{"title":"Comprehensive analysis of GPN1 in human cancer and its effects on the migration of hepatocellular carcinoma cells.","authors":"Rongtao Zhu, Senfeng Zhao, Jiahui Cao, Yin Liu, Ruopeng Liang","doi":"10.17305/bb.2024.11310","DOIUrl":"10.17305/bb.2024.11310","url":null,"abstract":"<p><p>To investigate the prognostic value of GPN1 in cancer and its role in the migration of hepatocellular carcinoma (HCC or LIHC) cells, we used several databases to assess GPN1 expression levels and effects in human tumors. Furthermore, experiments were conducted to verify changes in GPN1 expression in HCC cell lines and explore its biological function. We found that GPN1 gene and protein expression were significantly increased in several tumor tissues. Higher GPN1 expression was associated with unfavorable overall survival. Additionally, there was a strong association between GPN1 expression and several clinicopathological features, according to multivariate Cox regression analysis. Moreover, GPN1 gene mutation and methylation were present in some tumors. A relationship was also found between GPN1 expression and immune infiltration. Notably, immune checkpoint analysis showed that GPN1 expression was correlated with PD-1/PDL-1 and CTLA-4, suggesting it may serve as a biomarker for predicting immune subtypes and response to immunotherapy in HCC. Enrichment analysis in HCC indicated that GPN1 is primarily involved in RNA metabolism. Additionally, drug sensitivity analysis revealed that GPN1 appeared to be responsive to 16 drugs. Finally, GPN1 upregulation was confirmed to promote the migration of HCC cells. This study provides a comprehensive overview of GPN1 in human cancer and demonstrates that GPN1 contributes to the migration of HCC cells, potentially serving as a prognostic and immunotherapy biomarker.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1111-1125"},"PeriodicalIF":0.0,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11984376/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142633795","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}
Qiuxia Zhang, Min Wang, Li You, Chen Chen, Jia Feng, Miao Song, Kui Yang, Xuexue Liu, Guangrong Li, Jinbo Liu
{"title":"Research progress and application status of organoid in breast cancer subtypes.","authors":"Qiuxia Zhang, Min Wang, Li You, Chen Chen, Jia Feng, Miao Song, Kui Yang, Xuexue Liu, Guangrong Li, Jinbo Liu","doi":"10.17305/bb.2024.11450","DOIUrl":"10.17305/bb.2024.11450","url":null,"abstract":"<p><p>Breast cancer (BC) is a prevalent malignant tumor that poses a significant health risk to women. The complexity of basic BC research and clinical treatment is influenced by multiple factors, including age, fertility, hormone metabolism, molecular subtypes, and tumor grading and staging. Traditional in vitro models often fall short of meeting modern research demands, whereas organoids-an emerging 3D primary culture technology-offer a unique platform that better replicates the tumor microenvironment (TME). Coupled with advances in high-throughput sequencing technologies, organoids have become increasingly valuable in biological and chemical research. Currently, the most widely used organoid model in BC research is the patient-derived organoid (PDO) model, which is generated directly from original tumor tissues. This paper aims to summarize the current status of PDO models across various BC subtypes, highlighting recent advances in genetics, mechanisms of drug resistance, identification of new therapeutic targets, and approaches to personalized treatment. In conclusion, the development of clinical precision medicine urgently requires in vitro models capable of accurately simulating the unique molecular subtypes of patients. This review will examine the challenges and future prospects of organoid models in BC research, offering new insights into the fundamental mechanisms of BC and paving the way for more effective personalized therapies.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"976-985"},"PeriodicalIF":0.0,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11984363/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142886548","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}
Xiaomin Wang, Hui Li, Aoxuan Xu, Jie Peng, Yanqing Wu, Yunfan Liu, Junjie Zhang, Changqi Cai, Shiyin Ma, Kai Zhang
