Molecular Biology Reports最新文献

{"title":"Curcumin and acute myeloid leukemia: a golden hope, updated insights.","authors":"Hamed Soleimani Samarkhazan, Hanieh Noormohamadi, Fatemeh Sadat Shafiei, Niloofar Pilehvari, Amir Hossein Aghaei, Mohammad Hossein Mohammadi, Mehrnoosh Shanaki","doi":"10.1007/s11033-025-10692-z","DOIUrl":"https://doi.org/10.1007/s11033-025-10692-z","url":null,"abstract":"<p><p>Acute myeloid leukemia (AML) is marked by uncontrolled growth of malignant cells in the bone marrow, presenting a major challenge in hematology despite treatment advances. Curcumin, a polyphenol from turmeric, shows promise as an anticancer agent with multiple mechanisms targeting pathways like NF-κB, STAT3, PI3K/AKT, and MAPK. This review highlights curcumin's antileukemic effects, including apoptosis induction, cell proliferation inhibition, and angiogenesis modulation. Although low bioavailability limits its clinical use, nanoformulations such as liposomes and micelles have improved curcumin's stability and uptake. Combining curcumin with standard chemotherapies has shown synergistic effects, enhancing anticancer efficacy. Preclinical studies consistently demonstrate curcumin's antileukemic impact in AML cell lines and animal models, showing reduced tumor load and prolonged survival. Ongoing clinical trials are assessing curcumin's safety and efficacy in AML patients, with early results indicating potential. However, larger randomized trials are needed for confirmation. In conclusion, curcumin's anticancer properties and safety profile make it a valuable candidate for AML treatment. Further research is necessary to refine delivery methods, optimize combination therapies, and substantiate its role through clinical trials.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"583"},"PeriodicalIF":2.6,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144266731","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":"The importance of ALPK1 kinase functionality as a potential biomarker for inflammatory diseases.","authors":"Yessica Zamudio-Cuevas, Javier Fernández-Torres, Karina Martínez-Flores, Ambar López-Macay","doi":"10.1007/s11033-025-10528-w","DOIUrl":"https://doi.org/10.1007/s11033-025-10528-w","url":null,"abstract":"<p><p>Currently, molecules with the potential to act as biomarkers in the prevention and early diagnosis of diseases are being sought. The above implies that these molecules play key roles in specific stages of the disease or are associated with them. However, before proposing these types of molecules as biomarkers or therapeutic targets, it is essential to thoroughly understand their action mechanism. In this work, the most relevant findings on the function, regulation, disease´s association studies of the ALPK1 protein with kinase activity (α kinase-1) are highlighted. Unlike other protein kinases, ALPK1 specifically recognizes the conformation part of the alpha helix as the phosphorylation site. The objective of this review is to analyze the functions of ALPK1 in different pathologies and to determine whether this protein plays an important role in these diseases, and if it could be used as a biomarker for the progression or prediction of an inflammatory disease.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"575"},"PeriodicalIF":2.6,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144258571","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":"LRG1 in cancer: mechanisms, potential therapeutic target, and use in clinical diagnosis.","authors":"Federico Osorio-Antonio, Daniela Michel Diaz-González, Elizabeth Bautista-Rodríguez, Gabriela Elizabeth Campos-Viguri, Oscar Peralta-Zaragoza, José Manuel Sánchez-López, José Luis Cortez-Sánchez, Cristina Muñoz-Olivos, Francisco Castelán, Verónica Velázquez-Orozco","doi":"10.1007/s11033-025-10669-y","DOIUrl":"https://doi.org/10.1007/s11033-025-10669-y","url":null,"abstract":"<p><p>Leucine-rich alpha-2 glycoprotein 1 (LRG1) is an extracellular protein whose elevated expression has been linked to cancers with poor prognosis and low survival rates. Given its significance as a biomarker, this manuscript explores the role of LRG1 in cancer, as several studies have identified it as a promoter of proliferation, angiogenesis, invasion, and metastasis in breast, ovarian, pancreatic, and neuroblastoma cancers. However, contrasting evidence suggests that LRG1 inhibits proliferation in hepatocellular carcinoma cells and suppresses migration and invasion in esophageal squamous cell carcinoma. We also examine its regulation and the associated signaling pathways, including TGF-β and PI3K/AKT/mTOR.