南方医科大学学报杂志最新文献

{"title":"[Protective effect of graphene heating film far-infrared hyperthermia against frostbite in mice].","authors":"Jinshui Zhang, Shuo Li, Dongdong Wei, Xin Cheng, Yun Deng, Youzhi Zhang","doi":"10.12122/j.issn.1673-4254.2025.03.10","DOIUrl":"https://doi.org/10.12122/j.issn.1673-4254.2025.03.10","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the protective effects of graphene heating film far-infrared (FIR) hyperthermia therapy against frostbite in mice and its impacts on microcirculation and coagulation function.</p><p><strong>Methods: </strong>Seventy-six C57BL/6J mice were randomized into control, model, graphene-FIR, and carbon fiber-FIR groups. After 7-day FIR intervention (4 h/day), the mice were subjected to acute (4 ℃, 4 h) and intermittent (4 ℃, 4 h/day for 3 days) cold exposure and the changes in rectal temperature were monitored. In liquid nitrogen frostbite experiment, 24 ICR mice were divided into model, graphene-FIR, and carbon fiber-FIR groups, and after a 7-day FIR pretreatment (4 h/day), the liquid nitrogen frostbite models were established and apparent scores of the wounds were assessed on days 3 and 6 after modeling. In carrageenan-induced thrombosis experiment, 40 ICR mice were allocated to control, model, graphene-FIR, carbon fiber-FIR, and prazosin groups to test the effect of a 7-day FIR intervention on thrombosis induced by intraperitoneal carrageenan injection (2.5 mg/kg) by measuring thrombus length, blood perfusion, and serum biomarkers (6-keto-PGF1α, TXB2, t-PA, IL-6, IL-1β, TNF‑α) 24 h after the injection.</p><p><strong>Results: </strong>The mice in graphene-FIR group showed significantly elevated rectal temperature in cold exposure tests. In mice with liquid nitrogen-induced frostbite, graphene-FIR treatment significantly reduced the wound scores and reduced frostbite area, producing better effects than carbon fiber. In mice with carrageenan-induced thrombosis, graphene-FIR treatment significantly decreased tail thrombosis length and thrombosis area, increased blood perfusion, lowered serum levels of TXB2, TNF-α and IL-6, and increased the levels of 6-keto-PGF1α and t-PA.</p><p><strong>Conclusions: </strong>Graphene heating film FIR therapy can alleviate frostbite injury in mice by improving microcirculation, suppressing thrombosis and inflammatory responses, and reducing coagulation dysfunction.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 3","pages":"522-530"},"PeriodicalIF":0.0,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143753683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Protein C activator derived from snake venom protects human umbilical vein endothelial cells against hypoxia-reoxygenation injury by suppressing ROS <i>via</i> upregulating HIF-1α and BNIP3].","authors":"Ming Liao, Wenhua Zhong, Ran Zhang, Juan Liang, Wentaorui Xu, Wenjun Wan, Chao Li Shu Wu, 曙 李","doi":"10.12122/j.issn.1673-4254.2025.03.19","DOIUrl":"https://doi.org/10.12122/j.issn.1673-4254.2025.03.19","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the antioxidative mechanism of snake venom-derived protein C activator (PCA) in mitigating vascular endothelial cell injury.</p><p><strong>Methods: </strong>Human umbilical vein endothelial cells (HUVECs) were cultured in DMEM containing 1.0 g/L D-glucose and exposed to hypoxia (1% O₂) for 6 h followed by reoxygenation for 2 h to establish a cell model of oxygen-glucose deprivation/reoxygenation (OGD/R). The cell model was treated with 2 μg/mL PCA alone or in combination with 2-ME2 (a HIF-1α inhibitor) or DMOG (a HIF-1α stabilizer), and intracellular production of reactive oxygen species (ROS) and protein expression levels of HIF-1α, BNIP3, and Beclin-1 were detected using DCFH-DA fluorescence probe, flow cytometry, and Western blotting. The OGD/R cell model was transfected with a BNIP3-specific siRNA or a scrambled control sequence prior to PCA treatment, and the changes in protein expressions of HIF-1α, BNIP3 and Beclin-1 and intracellular ROS production were examined.</p><p><strong>Results: </strong>In the OGD/R cell model, PCA treatment significantly upregulated HIF-1α, BNIP3 and Beclin-1 expressions and reduced ROS production. The effects of PCA were obviously attenuated by co-treatment with 2-ME2 but augmented by treatment with DMOG (a HIF-1α stabilizer). In the cell model with BNIP3 knockdown, PCA treatment increased BNIP3 expression and decreased ROS production without causing significant changes in HIF-1α expression. Compared with HUVECs with PCA treatment only, the cells with BNIP3 knockdown prior to PCA treatment showed significantly lower Beclin-1 expression and higher ROS levels.