{"title":"Inhibition of the long non-coding RNA MALAT1 downregulates MAP2K1, suppressing the progression of hypopharyngeal squamous cell carcinoma.","authors":"Xiaomin Wang, Hui Li, Aoxuan Xu, Jie Peng, Yanqing Wu, Yunfan Liu, Junjie Zhang, Changqi Cai, Shiyin Ma, Kai Zhang","doi":"10.17305/bb.2024.11151","DOIUrl":"10.17305/bb.2024.11151","url":null,"abstract":"<p><p>This study aimed to explore the role of long non-coding RNAs metastasis-associated lung adenocarcinoma transcript (lncRNA MALAT1), and its underlying mechanisms in hypopharyngeal squamous cell carcinoma (HSCC). Quantitative real-time PCR (qRT-PCR) was employed to measure lncRNA MALAT1 expression in HSCC and adjacent non-cancerous tissues, along with the expression of the downstream target mitogen-activated protein kinase kinase 1 (MAP2K1). The independent prognostic significance of lncRNA MALAT1 was assessed using Cox regression analysis. Potential downstream targets of MALAT1 were identified through parallel reaction monitoring (PRM) analysis and validated using the TCGA-HNSC database, Western blotting, and immunohistochemistry. CCK-8, flow cytometry, and Transwell assays were conducted to assess the effects of the lncRNA MALAT1/MAP2K1 axis on FaDu cells. Additionally, a nude mouse xenograft model was used to confirm the role of lncRNA MALAT1/MAP2K1 in tumor growth. LncRNA MALAT1 was significantly upregulated in HSCC tissues and closely associated with poor prognosis. Bioinformatics analysis, including PRM screening and TCGA-HNSC data, identified FERMT2, CSNK2A2, and MAP2K1 as potential downstream targets of MALAT1. Validation through qPCR, Western blotting, and immunohistochemistry confirmed MAP2K1 as a downstream target. In vitro and in vivo experiments demonstrated that inhibiting lncRNA MALAT1 suppressed cell proliferation, migration, and epithelial-to-mesenchymal transition (EMT) by downregulating MAP2K1 expression. Additionally, it induced apoptosis, affected the cell cycle, and inhibited tumor growth. Our study uniquely demonstrates that targeting MALAT1 significantly impedes HSCC progression by downregulating its novel downstream target, MAP2K1, offering new insights into potential therapeutic strategies.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1023-1037"},"PeriodicalIF":0.0,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11984367/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142333644","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}
Miao Ao, You Wu, Zhiping Huo, He Zhang, Wei Mao, Bin Li
{"title":"Surgical approach and recurrence risk in struma ovarii: A retrospective and systematic analysis.","authors":"Miao Ao, You Wu, Zhiping Huo, He Zhang, Wei Mao, Bin Li","doi":"10.17305/bb.2024.11287","DOIUrl":"10.17305/bb.2024.11287","url":null,"abstract":"<p><p>Struma ovarii (SO) represents a rare subset of ovarian germ cell tumors, with approximately 5% transforming into malignant SO (MSO). This study retrospectively analyzed clinical data from 23 SO patients treated at the Cancer Hospital of the Chinese Academy of Medical Sciences between January 2013 and December 2023, including 17 benign SO and 6 MSO cases. Additionally, a systematic review of 164 cases of MSO confined to the ovary, reported in the literature from 1946 to 2024, was conducted. Data on pathological type, treatment, and prognosis were extracted, and univariate and multivariate Cox regression analyses were performed to identify risk factors for recurrence in stage I MSO. The median age at diagnosis was higher for benign SO compared to MSO (58 vs. 42.5 years), with 70.6% of patients being postmenopausal. Benign SO commonly presented with abdominal distension or mass, with more than half having ascites, while MSO patients were asymptomatic and lacked ascites. Cox regression analyses revealed that ovarian cystectomy was adversely associated with recurrence risk in stage I MSO, likely due to surgically induced capsular rent and potential tumor spillage. Significantly lower recurrence risks were observed in patients who underwent unilateral or bilateral salpingo-oophorectomy (HR = 0.36, P = 0.019; HR = 0.19, P = 0.004, respectively). This study highlights the importance of the surgical approach in the management of stage I MSO. A thorough preoperative discussion of the benefits and risks of different surgical approaches is recommended for patients desiring fertility preservation. Postoperative adjuvant therapy has not been shown to have a significant impact on prognosis. For the treatment of recurrent MSO, selecting appropriate surgical and adjuvant therapeutic strategies is essential to improve the long-term prognosis of MSO patients.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1092-1098"},"PeriodicalIF":0.0,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11984365/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142513969","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}
