. In cultured A549 cells, the changes in cell proliferation, migration, and invasion following transfection with a SNHG15 knockdown plasmid (sh-SNHG15), a miR-30b-3p inhibitor, or their co-transfection were assessed with EdU, wound healing, and Transwell assays. Bioinformatics analyses were used to predict the regulatory relationship between lncRNA SNHG15 and COX6B1, and the results were verified using Western blotting and rescue experiments in A549 cells transfected with sh-SNHG15, a COX6B1-overexpressing plasmid, or both.</p><p><strong>Results: </strong>LncRNA SNHG15 was shown to target miR-30b-3p, and the former was highly expressed in lung adenocarcinoma, and associated with a poor patient prognosis. LncRNA SNHG15 was localized in the cytoplasm and expressed at higher levels in A549 and NCI-H1299 cells than in BEAS-2B cells. In A549 cells, lncRNA SNHG15 knockdown significantly inhibited cell migration, invasion and proliferation, and these changes were reversed by miR-30b-3p inhibitor. A regulatory relationship was found between lncRNA SNHG15 and COX6B1, and their expression levels were positively correlated (<i>r</i>=0.128, <i>P</i>=0.003). MiR-30b-3p knockdown obviously decreased COX6B1 expression in A549 cells, and COX6B1 overexpression rescued the cells from the inhibitory effects of lncRNA-SNHG15 knockdown.</p><p><strong>Conclusions: </strong>LncRNA SNHG15 may compete with COX6B1 to bind miR-30b-3p through a ceRNA mechanism to affect proliferation, migration, and invasion of lung adenocarcinoma cells.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 7","pages":"1498-1505"},"PeriodicalIF":0.0,"publicationDate":"2025-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12268920/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144649959","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[A multi-feature fusion-based model for fetal orientation classification from intrapartum ultrasound videos].","authors":"Ziyu Zheng, Xiaying Yang, Shengjie Wu, Shijie Zhang, Guorong Lyu, Peizhong Liu, Jun Wang, Shaozheng He","doi":"10.12122/j.issn.1673-4254.2025.07.24","DOIUrl":"10.12122/j.issn.1673-4254.2025.07.24","url":null,"abstract":"<p><strong>Objectives: </strong>To construct an intelligent analysis model for classifying fetal orientation during intrapartum ultrasound videos based on multi-feature fusion.</p><p><strong>Methods: </strong>The proposed model consists of the Input, Backbone Network and Classification Head modules. The Input module carries out data augmentation to improve the sample quality and generalization ability of the model. The Backbone Network was responsible for feature extraction based on Yolov8 combined with CBAM, ECA, PSA attention mechanism and AIFI feature interaction module. The Classification Head consists of a convolutional layer and a softmax function to output the final probability value of each class. The images of the key structures (the eyes, face, head, thalamus, and spine) were annotated with frames by physicians for model training to improve the classification accuracy of the anterior occipital, posterior occipital, and transverse occipital orientations.</p><p><strong>Results: </strong>The experimental results showed that the proposed model had excellent performance in the tire orientation classification task with the classification accuracy reaching 0.984, an area under the PR curve (average accuracy) of 0.993, and area under the ROC curve of 0.984, and a kappa consistency test score of 0.974. The prediction results by the deep learning model were highly consistent with the actual classification results.</p><p><strong>Conclusions: </strong>The multi-feature fusion model proposed in this study can efficiently and accurately classify fetal orientation in intrapartum ultrasound videos.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 7","pages":"1563-1570"},"PeriodicalIF":0.0,"publicationDate":"2025-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12268913/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144649950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[High expression of ELFN1 is a prognostic biomarker and promotes proliferation and metastasis of colorectal cancer cells].","authors":"Kang Wang, Haibin Li, Jing Yu, Yuan Meng, Hongli Zhang","doi":"10.12122/j.issn.1673-4254.2025.07.22","DOIUrl":"10.12122/j.issn.1673-4254.2025.07.22","url":null,"abstract":"<p><strong>Objectives: </strong>To explore the correlation of ELFN1 expression level with prognosis of colorectal cancer and its regulatory role in colorectal cancer cell proliferation and metastasis.</p><p><strong>Methods: </strong>We analyzed the expression levels of ELFN1 across 33 cancer types using publicly available databases and identified differential genes related to ELFN1 in colorectal cancer. Gene function annotation and enrichment analysis were used to identify the involved signaling pathways. Logistic analysis, Kaplan-Meier analysis and Cox regression analysis were performed to evaluate the correlation between ELFN1 expression and clinicopathological parameters and survival of colorectal cancer patients. qPCR and Western blotting were used to validate the expression levels of ELFN1 in different colorectal cancer cell lines and tissues, and Transwell and EDU experiments were carried out to assess the effect of ELFN1 knockdown on biological behaviors of SW480 cells.</p><p><strong>Results: </strong>ELFN1 was highly expressed in 14 cancers, and its expression was significantly higher in colon cancer tissues than in adjacent tissues. A high expression of ELFN1 mRNA was associated with a poorer overall survival of colorectal cancer patients. Cox regression analysis indicated that ELFN1 expression was an independent prognostic factor for overall survival of the patients. ELFN1 was significantly enriched in tumor metastasis and proliferation and participated in several tumor signaling pathways. The colon cancer cell lines showed significantly higher expression levels of ELFN1 than normal cells, ELFN1 knockdown obviously inhibited proliferation and migration of SW480 cells <i>in vitro</i>.</p><p><strong>Conclusions: </strong>ELFN1 is overexpressed in colorectal cancer and is associated with poor clinical prognosis of the patients. A high ELFN1 expression is associated with malignant phenotypes of colorectal cancer and promotes cancer cell proliferation and metastasis, suggesting its potential as a prognostic biomarker for colorectal cancer.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 7","pages":"1543-1553"},"PeriodicalIF":0.0,"publicationDate":"2025-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12268922/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144649955","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}