Turkish Journal of Biochemistry最新文献_第2页

Exercise combined with cognitive rehabilitation training affects miR-103a-3p/BDNF expression to improve Alzheimer’s disease 运动联合认知康复训练影响miR-103a-3p/BDNF表达改善阿尔茨海默病

Turkish Journal of Biochemistry Pub Date : 2025-11-19 DOI: 10.1515/tjb-2025-0350

Hui Xu, Xue Ping Wang, S.H. VAN DER MEI, Zhu Song, Jie Yang

{"title":"Exercise combined with cognitive rehabilitation training affects miR-103a-3p/BDNF expression to improve Alzheimer’s disease","authors":"Hui Xu, Xue Ping Wang, S.H. VAN DER MEI, Zhu Song, Jie Yang","doi":"10.1515/tjb-2025-0350","DOIUrl":"https://doi.org/10.1515/tjb-2025-0350","url":null,"abstract":"Abstract Objectives Exercise and cognitive rehabilitation exercises (EC) have been shown to slow the progression of Alzheimer’s disease (AD). To evaluate the regulation of EC for the miR-103a-3p/BDNF expression to delay the progression of AD. Methods AD patients were assigned to control (n=30) and EC groups (n=30) using a random number table method. Cognition was assessed using the Mini-Mental State Examination (MMSE), ‌Activity of Daily Living (ADL), and the Alzheimer’s Disease Assessment Scale–Cognition (ADAS-Cog) before and after treatment.in AD patients. The expression of miR-103a-3p in AD patients was detected by the RT-qPCR method. The expression of amyloid β-protein (Aβ), phosphorylated Tau proteins (p-Tau), BDNF, Tumor Necrosis Factor-α (TNF-α), and Interleukin-1 beta (IL-1β) in the serum of AD patients was measured by ELISA. Results After six months of EC treatment for them, MMSE and ALD scores were elevated, and ADAS-cog scores were reduced in AD patients. In addition, serum Aβ 1-42 was elevated and p-Tau was decreased in AD patients after EC treatment. RT-qPCR results indicated that the expression of miR-103a-3p was reduced in AD patients after EC treatment. The results of ELISA indicated that the expression of BDNF was increased while TNF-α and IL-1β were decreased in AD patients after EC treatment. Dual-luciferase reporter assay confirmed miR-103a-3p targeting of BDNF. Conclusions EC may affect miR-103a-3p/BDNF expression to inhibit the expression of pro-inflammatory factors (TNF-α and IL-1β), thus alleviating AD.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147899521","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}

引用次数: 0

Tanshinone ⅡA suppresses hypoxia-induced human pulmonary artery smooth muscle cell over-proliferation via the LINC01013/miR-548c-3p/IL6 pathway 丹参酮ⅡA通过LINC01013/miR-548c-3p/IL6途径抑制缺氧诱导的人肺动脉平滑肌细胞过度增殖

Turkish Journal of Biochemistry Pub Date : 2025-11-01 DOI: 10.1515/tjb-2025-0133

Nuan Zhang, Kai Xing

{"title":"Tanshinone ⅡA suppresses hypoxia-induced human pulmonary artery smooth muscle cell over-proliferation via the LINC01013/miR-548c-3p/IL6 pathway","authors":"Nuan Zhang, Kai Xing","doi":"10.1515/tjb-2025-0133","DOIUrl":"https://doi.org/10.1515/tjb-2025-0133","url":null,"abstract":"Abstract Objectives The high proliferation of pulmonary artery endothelial cells and smooth muscle cells (PASMCs) is one of the mechanisms of pulmonary hypertension (PH), which can eventually lead to death. The purpose of this study is to explore the effect of tanshinone ⅡA on PASMC proliferation and its action mechanism. Methods PASMCs were treated with hypoxia to simulate the PH cell model, and they were cultured by the medium containing different concentrations of tanshinone ⅡA to evaluate its effect on cell viability. CCK-8 reagent was for the viability detection of PASMCs. The expressions of LINC01013, miR-548c-3p, and interleukin 6 (IL6) were detected by RT-qPCR or western blotting, and their targeting relationships were demonstrated by a dual-luciferase reporter assay. The proliferation capacity of PASMCs was evaluated by CCK-8 and the expressions of markers. Glycolysis was measured by detecting phosphofructokinase-1 (PFK-1) activity and pyruvic acid level. Results Tanshinone ⅡA restrained hypoxic PASMC viability in a concentration-dependent manner. Overexpression of LINC01013 decreased miR-548c-3p level by binding to it. IL6 was a target of miR-548c-3p, and its expression was hindered by the miR-548c-3p mimics. LINC01013 and IL6 promoted the proliferation and glycolysis of hypoxic PASMCs, and miR-548c-3 acted with inhibiting effects on which. Tanshinone ⅡA suppressed LINC01013/IL6 expression and up-regulated miR-548c-3p. Conclusions Tanshinone ⅡA inhibited the glycolysis-mediated growth in hypoxic PASMCs by regulating the LINC01013/miR-548c-3p/IL6 pathway.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.degruyterbrill.com/document/doi/10.1515/tjb-2025-0133/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147884319","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}