Peipei Shen, Yu Xu, Jiahao Zhu, Danqi Qian, Bo Yang, Yong Mao, Shengjun Ji, Ke Gu, Yutian Zhao
{"title":"Predictive and prognostic value of preoperative pan-immune-inflammation value in patients with locally advanced rectal cancer.","authors":"Peipei Shen, Yu Xu, Jiahao Zhu, Danqi Qian, Bo Yang, Yong Mao, Shengjun Ji, Ke Gu, Yutian Zhao","doi":"10.17305/bb.2024.10658","DOIUrl":"10.17305/bb.2024.10658","url":null,"abstract":"<p><p>This study aimed to investigate the prognostic value of the pan-immune-inflammation value (PIV) in patients with locally advanced rectal cancer (LARC) who received neoadjuvant chemoradiotherapy (nCRT) followed by total mesorectal excision. We retrospectively collected and analyzed the clinicopathological data of 215 resected LARC patients. X-tile software was used to determine the optimal threshold value for PIV in predicting overall survival (OS). The predictive ability of PIV for pathological complete regression (pCR), OS, and disease-free survival (DFS) was evaluated and compared with other inflammation markers. Univariate and multivariate logistic regression analyses for pCR and Cox regression analyses for OS and DFS were conducted. The optimal threshold value for PIV was determined to be 454.7 based on the X-tile software. Patients were then categorized into low (≤ 454.7) and high (> 454.7) PIV groups comprising 153 and 62 patients, respectively. PIV demonstrated superior predictive ability for pCR, OS, and DFS compared to other inflammation markers. LARC patients with low PIV had significantly higher pCR (P = 0.029), OS (P = 0.002), and DFS (P = 0.001) rates compared to those with high PIV. Multivariate regression analysis identified PIV as an independent prognostic factor for pCR (odds ratio = 0.32; 95% confidence interval [CI], 0.10-0.80; P = 0.014), OS (hazard ratio = 3.08; 95% CI, 1.77-5.35; P = 0.001), and DFS (hazard ratio = 2.53; 95% CI, 1.58-4.06; P = 0.002). This study confirmed that preoperative PIV could serve as a useful independent prognostic factor in LARC patients treated with nCRT.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1000-1008"},"PeriodicalIF":0.0,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11984369/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142115561","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":"Silencing FOXA1 suppresses inflammation caused by LPS and promotes osteogenic differentiation of periodontal ligament stem cells through the TLR4/MyD88/NF-κB pathway.","authors":"Miao He, Yangdong Lin","doi":"10.17305/bb.2024.11367","DOIUrl":"10.17305/bb.2024.11367","url":null,"abstract":"<p><p>Human periodontal ligament stem cells (hPDLSCs) play a critical role in the regeneration of periodontal tissue. Forkhead box protein A1 (FOXA1) has been implicated in the inflammatory mechanisms of various diseases. However, the role of FOXA1 in periodontal inflammation and its effect on the osteogenic differentiation of hPDLSCs remains unclear. In this study, healthy tooth root-derived hPDLSCs were isolated, and flow cytometry was used to detect cell surface markers. Western blot and immunofluorescence analyses were performed to assess FOXA1 levels in different tissues. The levels of inflammatory factors were measured using Western blot and ELISA kits. Alkaline phosphatase (ALP) staining, alizarin red S staining, and Western blot were employed to evaluate the impact of FOXA1 silencing on the osteogenic differentiation of hPDLSCs. Finally, the protein levels in the Toll-like receptor 4 (TLR4)/Myeloid differentiation factor-88 (MyD88)/NF-κB pathway were analyzed using Western blot. Results showed that periodontal membrane tissues from patients with periodontitis exhibited a marked increase in FOXA1 levels. Lipopolysaccharide (LPS) treatment significantly upregulated FOXA1 expression in hPDLSCs, elevated inflammatory factor levels, and inhibited osteogenic differentiation. However, silencing FOXA1 mitigated the effects of LPS. Furthermore, LPS treatment activated the TLR4/MyD88/NF-κB pathway, while FOXA1 silencing impeded this activation. Notably, the application of the TLR4 agonist CRX-527 reversed the inhibitory effects of FOXA1 silencing on LPS-induced responses. In summary, silencing FOXA1 reduced cellular inflammation by inhibiting the TLR4/MyD88/NF-κB pathway and alleviated the suppressive effects of LPS on the osteogenic differentiation of hPDLSCs.