Current Proteomics最新文献

{"title":"Proteomics and metabolomics analysis of Mongolian acupuncture therapy for type 2 diabetes mellitus with atherosclerosis","authors":"Xueyong Li, Mei Miao, Junfeng Zhang, Hu He Mu Ren, Long Bai, Bu He Chao Lu Wang, Mu Ri Gen Ji Ya, Si Leng Ge, A Ru Na, Ai Ji Ma, A Di Na, Yao Ha Si, Wu Lan","doi":"10.1016/j.curpro.2025.100058","DOIUrl":"https://doi.org/10.1016/j.curpro.2025.100058","url":null,"abstract":"Mongolian acupuncture therapy, a traditional modality involving stimulation of specific acupoints, has shown notable benefits in managing diabetes mellitus (DM) and its complications. However, its effects and molecular mechanisms in type 2 DM (T2DM) complicated with atherosclerosis remain unclear. This study aimed to evaluate the therapeutic efficacy and elucidate the molecular mechanisms of Mongolian acupuncture in a rat model of T2DM with atherosclerosis. A T2DM with atherosclerosis rat model was established using high-fat/high-sugar diet feeding, streptozotocin injection, and vitamin D3 administration. Rats were treated with Mongolian acupuncture for 28 days. Serum biochemical parameters and inflammatory markers were assessed. Histopathological changes in the carotid artery were examined by hematoxylin and eosin (H&E) staining. Proteomic and metabolomic analyses were performed to identify differentially expressed proteins (DEPs) and metabolites (DEMs), and key protein changes were validated by Western blot. Mongolian acupuncture significantly improved inflammatory cytokine levels, renal function markers, lipid profiles, and carotid artery histopathology compared with untreated model rats. Proteomics identified 625 DEPs enriched mainly in fatty acid metabolism and energy metabolism pathways. Metabolomics revealed 184 DEMs, with enrichment in linoleic acid, sphingolipid, and amino acid metabolism. Integrated analysis suggested that the therapeutic effects were largely mediated by regulation of fatty acid metabolism, supported by increased expression of HADH, ACADL, ACSF3, and CPT1B, and elevated palmitoleic acid levels. Mongolian acupuncture alleviates vascular and metabolic dysfunction in T2DM with atherosclerosis, potentially through modulation of fatty acid metabolism and energy homeostasis. These findings provide mechanistic insights and experimental evidence supporting the potential clinical application of Mongolian acupuncture for T2DM-associated macrovascular complications.","PeriodicalId":50601,"journal":{"name":"Current Proteomics","volume":"22 5","pages":"100058-100058"},"PeriodicalIF":0.0,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147900168","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NSUN2/FOXM1 positive feedback pathway promotes the malignant development of non-small cell lung cancer","authors":"Lin Wang, Dujuan Zhou, Yangjing Ou","doi":"10.1016/j.curpro.2025.100029","DOIUrl":"https://doi.org/10.1016/j.curpro.2025.100029","url":null,"abstract":"• FOXM1 expression was upregulated in NSCLC tissues and cells. • FOXM1 silencing inhibited NSCLC cell proliferation, invasion, and M2 macrophage polarization and induced cell apoptosis and ferroptosis. • NSUN2 stabilized FOXM1 expression in a YBX1-dependent manner. • FOXM1 transcriptionally activated NSUN2 in NSCLC cells. • NSUN2 knockdown repressed tumor formation by regulating FOXM1. Non-small cell lung cancer (NSCLC) constitutes the majority of lung cancer cases and is associated with poor prognosis. The forkhead box M1 (FOXM1) transcription factor is implicated in cancer progression, yet the precise mechanisms regulating its activity in NSCLC remain poorly understood. Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to assess mRNA expression levels. Immunohistochemistry (IHC) and western blotting were utilized to analyze protein expression. Cell viability was evaluated using a cell counting kit-8 (CCK-8) assay, while 5-ethynyl-2′-deoxyuridine (EdU) assay was used to measure cell proliferation. Cell invasion was determined through a transwell assay. Flow cytometry was performed to quantify CD206-positive M2 macrophages, measure reactive oxygen species (ROS) levels, and analyze cell apoptosis. The colorimetric method was used to analyze Fe 2+ , malondialdehyde (MDA), and glutathione (GSH) levels. M5C methylated RNA immunoprecipitation (MeRIP), RNA immunoprecipitation (RIP), chromatin immunoprecipitation and dual-luciferase reporter assays were conducted to validate the interaction between FOXM1, NOL1/NOP2/Sun domain family, member 2 (NSUN2), and Y-box binding protein 1 (YBX1). In vivo effects of NSUN2 silencing and FOXM1 overexpression on NSCLC cell malignancy were examined using a mouse model assay. FOXM1 expression was elevated in NSCLC