引用次数: 0

Study on the role of miR-146b-3p in the occurrence and development of endometriosis miR-146b-3p在子宫内膜异位症发生发展中的作用研究

Turkish Journal of Biochemistry Pub Date : 2025-10-16 DOI: 10.1515/tjb-2025-0222

Yan Zhang, D W Han

{"title":"Study on the role of miR-146b-3p in the occurrence and development of endometriosis","authors":"Yan Zhang, D W Han","doi":"10.1515/tjb-2025-0222","DOIUrl":"https://doi.org/10.1515/tjb-2025-0222","url":null,"abstract":"Abstract Objectives A chronic inflammatory disease, endometriosis is recognized by the ectopic tissue growth of endometrium, but its pathogenesis has not been fully elucidated. Recently, miRNAs have been identified as a key regulator in the pathological process of endometriosis. This study investigated the function and molecular mechanism of miR-146b-3p in the occurrence and development of endometriosis. Methods In this study, 90 patients with endometriosis and 90 age-matched patients who had surgery for uterine fibroids or simple ovarian cysts were selected for the research objects. miR-146b-3p and UNC5C levels were examined by qRT-PCR in clinical endometriotic tissues and normal tissues. The impact of miR-146b-3p on endometriotic cells was verified through transfection of miR-146b-3p mimic or inhibitor. Apoptosis and proliferation were detected using flow cytometry and CCK8 assay. Transwell method was employed for examination of cell migration and invasion. The interaction of miR-146b-3p and UNC5C was detected via luciferase activity. Results miR-146b-3p levels were significantly elevated in endometriotic tissues and gradually raised with increasing rASRM grade. In endometriotic cells, up-regulation of miR-146b-3p inhibited apoptosis, facilitated cell proliferation, migration and invasion, and elevated IL-6 and TNF-α, whereas downregulation of miR-146b-3p exhibited opposite trend. In addition, miR-146b-3p targeted UNC5C, which altered the influences of miR-146b-3p on apoptosis, proliferation, migration, invasion, and inflammatory responses. Conclusions This study found that miR-146b-3p regulates inflammatory response and progression of endometriosis by targeting UNC5C, which provided a theoretical basis for the exploitation of new diagnostic biomarkers or searching for potential therapeutic targets.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147912856","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}

引用次数: 0

Study on the roles of glycolipid metabolism indicators and microRNAs in benign prostatic hyperplasia 糖脂代谢指标及microrna在良性前列腺增生中的作用研究