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1138-1149"},"PeriodicalIF":0.0,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11984371/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142933951","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":"miR-145-5p regulates hepatocellular carcinoma malignant advancement and immune escape via down-regulation of AcylCoA synthase ACSL4.","authors":"Dingxue Wang, Wenqi Huang, Gao Li","doi":"10.17305/bb.2024.11209","DOIUrl":"10.17305/bb.2024.11209","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) exhibits a subtle onset, high incidence rates, and low survival rates, becoming a substantial threat to human health. Hence, it is crucial to discover fresh biomarkers and treatment targets for the early detection and management of HCC. CCK-8, scratch-wound, and transwell assays were used to evaluate the biological properties of HCC cell lines (Huh-7 and Hep3B). Bioinformatics analysis identified the downstream target mRNA of miR-145-5p as acyl-CoA synthetase long-chain family member 4 (ACSL4). RT-qPCR was used to test miR-145-5p and ACSL4 levels. Transwell chambers were used to co-incubate purified CD8+ T cells and HCC cells for 48 h, and the effect of CD8+ T cells on apoptosis in HCC cells was detected by flow cytometry. A subcutaneous graft tumor model was constructed, and ELISA kits were used to assess cytokine levels and CD8+ T cell activation markers. HCC cells showed a decline in miR-145-5p levels and a rise in ACSL4 levels. Overexpression of miR-145-5p hindered HCC cell proliferation, migration, and invasion, while stimulating CD8+ T cell activation. Conversely, overexpression of ACSL4 enhanced the malignant biological properties of HCC cells and reduced the effect of CD8+ T cells, while silencing ACSL4 had the opposite effect. miR-145-5p targeted and downregulated ACSL4, while overexpression of miR-145-5p weakened the promotion of HCC malignant progression caused by ACSL4 overexpression. Additionally, overexpression of miR-145-5p and silencing ACSL4 were effective in inhibiting tumor growth in vivo. In conclusion, miR-145-5p targets and downregulates ACSL4, leading to the inhibition of HCC malignant progression and preventing immune escape in HCC cells.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1184-1196"},"PeriodicalIF":0.0,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11984366/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142803606","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}
Tatiana Zavarykina, Maria Kapralova, Polina Lomskova, Aleksandra Asaturova, Grigory Khabas, Lyailya Kayumova, Dmitry Khodyrev, Irina Pronina, Maya Sannikova, Svetlana Khokhlova
{"title":"The association of rs25487 of the <i>XRCC1</i> gene and rs13181 of the <i>ERCC2 </i>gene polymorphisms with the ovarian cancer risk.","authors":"Tatiana Zavarykina, Maria Kapralova, Polina Lomskova, Aleksandra Asaturova, Grigory Khabas, Lyailya Kayumova, Dmitry Khodyrev, Irina Pronina, Maya Sannikova, Svetlana Khokhlova","doi":"10.17305/bb.2024.11314","DOIUrl":"10.17305/bb.2024.11314","url":null,"abstract":"<p><p>Ovarian cancer (OC) is the most lethal gynecological cancer worldwide. DNA damage plays an important role in cancer development, and the proteins encoded by XRCC1 and ERCC2 are important components of the DNA repair system. This study aimed to examine the relationship between the rs25487 XRCC1 and rs13181 ERCC2 polymorphisms and the risk of OC development in women from the Moscow region. DNA was isolated from the blood of 129 healthy donors and tissues and blood samples from 125 patients with OC and studied using real-time PCR. An increase in odds ratios (OR) was obtained for OC tissue and blood for both T (OR = 1.46, 95% confidence interval [CI] = 1.22-1.76, P = 0.00005), and for T/T of rs25487 XRCC1. The most significant OR values were found for the T/T genotype using the codominant model (OR = 2.11, 95% CI = 1.44-3.07, P = 0.00006) and dominant model (OR = 3.13, 95% CI = 1.44-6.79, P = 0.0025) for the pooled blood and tissue groups. For rs13181 ERCC2, differences were observed for the T/G genotype in OC tissues (OR = 0.69, 95% CI = 0.51-0.92, P = 0.011) in the codominant model. In this study, the association of allele T and genotypes of rs25487 XRCC1 and T/G of rs13181 ERCC2 with OC was shown. Our results indicate that these polymorphisms may be involved in the pathogenesis of OC and are promising for further studies on therapeutic applications in OC.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1197-1204"},"PeriodicalIF":0.0,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11984361/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142857201","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}
