{"title":"Expression of DDX49 in breast cancer and its mechanism regulating the proliferation and metastasis of breast cancer cells.","authors":"Yuanbin Wang, Lijun Yang, Xiangli Li, Qing Yang, Ruimin Ma, Zhihao Wu","doi":"10.1080/08977194.2025.2484007","DOIUrl":"https://doi.org/10.1080/08977194.2025.2484007","url":null,"abstract":"<p><p>DEAD-box RNA helicase (DDX) is linked to the invasion, drug resistance, proliferation, and epithelial-mesenchymal transition of tumour cells. This study examined the potential mechanisms of DDX49 in breast cancer. The expression of DDX49 in breast cancer tissues and cells was evaluated. The effects of DDX49 on proliferation, invasion, migration and apoptosis of breast cancer cells were evaluated. The expression of proteins associated with the JAK/STAT pathway was examined. A xenograft tumour model was established. DDX49 expression is elevated in breast cancer tissues and cell lines. shDDX49 suppressed the ability of breast cancer cells to proliferate, invade, and migrate, but promoted apoptosis. Conversely, overexpression of DDX49 exerted an opposite effect. The activation of the JAK-STAT signalling pathway is inhibited by the shDDX49. shDDX49 efficiently inhibits tumour growth in mice with breast cancer. shDDX49 may hinder the growth and spread of breast cancer cells by inhibiting the JAK-STAT pathway.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":" ","pages":"1-11"},"PeriodicalIF":1.8,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143779767","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Super-activated platelet lysate promotes mesenchymal stem cell proliferation, migration, and chondrogenic differentiation: an in vitro study.","authors":"Chunxiang Liu, Tianqi Zhang, Lingqi Meng, Ihsan Ullah, Heng Li, Fuge Sui, Yi Zhang","doi":"10.1080/08977194.2025.2484614","DOIUrl":"https://doi.org/10.1080/08977194.2025.2484614","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to investigate the effects of super-activated platelet lysate (sPL) on the proliferation, migration, and chondrogenic differentiation of human umbilical cord mesenchymal stem cells (hUCMSCs).</p><p><strong>Methods: </strong>Cell proliferation and migration assay, enzyme-linked immunosorbent analysis, RT-qPCR, chondrogenic differentiation, and Western blot were performed on sPL-treated hUCMSCs.</p><p><strong>Results: </strong>The extraction of sPL from PRP yielded a significant release of growth factors. The proliferation of hUCMSCs was significantly enhanced by both 5% and 10% sPL, and the 5% sPL showed the most promising results. Additionally, 10% sPL demonstrated the strongest positive effect on hUCMSC migration. The 20% sPL group showed a significant decrease in inflammatory factor levels compared to the 0% sPL group when hIL-1β was added to the differentiation system. Notably, hUCMSCs in the 5% sPL, 10% sPL and 20% sPL groups displayed excellent chondrogenic differentiation.</p><p><strong>Conclusion: </strong>In summary, sPL demonstrates the ability to promote stem cell proliferation, migration, and chondrogenic differentiation, while also suppressing inflammation.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":" ","pages":"1-13"},"PeriodicalIF":1.8,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143752369","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Growth factorsPub Date : 2025-03-13DOI: 10.1080/08977194.2025.2470185
James Dimou, Giovanna D'Abaco, Lucy Paradiso, Nicole Kountouri, Wayne Ng, Stanley Stylli, Katharine Drummond, Antony Burgess, Andrew Kaye, Andrew Morokoff
{"title":"Akt inhibition is effective against PTEN-deleted, chemoirradiation-resistant glioblastoma stem cells.","authors":"James Dimou, Giovanna D'Abaco, Lucy Paradiso, Nicole Kountouri, Wayne Ng, Stanley Stylli, Katharine Drummond, Antony Burgess, Andrew Kaye, Andrew Morokoff","doi":"10.1080/08977194.2025.2470185","DOIUrl":"https://doi.org/10.1080/08977194.2025.2470185","url":null,"abstract":"<p><p>Activated Akt and loss of phosphatase and tensin homolog (PTEN) tumour suppression aid chemo- and radio-resistance in glioblastoma stem cells (GSC), contributing to treatment failure in glioblastoma. In this study, sixteen GSC lines were generated from 66 individual glioma samples, in gliomasphere culture conditions. Thirteen of 16 GSC lines expressed hyperphosphorylated Akt (Ser473); Akt phosphorylation did not correlated with EGFR expression. An LDH colorimetric assay was used to measure the in vitro cytotoxicity of eight of these lines. Akt X (20 µM) proved more effective at inducing in vitro GSC cytotoxicity (range: 22-73%) over 48 hours than triciribine (20 µM) (0-27%), although both agents inhibited Akt phosphorylation as detected by western blot analysis. A statistically significant correlation between PTEN loss (western blot) and the extent of Akt X-induced cytotoxicity was found (p = 0.03). Akt inhibition reduces in vitro proliferation of treatment-resistant GSC lines, especially in PTEN-deficient lines, warranting further translational investigation in glioblastoma.