Turkish Journal of Biochemistry Pub Date : 2025-10-16 DOI: 10.1515/tjb-2025-0043

Yanping Li, H. Zhang, Yanjun Yue

{"title":"Study on the roles of glycolipid metabolism indicators and microRNAs in benign prostatic hyperplasia","authors":"Yanping Li, H. Zhang, Yanjun Yue","doi":"10.1515/tjb-2025-0043","DOIUrl":"https://doi.org/10.1515/tjb-2025-0043","url":null,"abstract":"Abstract Objectives As a highly prevalent disease in older men, the incidence of benign prostatic hyperplasia (BPH) is increasing as aggravating aging of the global population. This study aimed to explore the pathogenesis of BPH and its potential biomarkers. Methods Expression of miR-96-5p/miR-181a-5p and glycolipid metabolism indicators (GLMI) were detected by collecting the peripheral blood samples from 100 healthy volunteers and 110 patients with BPH. The diagnostic value of clinical factors for BPH was evaluated through the receiver operating characteristic (ROC) curve. The inhibitors of miR-96-5p and miR-181a-5p were introduced to detect their roles in BPH pathogenesis and regulation of FOXP2 expression. Interaction between miR-96-5p/miR-181a-5p and FOXP2 mRNA was verified through dual luciferase assay. Silencing FOXP2 to explore its role in the progression of BPH. Results GLMI, miR-96-5p, and miR-181a-5p levels are high in BPH patients and increased with the severity of disease, and their blood levels are positively correlated with International Prostate Symptom Score (IPSS). MiR-96-5p combined with miR-181a-5p is a good prediction model for the occurrence and severe progression of BPH, with area under curve (AUC) of 0.901 and 0.927, respectively; and they combined with GLMI showed a high authenticity, with AUC of 0.927 and 0.962, respectively. MiR-96-5p/miR-181a-5p inhibited FOXP2 expression by adsorption of its mRNA, and their inhibition reduced the viability and promoted apoptosis of WPMY-1 and BPH-1 cells, which was reversed by the silence of FOXP2. Conclusions GLMI, miR-96-5p, and miR-181a-5p presented a close clinical correlation with BPH, which are valuable biomarkers of BPH, and these two miRNAs may contribute to BPH progression by regulating FOXP2 negatively.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"51 2","pages":"243-252"},"PeriodicalIF":0.0,"publicationDate":"2025-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147917191","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}

引用次数: 0

The role of miR-361-5p in delayed fracture healing and its clinical predictive value miR-361-5p在骨折延迟愈合中的作用及其临床预测价值

Turkish Journal of Biochemistry Pub Date : 2025-09-29 DOI: 10.1515/tjb-2025-0256

Yanqi Shang, Qianqian Cheng, Hongqing Wang, Meng Han

{"title":"The role of miR-361-5p in delayed fracture healing and its clinical predictive value","authors":"Yanqi Shang, Qianqian Cheng, Hongqing Wang, Meng Han","doi":"10.1515/tjb-2025-0256","DOIUrl":"https://doi.org/10.1515/tjb-2025-0256","url":null,"abstract":"Abstract Objectives Delayed fracture healing (DFH) is a common clinical complication in orthopedic trauma. This study aims to investigate the expression patterns and regulatory mechanisms of miR-361-5p in DFH. Methods Patients with normal fracture healing (NFH) and DFH were included in this study. miR-361-5p levels in the subjects were detected using RT-qPCR, and the predictive value of miR-361-5p for DFH was evaluated through Receiver Operating Characteristic (ROC) curve. MC3T3-E1 cells were induced to undergo osteogenic differentiation in vitro , and the functional role of miR-361-5p in this process was investigated. The expression levels of osteogenic differentiation markers, including alkaline phosphatase (ALP), osteocalcin (OCN), osteopontin (OPN), and runt-related transcription factor 2 (RUNX2), in the cells were quantitatively assessed using RT-qPCR. Dual luciferase reporter assay and RNA immunoprecipitation assay were used to verify the targeted binding relationship between miR-361-5p and FGF7. Results miR-361-5p significantly increased in patients with DFH. Serum miR-361-5p had a sensitivity of 87.93 % and a specificity of 74.14 % for the prediction of DFH. During the process of osteogenic induction, we observed that the expression level of miR-361-5p gradually decreased. And this molecule is negatively correlated with the level of osteogenic markers. We found that miR-361-5p directly targets FGF7. Transfection with miR-361-5p inhibitor can enhance the activity of ALP and increase the levels of osteogenic markers. However, specific inhibition of FGF7 partially counteracted these effects. Conclusions MiR-361-5p can be used as a potential predictor of DFH. miR-361-5p inhibits osteogenic differentiation by targeting FGF7, thereby delaying the process of fracture healing.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"51 2","pages":"192-199"},"PeriodicalIF":0.0,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147903778","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}