</p><p><strong>Conclusions: </strong>Snake venom PCA alleviates OGD/R-induced endothelial cell injury by upregulating HIF-1α/BNIP3 signaling to suppress ROS generation, suggesting its potential as a therapeutic agent against oxidative stress in vascular pathologies.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 3","pages":"614-621"},"PeriodicalIF":0.0,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143753685","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[High MYO1B expression promotes proliferation, migration and invasion of gastric cancer cells and is associated with poor patient prognosis].","authors":"Qingqing Huang, Wenjing Zhang, Xiaofeng Zhang, Lian Wang, Xue Song, Zhijun Geng, Lugen Zuo, Yueyue Wang, Jing Li, Jianguo Hu","doi":"10.12122/j.issn.1673-4254.2025.03.20","DOIUrl":"https://doi.org/10.12122/j.issn.1673-4254.2025.03.20","url":null,"abstract":"<p><strong>Objectives: </strong>To analyze MYO1B expression in gastric cancer, its association with long-term prognosis and its role in regulating biological behaviors of gastric cancer cells.</p><p><strong>Methods: </strong>We analyzed MYO1B expression in gastric cancer and its correlation with tumor grade, tumor stage, and patient survival using the Cancer Public Database. We also examined MYO1B expression with immunohistochemistry in gastric cancer and paired adjacent tissues from 105 patients receiving radical surgery and analyzed its correlation with cancer progression and postoperative 5-year survival of the patients. GO and KEGG enrichment analyses were used to explore the biological functions of MYO1B and the key pathways. In cultured gastric cancer cells, we examined the changes in cell proliferation, migration and invasion following MYO1B overexpression and knockdown.</p><p><strong>Results: </strong>Data from the Cancer Public Database showed that MYO1B expression was significantly higher in gastric cancer tissues than in normal tissues with strong correlations with tumor grade, stage and patient prognosis (<i>P</i><0.05). In the clinical tissue samples, MYO1B was significantly overexpressed in gastric cancer tissues in positive correlation with Ki67 expression (<i>r</i>=0.689, <i>P</i><0.05) and the parameters indicative of gastric cancer progression (CEA ≥5 μg/L, CA19-9 ≥37 kU/L, G3-4, T3-4, and N2-3) (<i>P</i><0.05). Kaplan-Meier analysis and multivariate Cox regression analysis suggested that high MYO1B expression was associated with decreased postoperative 5-year survival and was an independent risk factor (<i>HR</i>: 3.522, 95%<i>CI</i>: 1.783-6.985, <i>P</i><0.05). MYO1B expression level was a strong predictor of postoperative survival (cut-off value: 3.11, AUC: 0.753, <i>P</i><0.05). GO and KEGG analyses suggested that MYO1B may regulate cell migration and the mTOR signaling pathway. In cultured gastric cancer cells, MYO1B overexpression significantly enhanced cell proliferation, migration, and invasion and promoted the phosphorylation of Akt and mTOR.</p><p><strong>Conclusions: </strong>High MYO1B expression promotes proliferation, migration and invasion of gastric cancer cells and is correlated with poor patient prognosis.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 3","pages":"622-631"},"PeriodicalIF":0.0,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143753675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Prognosis-guided optimization of intensity-modulated radiation therapy plans for lung cancer].","authors":"Huali Li, Ting Song, Jiawen Liu, Yongbao Li, Zhaojing Jiang, Wen Dou, Linghong Zhou","doi":"10.12122/j.issn.1673-4254.2025.03.22","DOIUrl":"https://doi.org/10.12122/j.issn.1673-4254.2025.03.22","url":null,"abstract":"<p><strong>Objectives: </strong>To propose a new method for optimizing radiotherapy planning for lung cancer by incorporating prognostic models that take into account individual patient information and assess the feasibility of treatment planning optimization directly guided by minimizing the predicted prognostic risk.</p><p><strong>Methods: </strong>A mixed fluence map optimization objective was constructed, incorporating the outcome-based objective and the physical dose constraints. The outcome-based objective function was constructed as an equally weighted summation of prognostic prediction models for local control failure, radiation-induced cardiac toxicity, and radiation pneumonitis considering clinical risk factors. These models were derived using Cox regression analysis or Logistic regression. The primary goal was to minimize the outcome-based objective with the physical dose constraints recommended by the clinical guidelines. The efficacy of the proposed method for optimizing treatment plans was tested in 15 cases of non-small cell lung cancer in comparison with the conventional dose-based optimization method (clinical plan), and the dosimetric indicators and predicted prognostic outcomes were compared between different plans.