tissues and cells. FOXM1 knockdown suppressed NSCLC cell proliferation, invasion, and M2 macrophage polarization, while promoted apoptosis and ferroptosis. In addition, NSUN2 stabilized FOXM1 mRNA through m5C modification and regulated FOXM1 expression in a YBX1-dependent manner. The results also showed that NSUN2 knockdown inhibited NSCLC cell proliferation, invasion, and M2 macrophage polarization, and induced apoptosis and ferroptosis by modulating FOXM1. Moreover, FOXM1 transcriptionally activated NSUN2 in A549 and 95D cells. Further, NSUN2 knockdown repressed tumor formation by regulating FOXM1. The NSUN2/FOXM1 positive feedback pathway accelerated the malignant development of NSCLC, suggesting that targeting this pathway may have significant clinical implications for NSCLC treatment.","PeriodicalId":50601,"journal":{"name":"Current Proteomics","volume":"22 4","pages":"100029-100029"},"PeriodicalIF":0.0,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147903220","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Proteomic analysis reveals the expression and impact of PRDX2 in ovarian cancer tissues","authors":"Ting Lan, Jing Wang, Cheng Qian, Xiaopeng Xu, Zheng Quan, Zhou Zhang","doi":"10.1016/j.curpro.2025.100031","DOIUrl":"https://doi.org/10.1016/j.curpro.2025.100031","url":null,"abstract":"The objective of this study is to elucidate the Peroxiredoxin 2(PRDX2) expression in ovarian cancer tissues and its effect on cancer progression using proteomic technology. Four ovarian cancer tissues and four normal ovarian tissues were subjected to proteomic analysis to identify differentially expressed proteins. Subsequent bioinformatics analysis focused on PRDX2. PRDX2 expression in ovarian cancer tissues and cells was validated via Western blot, Reverse Transcription- Quantitative Polymerase Chain Reaction (RT-qPCR), Immunofluorescence, and Immunohistochemistry. PRDX2 was knocked down in ovarian cancer cells using small interfering RNA (siRNA) technology. Functional assays, including Cell Counting Kit-8(CCK8) and scratch assays, were utilized to evaluate the impact of PRDX2 depletion on ovarian cancer cell proliferation and migration. The prognostic significance of PRDX2 in ovarian cancer patients was assessed using the Kaplan-Meier Plotter tool. Proteomics analysis identified 4375 proteins, of which 305 were upregulated and 410 were downregulated. Among these, PRDX2 was significantly differentially expressed and primarily associated with oxidative stress pathways. In ovarian cancer, PRDX2 is associated with 23 related proteins. Ovarian cancer tissues and cells showed decreased PRDX2 expression. Knockdown of PRDX2 promoted the proliferation and migration of ovarian cancer cells (A2780). Patients with low PRDX2 expression had a poorer prognosis. This study revealed decreased expression of PRDX2 in ovarian cancer, indicating its inhibitory role in ovarian cancer progression. Patients with low PRDX2 expression exhibited a poorer prognosis, suggesting that PRDX2 might be a promising target for the diagnosis and treatment of ovarian cancer.","PeriodicalId":50601,"journal":{"name":"Current Proteomics","volume":"22 4","pages":"100031-100031"},"PeriodicalIF":0.0,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147905133","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploration of atractylenolide III targeting MDM2/p53 axis in breast cancer cell progression based on network pharmacology, molecular docking and ubiquitination analysis","authors":"Yuanyuan Zou, Ziru Guo, Ruonan Rong, He Zhang, Shuya Han","doi":"10.1016/j.curpro.2025.100016","DOIUrl":"https://doi.org/10.1016/j.curpro.2025.100016","url":null,"abstract":"Atractylenolide III (AT III) is a promising drug used for cancer treatment. Herein, this study aimed to explore the anti-tumor mechanism of AT III in breast cancer (BC) associated with murine double minute 2 (MDM2) and p53 through network pharmacology, molecular docking, ubiquitination analysis and cell experiments. The common targets between AT III and BC were obtained using Venn diagram followed by screening of hub targets using network pharmacology analysis. Molecular docking between AT III and hub targets (MAPK1, MDM2, and PPARG) was performed by AutoDock vina software, and docking results were evaluated by molecular dynamics simulation. Cell viability, proliferation, apoptosis, and migration/invasion were assessed through cell counting kit-8 (CCK-8), colony formation assay, flow cytometry and transwell assay. Western blot was performed for protein detection. AT III and MDM2 binding was analyzed by cellular thermal shift assay (CETSA). The ubiquitination effect of AT III on p53 was researched using ubiquitination assay. Network