引用次数: 0

Shenfu injection combats pathological myocardial hypertrophy by targeting TNF and TGFB1 to inhibit angiotensin II-induced autophagy 参附注射液通过靶向TNF和TGFB1抑制血管紧张素ii诱导的自噬来对抗病理性心肌肥大

Turkish Journal of Biochemistry Pub Date : 2025-09-27 DOI: 10.1515/tjb-2024-0382

Tiansheng Su, Jihong Luo, Candong Li, Zhangwu Xiao

{"title":"Shenfu injection combats pathological myocardial hypertrophy by targeting <i>TNF</i> and <i>TGFB1</i> to inhibit angiotensin II-induced autophagy","authors":"Tiansheng Su, Jihong Luo, Candong Li, Zhangwu Xiao","doi":"10.1515/tjb-2024-0382","DOIUrl":"https://doi.org/10.1515/tjb-2024-0382","url":null,"abstract":"Abstract Objectives This study aimed to explore the mechanism of action of Shenfu injection (SFI) on pathological myocardial hypertrophy. Methods The compound targets of the active ingredients in SFI were collected and intersected with the gene targets related to pathological myocardial hypertrophy. We performed protein-protein interactions (PPI), network construction, KEGG pathway enrichment analysis, and molecular docking on these targets. We used RT-qPCR and Western blot to measure the number of related genes and proteins and analyze their mechanisms of action. Results SFI relieved the hypertrophy of H9C2 cells induced by angiotensin II (Ang II). Eleven possible targets of SFI against myocardial hypertrophy were obtained. After conducting KEGG pathway enrichment analysis, these genes are closely related to heart disease-related pathways. SFI reversed the increase in the expression levels of TNF , TGFB1 , mTORC1 , and p-ULK1-Ser555 caused by Ang II. SFI can reduce the Ang II-induced increase in LC3-positive cells. Conclusions Our findings demonstrate that SFI inhibits Ang II-induced myocardial hypertrophy by attenuating pathological autophagy, an effect mediated through targeting TNF and TGFB1 pathways. These results position SFI as a promising multi-target therapeutic strategy targeting dysregulated cytokine signaling and autophagy in cardiac remodeling.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"51 2","pages":"342-350"},"PeriodicalIF":0.0,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147891244","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}

引用次数: 0

LncRNA EBLN3P inhibits myocardial inflammation and apoptosis after acute myocardial infarction via targeting miR-675-3p LncRNA EBLN3P通过靶向miR-675-3p抑制急性心肌梗死后心肌炎症和凋亡

Turkish Journal of Biochemistry Pub Date : 2025-09-15 DOI: 10.1515/tjb-2025-0060

Wan-Rong Bi, Qing Peng, Yushi Feng, Jingjing Liu

{"title":"LncRNA EBLN3P inhibits myocardial inflammation and apoptosis after acute myocardial infarction via targeting miR-675-3p","authors":"Wan-Rong Bi, Qing Peng, Yushi Feng, Jingjing Liu","doi":"10.1515/tjb-2025-0060","DOIUrl":"https://doi.org/10.1515/tjb-2025-0060","url":null,"abstract":"Abstract Objectives Acute myocardial infarction (AMI) is myocardial necrosis caused by acute and persistent ischemia and hypoxia of the coronary arteries. This study aimed to investigate the potential mechanisms of lncRNA EBLN3P in the development of AMI. Methods This study recruited 109 patients with AMI and 117 healthy controls. The hypoxia/reoxygenation (H/R) cell model was primarily utilized to simulate in vivo ischemia-reperfusion injury of tissues and organs. The expression levels of EBLN3P were assessed using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The concentrations of TNF-α, IL-6, and IL-1β were quantified via enzyme-linked immunosorbent assay (ELISA). Apoptosis was evaluated using flow cytometry. Additionally, the dual-luciferase reporter assay was utilized to confirm the targeting relationship between EBLN3P and miR-675-3p. Results EBLN3P was significantly downregulated in the serum of AMI patients. The receiver operating characteristic (ROC) curve analysis demonstrated that EBLN3P exhibited high diagnostic accuracy for AMI. Hypoxia/reoxygenation (H/R) treatment led to a marked decrease in EBLN3P expression levels, which could be significantly restored by transfecting EBLN3P post H/R treatment. H/R treatment significantly elevated the levels of TNF-α, IL-1β, and IL-6, but EBLN3P transfection partially reversed this effect. Additionally, H/R treatment resulted in a significant increase in the apoptosis rate, which EBLN3P transfection markedly reduced following H/R. EBLN3P targeted and regulated miR-675-3p, with their expression levels being negatively correlated. Furthermore, under H/R conditions, co-expression of EBLN3P and miR-mimic partially alleviated the effects of EBLN3P on cell behavior. Conclusions EBLN3P was involved in the regulatory mechanism of AMI by targeting miR-675-3p.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"51 2","pages":"271-282"},"PeriodicalIF":0.0,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147883591","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}