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"577"},"PeriodicalIF":2.6,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144258558","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":"Combined effects of IRAK inhibition and pioglitazone on hepatic inflammation and apoptosis in a mouse model of MASLD.","authors":"Hossein Fallah, Behnaz Danesh, Beydolah Shahouzehi","doi":"10.1007/s11033-025-10675-0","DOIUrl":"https://doi.org/10.1007/s11033-025-10675-0","url":null,"abstract":"<p><strong>Background: </strong>Inflammation and apoptosis play crucial role in the progression of liver diseases. This study aimed to evaluate the effects of Interleukin-1 receptor-associated kinase inhibitor (IRAKi) in combination with pioglitazone on the expression of inflammatory and apoptotic markers in the liver of C57BL/6J mice subjected to a high-fat diet (HFD).</p><p><strong>Methods: </strong>Male C57BL/6J mice were divided into five groups: Control (normal diet, ND), HFD, HFD-IRAKi, HFD-pioglitazone (HFD-PIO), and HFD-IRAKi-PIO. All groups, except ND, were administered HFD for 12 weeks. Subsequently, IRAKi (2 mg/kg, intraperitoneally, three times per week) and pioglitazone (10 mg/kg, orally, daily) were administered for 14 days. Gene and protein expression levels were assessed using real-time PCR and western blot analysis.</p><p><strong>Results: </strong>Separate administration of IRAKi and pioglitazone significantly reduced the mRNA levels of inflammatory markers IL-1β, IL-6, TNF-α, and NF-κB (p < 0.001). Combined treatment with IRAKi and pioglitazone significantly reduced hepatic triglyceride (TG) and cholesterol content (p < 0.05) and attenuated expression of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α, NF-κB) and apoptotic markers (cleaved-CASPASE3, Bax), while enhancing Il10 expression. These findings support the therapeutic potential of this combination in metabolic liver diseases such as MASLD.</p><p><strong>Conclusion: </strong>Co-administration of IRAKi and PIO attenuated markers of inflammation and apoptosis. These findings highlight the potential of IRAKi and pioglitazone as therapeutic agents for metabolic and inflammatory liver diseases, warranting further clinical evaluation.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"576"},"PeriodicalIF":2.6,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144258557","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":"Precore G1896A mutation of hepatitis B virus in patients with chronic hepatitis B, hepatic cirrhosis, and hepatocellular carcinoma in Burkina Faso.","authors":"Hodabalou Essoyomèwè Eugène Languie, Pegdwendé Abel Sorgho, Rogomenoma Alice Ouedraogo, Albert Théophane Yonli, Abdoul Karim Ouattara, Sidnooma Véronique Zongo, Théodora Mahoukèdè Zohoncon, Jacques Simpore","doi":"10.1007/s11033-025-10668-z","DOIUrl":"https://doi.org/10.1007/s11033-025-10668-z","url":null,"abstract":"<p><strong>Background: </strong>Hepatitis B virus (HBV) infection, which can progress to liver cancer and even death, remains a public health problem. The high variability of HBV leading to the accumulation of mutations influences the natural history of this infection. Mutations in the precore/core region, in particular the G1896A mutation, have been associated with severe forms of liver disease in certain populations around the world. The aim of this study was to determine the molecular epidemiology of the HBV precore G1896A mutation and its relationship to hepatic complications in HBV chronically infected patients.</p><p><strong>Methods: </strong>Classical nested PCR was used to amplify the HBV precore region. A total of 97 samples consisting of 53 cases of chronic hepatitis B (CHB), 18 cases of hepatic cirrhosis (HC) and 26 cases of hepatocellular carcinoma (HCC) were amplified. The G1896A mutation was determined by enzymatic digestion on 81 samples using the restriction enzyme Bsu36I. Serological (HBeAg, anti-HBe Ac), biochemical (ALT) and virological (HBV-DNA viral load) tests were performed.</p><p><strong>Results: </strong>The frequency of the G1896A mutation was 44.44% in our study population. It was 56.82% in CHB cases, 28.57% in HC cases and 30.43% in HCC. The G1896A mutation was found more in subjects with a negative HBeAg status than in those with a positive HBeAg (p = 0.05) in the CHB subgroup. The DNA level was higher in subjects carrying wild-type strains for the G1896A mutation (p > 0.05). ALT levels were lower in subjects carrying the G1896A mutation than in those infected with wild-type strains (p = 0.006) in the HBC subgroup.