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":" ","pages":"1-17"},"PeriodicalIF":1.8,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143614650","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Growth factorsPub Date : 2025-03-12DOI: 10.1080/08977194.2025.2478393
Nataša Todorović-Raković, Jelena Milovanović, Marko Radulovic, John Greenman
{"title":"Serum HER2 as potential prognostic biomarker in primary breast cancer patients.","authors":"Nataša Todorović-Raković, Jelena Milovanović, Marko Radulovic, John Greenman","doi":"10.1080/08977194.2025.2478393","DOIUrl":"https://doi.org/10.1080/08977194.2025.2478393","url":null,"abstract":"<p><p>Tissue expressed human epidermal growth factor receptor 2 (HER2) is an established parameter of breast cancer, and it is determined in routine clinical practice by histology. This study aims to assess the prognostic value of serum HER2 protein quantified using ELISA in 66 primary breast cancer patients. The median follow-up period was 94 months. Prognostic performance was assessed through receiver operating characteristic (ROC), Cox proportional hazards regression, and Kaplan-Meier analyses. There was a significant difference between serum HER2 levels of patients with and without recurrence. Prognostic associations were significant for age, grade, nodal status, follicle-stimulating hormone, oestradiol, and serum HER2. The cut-off point for serum HER2 levels was 6.0 ng/mL. Recurrence incidence was 29% in the serum HER2<b><sup>high</sup></b> subgroup, compared to only 10% in the serum HER2<b><sup>low</sup></b> subgroup. Serum HER2 testing by ELISA holds promise as an additional tool alongside routine tissue HER2 analysis for primary breast cancer patients.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":" ","pages":"1-8"},"PeriodicalIF":1.8,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143604685","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Growth factorsPub Date : 2025-02-22DOI: 10.1080/08977194.2025.2467135
Xiaowen Yu, Xuan Chen, Jun Ouyang, Biao Xi, Defeng Wu, Ling Wei, Dongyu Xie, Yaxiang Shi
{"title":"Exploring the mechanisms of Shugan-Jieyu-Jianpi formula against irritable bowel syndrome combined with non-alcoholic fatty liver disease by network pharmacology and experimental validation.","authors":"Xiaowen Yu, Xuan Chen, Jun Ouyang, Biao Xi, Defeng Wu, Ling Wei, Dongyu Xie, Yaxiang Shi","doi":"10.1080/08977194.2025.2467135","DOIUrl":"https://doi.org/10.1080/08977194.2025.2467135","url":null,"abstract":"<p><p>The study was aimed to investigate the clinical effect and mechanism of Shugan-Jieyu-Jianpi (SGJYJP) formula for the treatment of irritable bowel syndrome (IBS) combined with non-alcoholic fatty liver disease (NAFLD). The clinical efficacy of SGJYJP was evaluated in 54 patients with IBS-NAFLD. The potential molecular mechanism of SGJYJP formula was investigated by network pharmacology. Animal models were constructed to explore the related mechanism. From clinical studies, the total effective rate of patients in SGJYJP group was significantly higher than that in pinaverium group. The protein expression of TGFB1 was declined in IBS-NAFLD rats, together with the increased expression of PTGS2 and TNF, which was abolished by SGJYJP treatment. SGJYJP significantly reduced the expression of TNF signalling related molecules of TRAF2, caspase-8, and elevated the expression of Bcl-xl in IBS-NAFLD animal models. SGJYJP may exert therapeutic effect on IBS-NAFLD by targeting PTGS2, TGFB1, and TNF genes and TNF signalling.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":" ","pages":"1-19"},"PeriodicalIF":1.8,"publicationDate":"2025-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143476433","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Growth factorsPub Date : 2024-10-01Epub Date: 2024-12-25DOI: 10.1080/08977194.2024.2432951