</p><p><strong>Results: </strong>In terms of the dosemetric indicators, D_95% of the planning target volume obtained using the proposed method was basically consistent with that of the clinical plan (100.33% <i>vs</i> 102.57%, <i>P</i>=0.056), and the average dose of the heart and lungs was significantly decreased from 9.83 Gy and 9.50 Gy to 7.02 Gy (<i>t</i>=4.537, <i>P<</i>0.05) and 8.40 Gy (<i>t</i>=4.104, <i>P<</i>0.05), respectively. The predicted probability of local control failure was similar between the proposed plan and the clinical plan (60.05% <i>vs</i> 59.66%), while the probability of radiation-induced cardiac toxicity was reduced by 1.41% in the proposed plan.</p><p><strong>Conclusions: </strong>The proposed optimization method based on a mixed objective function of outcome prediction and physical dose provides effective protection against normal tissue exposure to improve the outcomes of lung cancer patients following radiotherapy.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 3","pages":"643-649"},"PeriodicalIF":0.0,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143753681","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[High serum cystatin C is an independent risk factor for poor renal prognosis in IgA nephropathy].","authors":"Tianwei Tang, Luan Li, Yuanhan Chen, Li Zhang, Lixia Xu, Zhilian Li, Zhonglin Feng, Huilin Zhang, Ruifang Hua, Zhiming Ye, Xinling Liang, Ruizhao Li","doi":"10.12122/j.issn.1673-4254.2025.02.19","DOIUrl":"10.12122/j.issn.1673-4254.2025.02.19","url":null,"abstract":"<p><strong>Objectives: </strong>To explore the value of serum cystatin C (CysC) levels in evaluating renal prognosis in IgA nephropathy (IgAN) patients.</p><p><strong>Methods: </strong>We retrospectively collected the clinical data of IgAN patients diagnosed by renal biopsy at Guangdong Provincial People's Hospital from January, 2014 to December, 2018. Based on baseline serum CysC levels, the patients were divided into high serum CysC (>1.03 mg/L) group and normal serum CysC (≤1.03 mg/L) group. The composite endpoint for poor renal prognosis was defined as ≥50% decline in estimated glomerular filtration rate (eGFR) and/or progression to end-stage renal disease (ESRD). Lasso regression, multivariate Cox regression and Kaplan-Meier survival analysis were used to identify the risk factors and compare renal survival rates between the two groups. Smooth curves fitting and threshold effect analysis were used to explore the relationship between serum CysC levels and the outcomes. A nomogram model was constructed and its predictive performance was evaluated using concordance index, calibration curve, receiver operating characteristic (ROC) curve and the area under curve (AUC).</p><p><strong>Results: </strong>A total of 356 IgAN patients were enrolled, who were followed up for 4.65±0.93 years. The composite endpoint occurred in 74 patients. High serum CysC was identified as an independent risk factor for poor renal prognosis in IgAN (<i>HR</i>=2.142, 95% <i>CI</i> 1.222 to 3.755), and the patients with high serum CysC levels had a lower renal survival rate (Log-rank χ²=47.970, <i>P</i><0.001). In patients with serum CysC below 2.12 mg/L, a higher CysC level was associated with an increased risk of poor renal prognosis (<i>β</i>=3.487, 95% <i>CI</i>: 2.561-4.413, <i>P</i><0.001), while above this level, the increase of the risk was not significant (<i>β</i>=0.676, 95% <i>CI</i>: -0.642-1.995, <i>P</i>=0.315). The nomogram model based on serum CysC and 3 other independent risk factors demonstrated good internal validity with a concordance index of 0.873 (95% <i>CI</i>: 0.839-0.907) and an AUC of 0.909 (95% <i>CI</i>: 0.873-0.945).</p><p><strong>Conclusions: </strong>Serum CysC levels are associated with renal prognosis in IgAN patients, and high serum CysC an independent risk factor for poor renal prognosis.