引用次数: 1

Clinical value of serum LncRNA EPB41L4A-AS1 in high-risk carotid artery stenosis and analysis of its mechanism 血清LncRNA EPB41L4A-AS1在高危颈动脉狭窄中的临床价值及机制分析

Turkish Journal of Biochemistry Pub Date : 2025-09-08 DOI: 10.1515/tjb-2025-0086

Lin Zhao, Yufeng He, Huhe Bateer, B. Li, Changjing Wu, Pengfei Li, Yan Gao

{"title":"Clinical value of serum LncRNA EPB41L4A-AS1 in high-risk carotid artery stenosis and analysis of its mechanism","authors":"Lin Zhao, Yufeng He, Huhe Bateer, B. Li, Changjing Wu, Pengfei Li, Yan Gao","doi":"10.1515/tjb-2025-0086","DOIUrl":"https://doi.org/10.1515/tjb-2025-0086","url":null,"abstract":"Abstract Objectives To investigate the diagnostic value of erythrocyte membrane protein band 4.1 like 4A gene antisense RNA 1 (EPB41L4A-AS1) for carotid artery stenosis (CAS) and its mechanism of action. Methods A total of 157 patients with CAS and 65 healthy individuals were included. Color doppler ultrasound determined the degree of carotid artery stenosis and plaque stability of the patients. Real-time quantitative PCR (RT-qPCR) detected the expression of EPB41L4A-AS1. Receiver operating characteristic (ROC) curve assessed the diagnostic value of EPB41L4A-AS1 for CAS. Cell counting kit-8 (CCK-8) observed the proliferative ability of the cells, Transwell detected the migration, and enzyme-linked immunoassay (ELISA) validated the expression of inflammatory factors. Results Blood pressure and low-density lipoprotein cholesterol (LDL-C) indexes were significantly elevated in CAS patients, and EPB41L4A-AS1 was significantly down-regulated, which was more pronounced in patients with heavy and unstable plaques. EPB41L4A-AS1 has diagnostic significance for the degree of carotid stenosis and plaque stability in CAS patients. Oxidized low-density lipoprotein (ox-LDL) induced cell proliferation and migration, and promotes inflammatory levels. However, overexpression of EPB41L4A-AS1 inhibited cell function and downregulated inflammatory levels. Conclusions Low EPB41L4A-AS1 was positively associated with the degree of carotid artery stenosis and plaque vulnerability in patients with CAS. Overexpression of EPB41L4A-AS1 may alleviate the degree of CAS by downregulating the expression of inflammatory factors.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"51 1","pages":"34-43"},"PeriodicalIF":0.0,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.degruyterbrill.com/document/doi/10.1515/tjb-2025-0086/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147891661","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}

引用次数: 0

Study on the association of LINC00924 with prognosis and malignant progression of thyroid cancer LINC00924与甲状腺癌预后及恶性进展的相关性研究