pharmacology analysis has screened three hub targets MAPK1, MDM2, and PPARG. Molecular docking and dynamic simulation showed the high binding between AT III and MAPK1, MDM2, or PPARG. AT III treatment significantly impeded proliferation, migration and invasion while promoting apoptosis of BC cells. AT III could bind to MDM2 and inhibit the ubiquitination of p53. MDM2/p53 reversed the anti-cancer regulation of AT III in BC cells. These results identified MDM2 as a target of AT III, and AT III played a tumor-inhibiting role in BC by mediating ubiquitination of p53 through targeting MDM2.","PeriodicalId":50601,"journal":{"name":"Current Proteomics","volume":"22 2","pages":"100016-100016"},"PeriodicalIF":0.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147916213","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SP1-mediated WTAP exacerbates the progression of colon adenocarcinoma by m6A methylation of KLK8","authors":"Zhijin Wu, Na Shen, Phil Hyun Song, Ben Wang, Chunming Li","doi":"10.1016/j.curpro.2025.100001","DOIUrl":"https://doi.org/10.1016/j.curpro.2025.100001","url":null,"abstract":"• KLK8 knockdown repressed COAD cell progression and promotes CD8 + T cell cytotoxicity. • KLK8 silencing blocks tumorigenesis of COAD in vivo . • WTAP knockdown inhibits COAD progression by regulating KLK8 expression through m6A methylation. • SP1 activates the transcription of WTAP. • KLK8 overexpression reverses SP1 downregulation-mediated impacts on COAD cell progression and CD8 + T cell cytotoxicity. The study focused on the functions of kallikrein related peptidase 8 (KLK8), WT1 associated protein (WTAP) and specific protein 1 (SP1) in colon adenocarcinoma (COAD) development. EdU and Transwell experiments were applied for cell proliferation, migration and invasion. Trypan blue experiment and flow cytometry analysis were adopted for evaluation of CD8 + T cell viability and apoptosis. qRT-PCR, western blot and IHC analysis were adopted to examine gene expression. The animal tests were utilized to investigate KLK8 role in tumor progression in vivo . meRIP analysis was conducted to estimate the relation between KLK8 and WTAP. CHIP and dual-luciferase reporter assays were performed to verify the relation between SP1 and WTAP. KLK8 expression was raised in COAD. Silencing of KLK8 inhibited COAD cell proliferation, migration, invasion, accelerated CD8 + T cell viability and repressed CD8 + T cell apoptosis. Deficiency of KLK8 also blocked tumor growth in vivo . WTAP modulated KLK8 expression through m6A methylation. WTAP silencing restrained COAD cell proliferation, migration, invasion and facilitated CD8 + T cell cytotoxicity, while KLK8 overexpression restored the effects. In addition, SP1 activated the transcription of WTAP. Deficiency of SP1 restrained COAD cell growth, metastasis and enhanced CD8 + T cell toxicity, with KLK8 enhancement abolished the effects. SP1-mediated upregulation of WTAP exacerbated the malignant COAD progression by modulating KLK8.","PeriodicalId":50601,"journal":{"name":"Current Proteomics","volume":"22 1","pages":"100001-100001"},"PeriodicalIF":0.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147909273","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigating the Effectiveness of Natural Analogs and DifferentMetabolites of Curcumin for the Inhibition of the Influenza Virus Proteinsin a Simulated Environment","authors":"Majid Asadi-Samani, Dhiya Altememy, Javad Saffari‐Chaleshtori, Mohammad-Taghi Moradi","doi":"10.2174/0115701646343074241210050400","DOIUrl":"https://doi.org/10.2174/0115701646343074241210050400","url":null,"abstract":"","PeriodicalId":50601,"journal":{"name":"Current Proteomics","volume":"22 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147918705","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":"Exploring Phytochemical Compounds: A Computational Study for HIV-1 Reverse Transcriptase Inhibition","authors":"Jyotsna Bandi, Madhan Chunduru, Satya Tulasi Mangamuri, Anand Kumar Nelapati, Jalaja Naravula, Viswajit Mulpuru","doi":"10.2174/0115701646316517240901091407","DOIUrl":"https://doi.org/10.2174/0115701646316517240901091407","url":null,"abstract":"Background: HIV-1 is the most virulent type, causing most AIDS cases worldwide. Therapeutics like NRTIs and NNRTIs terminate replication by terminating polymerization reactions. Natural-based therapeutics are increasingly being used to reduce side effects and combat disease. Method: The study focuses on identifying phytochemical compounds that effectively inhibit the HIV-1 reverse transcriptase process using molecular docking and molecular dynamic simulations. Result: Molecular docking results show anisomelolide has a significantly stronger binding