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 2","pages":"379-386"},"PeriodicalIF":0.0,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11875852/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143542725","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":"[Multiple arterial grafts does not increase perioperative or short- to medium-term risks of postoperative MACE in patients with impaired left ventricular function: 3-year follow-up results].","authors":"Ziru Li, Shengwei Bai, Jian Zhang, Hao Xu, Suhua Zang, Xin Zhang","doi":"10.12122/j.issn.1673-4254.2025.02.04","DOIUrl":"10.12122/j.issn.1673-4254.2025.02.04","url":null,"abstract":"<p><strong>Objectives: </strong>To compare perioperative and mid-term results of multiple versus single arterial off-pump coronary artery bypass grafting (OPCABG) in patients with impaired left ventricular function.</p><p><strong>Methods: </strong>This study was conducted among 86 patients with a left ventricular ejection fraction (LVEF) <50%, who underwent OPCABG at our hospital between January, 2018 and December, 2021. Of these patients, 22 underwent OPCABG with multiple arterial grafts (multiple graft group) and 64 received a single arterial graft in OPCABG (single graft group). The preoperative, intraoperative, and perioperative data were collected, and the patients were followed up for a mean of 29.28±14.84 months. The perioperative outcomes and follow-up results of the patients were compared, and the factors influencing major adverse cardiovascular events (MACE) were identified using logistic regression. Kaplan-Meier analysis was used to compare the postoperative survival rate without MACE.</p><p><strong>Results: </strong>The patients in multiple graft group had a significantly younger age than those in single graft group (P<0.05), but the other baseline data were similar between the two groups (<i>P</i>>0.05). Perioperative mortality, 24-h postoperative drainage volume, length of ICU stay, intubation time, and the incidence of new-onset atrial fibrillation were all similar between the two groups (<i>P</i>>0.05), but the rate of postoperative hypotension was significantly higher in multiple graft group (34.78% <i>vs</i> 11.54%, <i>P</i>=0.009). No significant differences were found in the incidence of MACE or echocardiographic data during the follow-up. Logistic regression identified the female sex (OR: 0.191, 95% <i>CI</i>: 0.049-0.075) and creatinine level (OR: 1.016, 95% <i>CI</i>: 1.000-1.033) as factors affecting postoperative MACE occurrence. Kaplan-Meier analysis showed no significant difference in MACE-free survival rate between the two groups.</p><p><strong>Conclusions: </strong>OPCABG with multiple arterial grafts does not increase severe perioperative complications or the risk of mid-term MACE in patients with impaired left ventricular function.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 2","pages":"239-244"},"PeriodicalIF":0.0,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11875857/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143542737","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":"[Nodakenin ameliorates TNBS-induced experimental colitis in mice by inhibiting pyroptosis of intestinal epithelial cells].","authors":"Ju Huang, Lixia Yin, Minzhu Niu, Zhijun Geng, Lugen Zuo, Jing Li, Jianguo Hu","doi":"10.12122/j.issn.1673-4254.2025.02.07","DOIUrl":"10.12122/j.issn.1673-4254.2025.02.07","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the therapeutic mechanism of nodakenin for Crohn's disease (CD)-like colitis in mice.</p><p><strong>Methods: </strong>Using a colonic organoid model with lipopolysaccharide (LPS)- and ATP-induced pyroptosis, we investigated the effects of nodakenin on pyroptosis, intestinal barrier function and inflammatory response by detecting key pyroptosis-regulating factors and assessing changes in permeability and pro-inflammatory factors. In a mouse model of 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced CD-like colitis, the therapeutic effect of nodakenin was evaluated by measuring changes in body weight, DAI score, colonic histopathologies, inflammation score, intestinal barrier function and intestinal epithelial cell pyroptosis. The mechanism of nodakenin protection against pyroptosis of intestinal epithelial cells was explored using network pharmacology analysis and <i>in vivo</i> and <i>in vitro</i> experiments.