G A Alsabri, F van der Horst, S A Alkaabi, S A Alavi, T Forouzanfar, M N Helder
{"title":"Evaluating growth-factor release in leukocyte- and platelet-rich fibrin, advanced platelet-rich fibrin, and injectable platelet-rich fibrin protocols: a narrative review.","authors":"G A Alsabri, F van der Horst, S A Alkaabi, S A Alavi, T Forouzanfar, M N Helder","doi":"10.1080/08977194.2024.2432951","DOIUrl":"10.1080/08977194.2024.2432951","url":null,"abstract":"<p><p>Since its introduction in 2001, multiple platelet-rich fibrin (PRF) centrifugation protocols have emerged, but the variations in growth factor release that result from these protocols remain unclear. This review aimed to evaluate growth factor release across three PRF protocols: leukocyte-PRF (L-PRF), advanced-PRF (A-PRF/+), and injectable-PRF (i-PRF). A comprehensive search was conducted using the MEDLINE and Embase databases, identifying 14 studies that met the inclusion criteria. Due to significant heterogeneity in study designs and methodologies, a meta-analysis was not feasible. However, our findings suggest that lower-speed centrifugation protocols, such as A-PRF/+ and i-PRF, tend to provide a more uniform cell distribution and sustain higher growth factor release over time compared to the conventional L-PRF protocol. Despite these observations, the current evidence is insufficient to draw definitive conclusions about the growth factor release levels among L-PRF, A-PRF/+, and i-PRF. Further well-designed, comparative studies are required to clarify these differences and establish optimal protocols for clinical use.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":" ","pages":"216-228"},"PeriodicalIF":1.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142894007","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Plasma levels and diagnostic utility of VEGF, MMP-9 and TIMP-2 in the diagnosis of psoriasis forms.","authors":"Imen Chihaoui, Arbia Abbes, Wiem Zidi, Nesrine Fourti, Dalenda El Euch, Amel Mebazaa, Moncef Feki, Mourad Mokni, Sameh Hadj Taieb, Monia Allal-Elasmi","doi":"10.1080/08977194.2024.2430205","DOIUrl":"10.1080/08977194.2024.2430205","url":null,"abstract":"<p><p>Psoriasis pathogenisis remain unknown despite the fact that it is considered as the most common autoimmune skin disease. We raised the hypothesis whether the selected biomarkers in this study provide actual evidence of psoriasis presence and severity. We aim in a first level to study serum level of pro-angiogenic marker VEGF variation and its correlation with MMP-9 and its specific inhibitor TIMP-2 in psoriatic patients serum. The study included 115 psoriatic patients and 51 controls. The biological parameters were measured by ELISA methods. Logistic regression analysis showed that VEGF, MMP-9, and inflammation Z-score are associated with psoriasis. ROC analysis showed that VEGF has low discriminant power for PsVG, However TIMP-2 and inflammation Z-scorewell discriminate this variant of psoriasis. The combined analysis of VEGF-TIMP-2 resulted in a significant increase in discriminant power for PsVG. Increase inflammatory phase may be reflecting the tissue destruction byMMP-9, emphasizing the deleterious expanse and the architectural changes of the skin which are more severe in PsP.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":" ","pages":"188-197"},"PeriodicalIF":1.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142695074","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Growth factorsPub Date : 2024-10-01Epub Date: 2024-10-10DOI: 10.1080/08977194.2024.2413623
Marie Rubin Sander, Agni Karolina Tsiatsiou, Kehuan Wang, Natalia Papadopoulos, Charlotte Rorsman, Frida Olsson, Johan Heldin, Ola Söderberg, Carl-Henrik Heldin, Johan Lennartsson
{"title":"PDGF-induced internalisation promotes proteolytic cleavage of PDGFRβ in mesenchymal cells.","authors":"Marie Rubin Sander, Agni Karolina Tsiatsiou, Kehuan Wang, Natalia Papadopoulos, Charlotte Rorsman, Frida Olsson, Johan Heldin, Ola Söderberg, Carl-Henrik Heldin, Johan Lennartsson","doi":"10.1080/08977194.2024.2413623","DOIUrl":"10.1080/08977194.2024.2413623","url":null,"abstract":"<p><p>Platelet-derived growth factor (PDGF)-induced signalling via PDGF receptor β (PDGFRβ) leads to activation of downstream signalling pathways which regulate multiple cellular responses. It is unclear how PDGFRβ is degraded; both lysosomal and proteasomal degradation have been suggested. In this