affinity (-29.9992KJ/mol) compared to nevirapine (-13.34696 KJ/mol), forming more hydrogen bonds and hydrophilic interactions, indicating a more stable and specific binding. MD simulations further support these findings, with anisomelolide exhibiting lower RMSD and RMSF values, suggesting greater structural stability and lower flexibility. Interaction energy analysis reveals robust binding and stability for anisomelolide over time. Additionally, hydrogen bond analysis indicates more frequent and stronger interactions for anisomelolide. Conclusion: The phytochemical compound anisomelolide exhibits superior binding affinity, structural stability, and interaction dynamics, making it a promising candidate for drug development against HIV-1 RT.","PeriodicalId":50601,"journal":{"name":"Current Proteomics","volume":"203 1","pages":""},"PeriodicalIF":0.8,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142258651","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":"Molecular Docking, Pharmacophore Mapping, and Virtual Screening of Novel Glucokinase Activators as Antidiabetic Agents","authors":"Anuradha Mehra, Amit Mittal, Divya Thakur","doi":"10.2174/0115701646323264240821072359","DOIUrl":"https://doi.org/10.2174/0115701646323264240821072359","url":null,"abstract":"Background: A pivotal impetus has led to the development of numerous small molecules to develop therapeutic strategies for type 2 diabetes. Novel heterocyclic derivatives are now available with expansive pharmacological activity designed specifically to activate Glucokinase (GK) in the body. This target is of particular significance in antidiabetic drug design since it is a newly validated target. Individuals with type 2 diabetes are unable to maintain blood glucose homeostasis due to impaired glucokinase function. The novel approach to managing type 2 diabetes relies on utilizing heterocyclic derivatives to activate the GK enzyme, also known as a metabolic enzyme. Objective: In this research endeavor, the primary objective was to improve drug delivery while minimizing adverse effects by using molecules that activate glucokinase Methods: There are 53,000 compounds included in Maybridge's online repository, which has been subjected to rigorous scrutiny. Eight two compounds that encompass the specific oxadiazole core were selectively extracted from this extensive collection. ChemBioDraw Ultra was used for structural drawing, and AutoDock Vina 1.5.6 was used to perform docking analysis. For the online prediction of log P, the SwissADME algorithm was employed. A PKCSM software program was used to predict toxicity for leading compounds. Results: Among all of the compounds, AD80 and AD27 displayed the highest affinity for GK receptors. These compounds, by adhering to Lipinski’s Rule of Five, exhibited good absorption and excretion profiles through the gastrointestinal (GI) tract. Lipinski’s Rule of Five refers to physicochemical properties that favor good oral bioavailability, and these specifications are zero to five hydrogen bond donors, zero to ten hydrogen bond acceptors, molecular weight below 500, and log P no more than five. These criteria ensure that the compounds of the invention have acceptable solubility and permeability, which are vital prerequisites when given orally, to be absorbed via the gastrointestinal wall, metabolized, and found in the urine. Therefore, the chance of drug candidates exhibiting favorable pharmacokinetic characteristics is increased, enhancing their chances of being developed for oral administration. In comparison with standard drugs Dorzagliatin as a glucokinase activator (GKA) and MRK (co-crystallized ligand), these compounds exhibit no skin sensitization, AMES toxicity, or hepatotoxicity. Conclusion: The recently designed lead molecules exhibit an improved pharmacokinetic profile, enhanced binding affinity, and minimal toxicity based on the computational study, potentially making them suitable candidates for further optimization as glucokinase activators.","PeriodicalId":50601,"journal":{"name":"Current Proteomics","volume":"24 1","pages":""},"PeriodicalIF":0.8,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142217975","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":"Comprehensive Analysis of Tertiary Lymphoid Structures in Pancreatic Cancer: Molecular Characteristics and Prognostic Implications","authors":"Jiana Fang, Jingru Huang, Jiazhong Zhang, Lin Chen, Jin Deng","doi":"10.2174/0115701646317271240821071544","DOIUrl":"https://doi.org/10.2174/0115701646317271240821071544","url":null,"abstract":"Purpose: The molecular properties of TLSs in pancreatic cancer are still not well comprehended. This research delved into the molecular properties