</p><p><strong>Results: </strong>In LPS- and ATP-induced colonic organoids, treatment with nodakenin significantly inhibited the expressions of NLRP3, GSDMD-N, cleaved caspase-1 and caspase-11, improved intestinal FITC-dextran (FD4, 4000) permeability, and decreased the levels of IL-1β and IL-18. In the mouse model of TNBS-induced colitis, nodakenin treatment significantly alleviated weight loss, reduced DAI score, inflammatory cell infiltration and inflammation score, and decreased serum FD4 and I-FABP levels and bacteria translocation to the mesenteric lymph nodes, spleen and liver. The mice with nodakenin treatment had also lowered expressions of NLRP3, GSDMD-N, cleaved caspase-1 and caspase-11 in the intestinal mucosa. Network pharmacology analysis suggested that the inhibitory effect of nodakenin on colitis was associated with the PI3K/Akt pathway. In both the colonic organoid model and mouse models of colitis, nodakenin effectively inhibited the activation of the PI3K/Akt pathway, and the application of IGF-1, a PI3K/Akt pathway activator, strongly attenuated the protective effect of nodakenin against intestinal epithelial cell pyroptosis and intestinal barrier dysfunction.</p><p><strong>Conclusions: </strong>Nodakenin protects intestinal barrier function and alleviates CD-like colitis in mice at least partly by inhibiting PI3K/Akt signaling to reduce intestinal epithelial cell pyroptosis.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 2","pages":"261-268"},"PeriodicalIF":0.0,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11875862/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143542683","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":"[SLC1A5 overexpression accelerates progression of hepatocellular carcinoma by promoting M2 polarization of macrophages].","authors":"Jinhua Zou, Hui Wang, Dongyan Zhang","doi":"10.12122/j.issn.1673-4254.2025.02.08","DOIUrl":"10.12122/j.issn.1673-4254.2025.02.08","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the clinical significance of SLC1A5 overexpression in pan-cancer and its mechanism for promoting hepatocellular carcinoma (HCC) progression.</p><p><strong>Methods: </strong>We analyzed the correlation of SLC1A5 expression with clinical stage, lymph node metastasis and prognosis in pan-cancer using TCGA and ICGC datasets and explored its association with immune cell infiltration using EPIC, CIBERSORT, and TIMER algorithms. In HCC cell lines, the effects of lentivirus-mediated SLC1A5 overexpression or RNA interference on cell proliferation were examined using CCK-8 assay, and the growth of HCC cell xenografts overexpressing SLC1A5 was observed in nude mice. The effects of SLC1A5 overexpression or silencing in HCC cells on macrophage polarization were evaluated in a cell co-culture system.</p><p><strong>Results: </strong>SLC1A5 was mainly localized on cell membrane and was highly expressed in most cancers in association with clinical stage, lymph node metastasis and poor prognosis. SLC1A5 expression was positively correlated with immunity score in 13 cancer types, especially in low-grade glioma (LGG), LIHC and thyroid cancer. SLC1A5 was positively correlated with macrophage infiltration level in LGG and LIHC but negatively correlated with macrophage infiltration in 5 cancers including lung squamous carcinoma, pancreatic carcinoma, and gastric carcinoma. Patients with SLC1A5 overexpression and high level of M2 macrophage infiltration had the worst survival outcomes. SLC1A5 was correlated with immunosuppression-related genes, cytokines, and cytokine receptors, which was the most obvious in LGG and LIHC. SLC1A5 was highly expressed in different HCC cell lines, and its overexpression promoted HCC cell proliferation both <i>in vitro</i> and in nude mice. In the cell co-culture experiment, SLC1A5 was positively correlated with the molecular markers of M2 polarization of macrophages, and its overexpression strongly promoted M2 polarization of the macrophages and inhibited T cell secretion of IFN-γ.</p><p><strong>Conclusions: </strong>SLC1A5 expression level is correlated with clinical stage, lymph node metastasis, prognosis, and immune cell infiltration in most cancers, and its overexpression promotes HCC progression by inhibiting T-cell function <i>via</i> promoting M2 polarization of macrophages.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 2","pages":"269-284"},"PeriodicalIF":0.0,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11875851/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143542690","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":"[Dihydroartemisinin enhances doxorubicin-induced apoptosis of triple negative breast cancer cells by negatively regulating the STAT3/HIF-1α pathway].","authors":"Di Chen, Ying Lü, Yixin Guo, Yirong Zhang, Ruixuan Wang, Xiaoruo Zhou, Yuxin Chen, Xiaohui Wu","doi":"10.12122/j.issn.1673-4254.2025.02.06","DOIUrl":"10.12122/j.issn.1673-4254.2025.02.06","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the effects of dihydroartemisinin (DHA) combined with doxorubicin (DOX) on proliferation and apoptosis of triple-negative breast cancer cells and explore the underlying molecular mechanism.