Turkish Journal of Biochemistry Pub Date : 2025-09-04 DOI: 10.1515/tjb-2025-0092

Luwei Niu, Qing Lu, Ran Li, Jiaxin Zhang

{"title":"Study on the association of LINC00924 with prognosis and malignant progression of thyroid cancer","authors":"Luwei Niu, Qing Lu, Ran Li, Jiaxin Zhang","doi":"10.1515/tjb-2025-0092","DOIUrl":"https://doi.org/10.1515/tjb-2025-0092","url":null,"abstract":"Abstract Objectives This study aimed to investigate the role of LINC00924 and its prognostic value in thyroid cancer (TC). Methods The study included cancer tissues from 101 TC patients and four TC cell lines. LINC00924 and miR-454-3p levels were measured using qRT-PCR. Patients were categorized into two groups according to LINC00924 levels. Cox regression analysis and Kaplan–Meier survival analysis were conducted to assess the correlation of LINC00924 with the pathological features of TC patients and its prognostic value. Additionally, validation of LINC00924 and miR-454-3p targeting relationship using dual luciferase reporter assay, and CCK-8 and Transwell assays were performed to evaluate TC cell proliferation, migration, and invasion. Results LINC00924 downregulated in TC tissues and cell lines, while miR-454-3p exhibited a marked upregulation. Lower LINC00924 expression correlated with advanced TNM stage, lymph node metastasis, and poorer overall survival. Cox analysis Kaplan-Meier survival analysis identified LINC00924 as an independent prognostic factor. Mechanistically, LINC00924 directly bound and negatively regulated miR-454-3p, acting as a molecular sponge. Functional experiments showed that LINC00924 suppressed TC cell proliferation, migration, and invasion, effects that were partially reversed by miR-454-3p. Conclusions LINC00924 may affect TC cell activity by regulating miR-454-3p. Furthermore, LINC00924 had potential as a clinical prognostic marker for TC.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"51 1","pages":"113-120"},"PeriodicalIF":0.0,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.degruyterbrill.com/document/doi/10.1515/tjb-2025-0092/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147909828","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}

引用次数: 0

MiR-221-3p improves the prognostic value of lung ultrasound score in acute respiratory distress syndrome and modulates the inflammatory response MiR-221-3p提高急性呼吸窘迫综合征肺超声评分的预后价值，调节炎症反应

Turkish Journal of Biochemistry Pub Date : 2025-08-18 DOI: 10.1515/tjb-2025-0157

Dan Liu, Di Yang, Yufeng Zhang, Yu Wang, Huijuan Yu, Caimei Liu, Jianhang Ge

{"title":"MiR-221-3p improves the prognostic value of lung ultrasound score in acute respiratory distress syndrome and modulates the inflammatory response","authors":"Dan Liu, Di Yang, Yufeng Zhang, Yu Wang, Huijuan Yu, Caimei Liu, Jianhang Ge","doi":"10.1515/tjb-2025-0157","DOIUrl":"https://doi.org/10.1515/tjb-2025-0157","url":null,"abstract":"Abstract Objectives Acute respiratory distress syndrome (ARDS) is linked to high mortality rates, with effective assessment of the condition critical to improving patient prognosis. The aim is to explore the value of serum miR-221-3p and lung ultrasound (LUS) score on the prognosis of ARDS, with the aim of providing meaningful references for clinical evaluation and therapeutic strategies. Methods The study cohort comprised 156 patients diagnosed with sepsis-induced ARDS. MiR-221-3p levels were quantified using RT-qPCR. Prognostic significance was determined by the ROC curve and Logistic analysis. Furthermore, a cell injury model was established in human pulmonary microvascular endothelial cells (HPMECs) induced by LPS, and the effects of miR-221-3p on cell viability and apoptosis of HPMECs were examined utilizing CCK-8 and flow cytometry. ELISA was utilized to evaluate the role of miR-221-3p on inflammatory factors and cell adhesion molecules. Results In deceased ARDS patients, elevated levels of serum miR-221-3p demonstrated a notable positive correlation with APACHE II score, SOFA score, procalcitonin, and LUS score. Notably, miR-221-3p and LUS score were identified as prognostic factors associated with patient mortality, and the integration of these two assays resulted in a more accurate assessment of patient prognoses. In HPMECs exposed to LPS, miR-221-3p silencing enhanced cell survival, suppressed apoptosis, and reduced levels of inflammatory cytokines (TNF-α, IL-6, IL-1β) and adhesion molecules (ICAM-1, E-selectin). Conclusions MiR-221-3p, combined with LUS assessment, holds prognostic value in ARDS. Its involvement in inflammation and cellular damage suggests a modulatory effect on disease advancement.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"51 1","pages":"60-68"},"PeriodicalIF":0.0,"publicationDate":"2025-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.degruyterbrill.com/document/doi/10.1515/tjb-2025-0157/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147917855","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}

引用次数: 0