Wei Wang, Lei Zhang, Ansheng Wang, Xiaohua Wang, Weidong Wu
{"title":"Unveiling the impact of C15orf48 on non-small cell lung cancer through NF-kappa B signaling.","authors":"Wei Wang, Lei Zhang, Ansheng Wang, Xiaohua Wang, Weidong Wu","doi":"10.17305/bb.2024.11113","DOIUrl":"10.17305/bb.2024.11113","url":null,"abstract":"<p><p>The role of the C15orf48 gene in lung cancer is not well understood. This study aimed to investigate the effect of C15orf48 in non-small cell lung cancer (NSCLC). Bioinformatics analyses were performed using Oncomine, The Cancer Genome Atlas (TCGA), Protein-Protein Interaction (PPI) networks, Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Set Enrichment Analysis (GSEA). Immunohistochemical staining was used to detect C15orf48 expression in tissue microarrays. Cellular assays, including CCK8, colony formation, wound healing, transwell migration, flow cytometry, and cell adhesion, were conducted to assess cell viability, proliferation, invasion, and apoptosis. A xenograft tumor model was used to examine tumor growth, and Western blotting was used to detect protein expression. C15orf48 expression was significantly upregulated in tumor tissues compared to normal tissues and was associated with poor prognosis. Knockdown of C15orf48 in A549 and H1299 cells reduced proliferation, invasion, and adhesion while increasing apoptosis. C15orf48 knockdown also inhibited tumor growth in vivo and was associated with immune cell infiltration. Although C15orf48 expression correlated with the epithelial-mesenchymal transition (EMT) score, no significant differences were observed. GSEA identified the NF-κB signaling pathway as a key pathway involved. Proteins PLAUR, IKBα, IL-1RN, ICAM1, and TMPRSS4 showed decreased expression in the shC15orf48 group compared to the shCtrl group. We concluded that C15orf48 promotes NSCLC progression, potentially through immune cell infiltration and the NF-κB signaling pathway.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1162-1174"},"PeriodicalIF":0.0,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11984370/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142693963","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":"L-theanine promotes angiogenesis in limb ischemic mice by modulating NRP1/VEGFR2 signaling.","authors":"Jingyi Wang, Yinghui Xu, Yating Ruan, Xinyang Hu","doi":"10.17305/bb.2024.11256","DOIUrl":"10.17305/bb.2024.11256","url":null,"abstract":"<p><p>Peripheral artery disease (PAD), primarily caused by atherosclerosis, leads to the narrowing or blockage of arteries that supply blood to the limbs. This study explores the pro-angiogenic effects of L-theanine and its underlying mechanisms in a mouse model of hindlimb ischemia (HLI). To evaluate L-theanine's pro-angiogenic effects, human umbilical vein endothelial cells (HUVECs) were subjected to tube formation, migration, sprouting, and proliferation assays. In vivo, C57BL/6 mice with induced HLI were treated with L-theanine. Blood flow recovery was measured via Doppler ultrasound, and vascular density was analyzed using immunofluorescence staining. RNA sequencing identified neuropilin-1 (NRP1) as a key regulator, and the expression levels of NRP1 and VEGFR2 were examined through qPCR and Western blotting. L-theanine significantly enhanced angiogenesis in HUVECs, as demonstrated by improved tube formation, migration, sprouting, and proliferation. In mice, L-theanine treatment resulted in increased vessel density and improved blood flow recovery. Furthermore, L-theanine was found to activate the NRP1/VEGFR2 signaling pathway in both HUVECs and the HLI mouse model. These findings indicate that L-theanine can promote angiogenesis and activate key pathways involved in vascular repair, suggesting its potential as a therapeutic agent for treating vascular defects associated with PAD.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1063-1078"},"PeriodicalIF":0.0,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11984362/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142973625","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}