</p><p><strong>Methods: </strong>MDA-MB-231 cells were treated with 50, 100 or 150 μmol/L DHA, 0.5 μmol/L DOX, or with 50 μmol/L DHA combined with 0.5 μmol/L DOX. The changes in proliferation and survival of the treated cells were examined with MTT assay and colony-forming assay, and cell apoptosis was analyzed with flow cytometry. Western blotting was performed to detect the changes in protein expression levels of PCNA, cleaved PARP, Bcl-2, Bax, STAT3, p-STAT3, HIF-1α and survivin.</p><p><strong>Results: </strong>The IC₅₀ of DHA was 131.37±29.87 μmol/L in MDA-MB-231 cells. The cells with the combined treatment with DHA and DOX showed significant suppression of cell proliferation. Treatment with DHA alone induced apoptosis of MDA-MB-231 cells in a dose-dependent manner, but the combined treatment produced a much stronger apoptosis-inducing effect than both DHA and DOX alone. DHA at 150 μmol/L significantly inhibited clone formation of MDA-MB-231 cells, markedly reduced cellular expression levels of PCNA, p-STAT3, HIF-1α and survivin proteins, and obviously increased the expression level of cleaved PARP protein and the Bax/Bcl-2 ratio, and the combined treatment further reduced the expression level of p-STAT3 protein and increased the Bax/Bcl-2 ratio.</p><p><strong>Conclusions: </strong>DHA combined with DOX produces significantly enhanced effects for inhibiting cell proliferation and inducing apoptosis in MDA-MB-231 cells possibly as result of DHA-mediated negative regulation of the STAT3/HIF-1α pathway.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 2","pages":"254-260"},"PeriodicalIF":0.0,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11875850/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143542714","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":"[GPSM2 is highly expressed in gastric cancer to affect patient prognosis by promoting tumor cell proliferation].","authors":"Xue Song, Yue Chen, Min Zhang, Nuo Zhang, Lugen Zuo, Jing Li, Zhijun Geng, Xiaofeng Zhang, Yueyue Wang, Lian Wang, Jianguo Hu","doi":"10.12122/j.issn.1673-4254.2025.02.03","DOIUrl":"10.12122/j.issn.1673-4254.2025.02.03","url":null,"abstract":"<p><strong>Objectives: </strong>To explore the association between GPSM2 expression level and gastric cancer progression and analyze the functional pathways and action mechanism of GPSM2.</p><p><strong>Methods: </strong>We analyzed GPSM2 expression levels in gastric cancer tumors based on data from the GEPIA database and the clinical data of 109 patients. Public databases enrichment analysis were used to assess the impact of GPSM2 expression level on survival outcomes and the functional pathways and action mechanism of GPSM2. We further observed the effects of GPSM2 knockdown and overexpression on proliferation, migration and apoptosis of MGC803 cells using CCK-8 assay, colony formation assay, flow cytometry and immunoblotting and on the growth of MGC803 cell xenografts in nude mice.</p><p><strong>Results: </strong>Bioinformatic analysis and immunohistochemical staining of the clinical specimens both revealed high GPSM2 expressions in gastric cancer (<i>P</i><0.01). A high GPSM2 expression was significantly correlated with T3-4 stages, N2-3 stages, a carcinoembryonic antigen (CEA) level ≥5 μg/L, and a carbohydrate antigen (CA) 19-9 level ≥37 kU/L (<i>P</i><0.05). Cox regression analysis identified high GPSM2 expression as an independent risk factor affecting 5-year survival of the patients (<i>P</i><0.05). Gene ontology (GO) analysis suggested that GPSM2 was involved in cell cycle regulation. In MGC803 cells, GPSM2 overexpression significantly promoted cell proliferation and G1/S transition and xenograft growth in nude mice. KEGG pathway enrichment analysis indicated that GPSM2 executed its biological functions by regulating the p53 signaling pathway, which was confirmed by the results of immunoblotting experiments showing suppression of p53 signaling pathway activity in GPSM2-over expressing MGC803 cells.</p><p><strong>Conclusions: </strong>GPSM2 is highly expressed in gastric cancer to affect patient prognosis by promoting tumor cell proliferation and G1/S transition possibly <i>via</i> inhibiting the p53 pathway.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 2","pages":"229-238"},"PeriodicalIF":0.0,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11875856/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143542716","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}