study, we have characterised the proteolytic cleavage of ligand-activated PDGFRβ, which results in two fragments: a larger fragment containing the extracellular domain, the transmembrane segment, and a part of the intracellular juxtamembrane region with a molecular mass of ∼130 kDa, and an intracellular ∼70 kDa fragment released into the cytoplasm. The proteolytic processing did not take place without internalisation of PDGFRβ. In addition, chelation of intracellular Ca<sup>2+</sup> inhibited proteolytic processing. Inhibition of the proteasome affected signal transduction by increasing the phosphorylation of PDGFRβ, PLCγ, and STAT3 while reducing it on Erk1/2 and not affecting Akt. The proteolytic cleavage was observed in fibroblasts or cells that had undergone epithelial-mesenchymal transition.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":" ","pages":"147-160"},"PeriodicalIF":1.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142463302","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Growth factorsPub Date : 2024-10-01Epub Date: 2024-11-14DOI: 10.1080/08977194.2024.2422014
Weiqiang Wei, Di Xu, Fan Hu, Tenglong Jiang, Hong Liu
{"title":"Platelet-rich plasma promotes wound repair in diabetic foot ulcer mice via the VEGFA/VEGFR2/ERK pathway.","authors":"Weiqiang Wei, Di Xu, Fan Hu, Tenglong Jiang, Hong Liu","doi":"10.1080/08977194.2024.2422014","DOIUrl":"10.1080/08977194.2024.2422014","url":null,"abstract":"<p><p>Diabetic foot ulcers (DFUs) are a severe microvascular complication. Platelet-rich plasma (PRP) pitches in DFU treatment. This study explored the mechanism of PRP facilitating wound repair in DFU mice via vascular endothelial growth factor A (VEGFA)/VEGF receptor 2 (VEGFR2)/extracellular signal-regulated kinase (ERK) pathway. The DFU mouse model was established, with wound skin injected with PRP, followed by the detections of wound area, histopathological changes, and CD31-positive cells. IL-6/TNF-α/VEGFA/VEGFR2/p-VEGFR2/(ERK1/2)/(p-ERK1/2) levels in wound tissue homogenates were assessed. VEGFA-VEGFR2 interaction was evaluated. PRP-treated DFU mice were simultaneously treated with fruquintinib/PD98059. PRP reduced wound area, IL-6 and TNF-α levels, elevated epidermal dermal thickness, CD31-positive cell number, and aligned tissue structure, which were mitigated by fruquintinib/PD98059. PRP promoted VEGFR2 phosphorylation. PRP and fruquintinib/PD98059 abated p-VEGFR2/VEGFR2 or p-ERK1/2/ERK1/2 levels in DFU mice. PRP activated the ERK pathway through VEGFA/VEGFR2. Collectively, PRP promoted VEGFR2 phosphorylation and activated the ERK pathway, thereby facilitating wound repair in DFU mice.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":" ","pages":"161-170"},"PeriodicalIF":1.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142618736","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"GDF15 promotes corneal neovascularization and RB cell progression via AKT/ERK signal pathway.","authors":"Haijian Zheng, Wen Zheng, Shiliang Cheng, Chunguang Li, Guanglan Liu, Miao Yu, Meng Li, Xinfeng Liu, Fangfang Li, Yanluan Wan, Ling Wang","doi":"10.1080/08977194.2024.2432948","DOIUrl":"10.1080/08977194.2024.2432948","url":null,"abstract":"<p><p>In this study, we aim to explore the involvement of growth differentiation factor 15 (GDF15) in both corneal neovascularization (CNV) and retinoblastoma (RB) progression. Cell migration and proliferation were assessed through Scratch assays and CCK-8 assays. Apoptosis was quantified using flow cytometry. In vitro angiogenesis was evaluated through a tube formation assay. RT-PCR and western blot analyses were employed to assess the angiogenesis-related factors. Results demonstrated that RhGDF15 has a promotional effect on the migration of RB cells. Conversely, si-GDF15 demonstrated an opposite effect. RhGDF15 exhibited an enhancement the tube formation, the levels of HIF-1α and SDF, as well as cell migration. Conversely, si-GDF15 demonstrated an opposite effect. The levels of factors were elevated by rhGDF15 in both HREC and RB cell lines. In conclusion, the downregulation of GDF15 has the potential to inhibit corneal angiogenesis and impede the migration of RB cells. These effects may be dependent on the AKT/ERK pathway.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":" ","pages":"205-215"},"PeriodicalIF":1.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142947773","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}