</p><p><strong>Conclusion: </strong>This study, conducted on patients with chronic hepatitis B, cirrhosis, and hepatocellular carcinoma (HCC), showed that the frequency of the precore G1896A mutation was 44.44%. We found no correlation between this mutation and cirrhosis and HCC. However, it was more found in subjects with chronic hepatitis B and was associated with HBeAg negativity in the latter. It would therefore be involved in the elimination of this protein partly responsible for the persistence of HBV infection and could be a molecular marker for clinicians in the management of patients infected with HBV with negative HBeAg and positive anti-HBe antibodies. However, studies on other mutations of the precore gene would be necessary to obtain more conclusive results in terms of effective treatment.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"578"},"PeriodicalIF":2.6,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144258570","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":"Novel therapeutic strategies targeting infections caused by P. aeruginosa biofilm.","authors":"Rajeshwari Lekhwar, Sunil Kumar, Mahima Tripathi, Saurabh Gangola, Anil Kumar Sharma","doi":"10.1007/s11033-025-10683-0","DOIUrl":"https://doi.org/10.1007/s11033-025-10683-0","url":null,"abstract":"<p><p>Pseudomonas aeruginosa is a gram-negative clinical pathogen, particularly affecting immunocompromised patients, those with cystic fibrosis, and burn victims. It causes chronic infections, especially in hospital settings, and is a significant contributor to nosocomial infections. Its capacity to create biofilms resistant to antibiotics is the reason for its infamous persistence in clinical settings. P. aeruginosa infections can affect any area of the body because the bacteria's biofilm enables it to stick to any surface, living or non-living. One of the primary clinical challenges in treating P. aeruginosa biofilm is its noteworthy resistance to many classes of antibiotics. The bacterium's ability to acquire resistance through efflux pumps, beta-lactamase production, and genetic mutations complicates treatment options. Recently, multidrug- resistant (MDR) strains of P. aeruginosa are becoming increasingly prevalent, limiting the efficacy of traditional antibiotics and leading to the need for alternative therapies. There is an ongoing need for novel treatment options, including bacteriophage therapy, antimicrobial peptides, and vaccines. The rapid adaptability of P. aeruginosa and its ability to develop resistance underscores the importance of continued research into new therapeutic strategies. This review discusses the various therapeutic strategies like; antimicrobial therapy, targeting efflux pumps and biofilms of P. aeruginosa, phage therapy, immunotherapy and nanotechnology to explore the mechanisms, through which antimicrobial compounds interact with biofilm structures and the bacteria within.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"571"},"PeriodicalIF":2.6,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144248743","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":"NETosis in hypersensitivity disorders.","authors":"Manouchehr Fadaee, Reza Aghaei, Niloufar Orooji, Sina Mahdavi, Masoud Lahouty, Shabnam Babaei, Mahdyar Shahizare, Golnaz Mobayen, Armin Ghahremanzadeh","doi":"10.1007/s11033-025-10629-6","DOIUrl":"https://doi.org/10.1007/s11033-025-10629-6","url":null,"abstract":"<p><p>Neutrophils are the first cells among the innate and adaptive immune cells, which quickly react to infections, injuries, and disease. Neutrophils have a wide range of antimicrobial proteins that are secreted from the cell through the NETosis process. Neutrophil extracellular traps (NETs) are intricate formations composed of chromatin decondensed and coated with granular and cytosolic proteins. The body's defensive mechanism first identified NETs as critical participants due to their capacity to immobilize and even eliminate germs. Follow-up investigations have shown that these substances have a role in developing numerous diseases, as their significant components harm nearby tissues. Hypersensitivity disorders are characterized by an unregulated and inappropriate immune response to innocuous antigens, resulting in numerous detrimental results. Both excessive NETosis and poor NET clearance contribute to the tissue damage observed in hypersensitivity disorders such as small vessel vasculitis (SVV), systemic lupus erythematosus (SLE), and psoriasis. NETs can also activate T cells to initiate inflammatory reactions and tissue damage. Here, we explore the recent advances in the role of NETosis in the pathogenesis of hypersensitivity disorders.