of intratumoral TLSs in pancreatic cancer through the exploration of multi-omics data. Methods: Seven key genes were identified through Cox regression analysis and random survival forest analysis from a total of 5908 genes related to TLSs. These genes were utilized to construct a prognosis model, which was subsequently validated in two independent cohorts. Additionally, the study investigated the molecular features of different populations of TLSs from multiple perspectives. The model’ s forecasting accuracy was verified by analyzing column-line graphs and decision curves, taking into account the patients’ clinical traits. Results: The analysis of immune cell infiltration showed a notably greater presence of Macrophage M0 cells in the group at high risk than in the low-risk group. The pathway enrichment analysis demonstrated the activation among common cancer-related pathways, including ECM receptor interaction, pathways in cancer, and focal adhesion, in the high-risk group. Additionally, the methylation study revealed notable disparities in DNA methylation between two TLS groups across four regions: TSS200, 5’ UTR, 1stExon, and Body. A variety of notably distinct sites were linked with PVT1. Furthermore, by constructing a competing endogenous RNA network, several mRNAs and lncRNAs were identified that compete for the binding of hsa-mir-221. Conclusion: Overall, this research sheds light on the molecular properties of TLSs across various pancreatic cancer stages and suggests possible focal points for the treatment of pancreatic cancer. result: The analysis of immune cell infiltration showed a notably greater presence of Macrophage M0 cells in the group at high-risk than in the low-risk group. Pathway enrichment analysis demonstrated the activation among common cancer-related pathways, including ECM receptor interaction, pathways in cancer, and focal adhesion, in the high-risk group. Additionally, the methylation study revealed notable disparities in DNA methylation between two TLSs groups across four regions: TSS200, 5’ UTR, 1stExon, and Body. A variety of notably distinct sites were linked with PVT1. By constructing a competing endogenous RNA network, multiple mRNAs and lncRNAs competing for the binding of hsa-mir-221 were identified.","PeriodicalId":50601,"journal":{"name":"Current Proteomics","volume":"5 1","pages":""},"PeriodicalIF":0.8,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142217977","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":"miR-124 in Neuroblastoma: Mechanistic Insights, Biomarker Potential, and Therapeutic Prospects","authors":"K M Monisha, Dhanu A S, D Mutthuraj, G Nandini, Sridhar Muthusami, Kanthesh M. Basalingappa","doi":"10.2174/0115701646331003240821061517","DOIUrl":"https://doi.org/10.2174/0115701646331003240821061517","url":null,"abstract":": Neuroblastoma, a malignancy predominantly affecting young children, originates from neural crest cells in the sympathetic nervous system. It primarily appears in the adrenal gland but can also affect nerve tissues in regions, such as the chest, neck, abdomen, and pelvis. Despite advancements in treatment, high-risk neuroblastoma patients often face poor prognoses, underscoring the need for ongoing research. This review paper examines the numerous factors responsible for neuroblastoma, emphasizing the importance of approaching the disorder with more strategic therapeutic methods. MicroRNAs, particularly miR-124, play critical roles in gene regulation and cancer pathogenesis. Abundant in the brain, miR-124 functions as a tumor suppressor by inhibiting cell growth, migration, and invasion and is often dysregulated in neuroblastoma. This study investigates the molecular functions of miR-124 in neuroblastoma, its potential as a biomarker, and its application in targeted therapy. MiR-124 regulates key pathways in neuroblastoma, including PI3K/AKT, TGF-β, and p53 signaling, impacting cell proliferation, apoptosis, and metastasis. The study also explores the promise of miR-124 as a biomarker for neuroblastoma through liquid biopsy, enabling non-invasive diagnosis and disease monitoring. Therapeutic strategies targeting miR-124 pathways show potential for overcoming chemotherapy resistance and improving treatment efficacy. The research underscores the significance of miR-124 in neuroblastoma, aiming to enhance early diagnosis, identify specific drug targets, and expand treatment options, ultimately improving patient outcomes.","PeriodicalId":50601,"journal":{"name":"Current Proteomics","volume":"163 1","pages":""},"PeriodicalIF":0.8,"publicationDate":"2024-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142217976","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}