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"574"},"PeriodicalIF":2.6,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144248742","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":"A novel DNA aptamer for Vibrio cholerae O139 detection: a whole-cell SELEX approach.","authors":"Masilamani Karthikeyan, Mohandass Ramya, Pasupathi Rathinasabapathi","doi":"10.1007/s11033-025-10677-y","DOIUrl":"https://doi.org/10.1007/s11033-025-10677-y","url":null,"abstract":"","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"569"},"PeriodicalIF":2.6,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144248735","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":"Immune profiling of kidney transplant recipients: the role of Tribbles-1, Perforin, and Granzyme B in chronic humoral rejection.","authors":"Marzie Esmaeili, Shima Afzali, Sepehr Dadfar, Samad Farashi Bonab, Maryam Rahbar, Aliakbar Amirzargar, Dariush Haghmorad","doi":"10.1007/s11033-025-10688-9","DOIUrl":"https://doi.org/10.1007/s11033-025-10688-9","url":null,"abstract":"<p><strong>Introduction: </strong>For patients with end-stage renal disease (ESRD), kidney transplantation is the most effective treatment option, yet chronic antibody-mediated rejection (cAMR) remains a key challenge to long-term graft survival. Natural killer (NK) cells are implicated in allograft rejection, but their precise role remains unclear. This study assessed NK cell activity and the expression of Tribbles-1, Perforin, and Granzyme B in kidney transplant recipients with either stable grafts or cAMR.</p><p><strong>Methods: </strong>Peripheral blood samples from 60 transplant recipients (30 stable grafts, 30 cAMR) were analyzed for NK cell percentages, activation (CD107a expression), and gene expression of Perforin, Granzyme B, and Tribbles-1 using real-time PCR.</p><p><strong>Results: </strong>NK cell numbers were similar in both groups, likely due to the influence of immunosuppressive therapy. However, cAMR patients exhibited significantly higher CD107a expression, suggesting heightened NK cell activation, potentially due to suboptimal immunosuppressive dosing. While Perforin and Tribbles-1 expression showed no significant differences between the two groups, Granzyme B expression was higher in stable graft recipients than in those with cAMR.</p><p><strong>Conclusion: </strong>These findings indicate that peripheral blood Granzyme B expression is not a specific biomarker for graft dysfunction, as elevated levels were also observed in stable graft recipients. Additionally, since Granzyme B is expressed in multiple immune cell types, its elevated levels in stable patients may indicate broader immune activation rather than graft dysfunction.</p><p><strong>Clinical trial number: </strong>Not applicable.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"573"},"PeriodicalIF":2.6,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144248739","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":"Targeting neurotrophic dysregulation in diabetic retinopathy: a novel therapeutic avenue.","authors":"Divya Rana, Sanchit Dhankhar, Rupali Chauhan, Monika Saini, Randhir Singh, Parveen Kumar, Thakur Gurjeet Singh, Samrat Chauhan, Sushma Devi","doi":"10.1007/s11033-025-10671-4","DOIUrl":"https://doi.org/10.1007/s11033-025-10671-4","url":null,"abstract":"<p><p>The gradual retinal damage caused by chronic hyperglycemia is known as Diabetic retinopathy (DR), and it is the main cause of visual impairment and blindness in adults. The importance of neurotrophic factors in DR pathogenesis has been emphasized by recent studies. In diabetes, several naturally occurring proteins undergo substantial changes that impact neuronal survival, development, and differentiation. A number of neurotrophic factors, such as Brain-derived neurotrophic factor (BDNF), Nerve growth factor (NGF), Ciliary neurotrophic factor (CNTF), Glial cell line-derived neurotrophic factor (GDNF), Insulin-like Growth Factor-1 (IGF-1), fibroblast growth factor (FGF) play interdependent roles in DR, and this review offers a new prospective into these relationships. The processes for downregulating these neurotrophic factors were investigated, together with their altered expression patterns, action mechanisms, and therapeutic target potential, in this review. The crosstalk between neurotrophic factors and inflammatory pathways, oxidative stress, and vascular dysfunction in the diabetic retina is elucidated, offering insights into the complex neurovascular interplay in DR. Furthermore, emerging therapeutic strategies aimed at modulating neurotrophic factors to prevent or ameliorate retinal neurodegeneration are discussed. This comprehensive overview underscores the necessity for integrated approaches targeting neurotrophic support to develop effective interventions for diabetic retinopathy.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"570"},"PeriodicalIF":2.6,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144248756","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}