International journal of molecular medicine最新文献

{"title":"Claudin 1, 4, 6 and 18 isoform 2 as targets for the treatment of cancer (Review).","authors":"Masuko Katoh, Masaru Katoh","doi":"10.3892/ijmm.2024.5424","DOIUrl":"https://doi.org/10.3892/ijmm.2024.5424","url":null,"abstract":"<p><p>The 24 claudin (<i>CLDN</i>) genes in the human genome encode 26 representative CLDN family proteins. CLDNs are tetraspan‑transmembrane proteins at tight junctions. Because several CLDN isoforms, such as CLDN6 and CLDN18.2, are specifically upregulated in human cancer, CLDN‑targeting monoclonal antibodies (mAbs), antibody‑drug conjugates (ADCs), bispecific antibodies (bsAbs) and chimeric antigen receptor (CAR) T cells have been developed. In the present review, CLDN1‑, 4‑, 6‑ and 18.2‑targeting investigational drugs in clinical trials are discussed. CLDN18.2‑directed therapy for patients with gastric and other types of cancer is the most advanced area in this field. The mouse/human chimeric anti‑CLDN18.2 mAb zolbetuximab has a single‑agent objective response rate (ORR) of 9%, and increases progression‑free and overall survival in combination with chemotherapy. The human/humanized anti‑CLDN18.2 mAb osemitamab, and ADCs AZD0901, IBI343 and LM‑302, with single‑agent ORRs of 28‑60%, have been tested in phase III clinical trials. In addition, bsAbs, CAR T cells and their derivatives targeting CLDN4, 6 or 18.2 are in phase I and/or II clinical trials. AZD0901, IBI343, zolbetuximab and the anti‑CLDN1 mAb ALE.C04 have been granted fast track designation or priority review designation by the US Food and Drug Administration.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":null,"pages":null},"PeriodicalIF":5.7,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11414526/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142286464","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of Agrin in tissue repair and regeneration: From mechanisms to therapeutic opportunities (Review).","authors":"Xiang Li, Yuan Xu, Jing-Xing Si, Fang Gu, Ying-Yu Ma","doi":"10.3892/ijmm.2024.5422","DOIUrl":"10.3892/ijmm.2024.5422","url":null,"abstract":"<p><p>Tissue regeneration is a complex process that involves the recruitment of various types of cells for healing after injury; it is mediated by numerous precise interactions. However, the identification of effective targets for improving tissue regeneration remains a challenge. As an extracellular matrix protein, Agrin plays a critical role in neuromuscular junction formation. Furthermore, recent studies have revealed the role of Agrin in regulating tissue proliferation and regeneration, which contributes to the repair process of injured tissues. An in‑depth understanding of the role of Agrin will therefore be of value. Given that repair and regeneration processes occur in various parts of the human body, the present systematic review focuses on the role of Agrin in typical tissue and highlights the potential signaling pathways that are involved in Agrin‑induced repair and regeneration. This review offers important insight into novel strategies for the future clinical applications of Agrin‑based therapies, which may represent a feasible treatment option for patients who require organ replacement or repair.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":null,"pages":null},"PeriodicalIF":5.7,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11410309/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142286478","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"miR‑155 promotes an inflammatory response in HaCaT cells via the IRF2BP2/KLF2/NF‑κB pathway in psoriasis.","authors":"Lu Chen, Chang Liu, Xuesong Xiang, Wenhong Qiu, Kaiwen Guo","doi":"10.3892/ijmm.2024.5415","DOIUrl":"10.3892/ijmm.2024.5415","url":null,"abstract":"<p><p>Psoriasis is a chronic inflammatory skin condition with numerous causes, including genetic, immunological and infectious factors. The course of psoriasis is long and recurrence is common; pathogenesis is not completely understood. However, there is an association between advancement of psoriasis and aberrant microRNA (miR or miRNA)‑155 expression. Through bioinformatics, the present study aimed to analyze the differentially expressed genes and miRNAs in psoriasis and its biological mechanism and function psoriatic inflammation. First of all, differentially expressed genes (DEGs) and miRNAs (DEMs) in patients with psoriasis were identified using GEO2R interactive web application. A psoriasis inflammatory model was established using lipopolysaccharide (LPS)‑treated HaCaT keratinocytes, which were transfected with miR‑155 mimic or inhibitor. Cell Counting Kit‑8 was used for the assessment of cell viability and proliferation, and changes in the cell cycle were examined using flow cytometry. ELISA and reverse transcription‑quantitative PCR (RT‑qPCR) were used to detect the expression levels of the inflammatory factors IL‑1β and IL‑6. The dual‑luciferase reporter assay was used to verify the targeting association between miR‑155‑5p and IFN regulatory factor 2 binding protein 2 (IRF2BP2). To verify the targeting association of miR‑155 and the IRF2BP2/kruppel‑like factor 2 (KLF2)/NF‑κB signaling pathway, expression levels of IRF2BP2, KLF2 and p65 were identified by RT‑qPCR and western blotting. IRF2BP2 levels were also confirmed by immunofluorescence, in conjunction with bioinformatics database analysis. Overexpression of miR‑155 inhibited proliferation of HaCaT cells and increased the number of cells in S phase and decreasing number of cells in G1 and G2 phase. In the LPS‑induced inflammatory state, miR‑155 overexpression heightened the inflammatory response of HaCaT cells while inhibition of miR‑155 lessened it. Suppression of inflammatory cytokine expression by miR‑155‑5p inhibitor was reversed by knockdown of IRF2BP2. miR‑155 was shown to interact with IRF2BP2 to negatively regulate its expression, leading to decreased KLF2 expression and increased p65 expression and secretion of inflammatory factors, intensifying the inflammatory response of HaCaT cells. Therefore, miR‑155 may contribute to development of psoriasis by inducing tissue and cell damage by increasing the inflammatory response of HaCaT cells via the IRF2BP2/KLF2/NF‑κB pathway. In conclusion, the results of the present study offer novel perspectives on the role of miR‑155 in the onset and progression of psoriasis.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":null,"pages":null},"PeriodicalIF":5.7,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11374146/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142107175","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Enhancing diabetic foot ulcer healing: Impact of the regulation of the FUS and ILF2 RNA‑binding proteins through negative pressure wound therapy.","authors":"Ying Tang, Hua Ji, Yanyan Yan, Die Hu, Murong Xu, Min Xu, Xiaotong Zhao, Mingwei Chen","doi":"10.3892/ijmm.2024.5427","DOIUrl":"10.3892/ijmm.2024.5427","url":null,"abstract":"<p><p>Diabetic foot ulcer (DFU) is a destructive complication of diabetes. Negative pressure wound therapy (NPWT) promotes DFU wound healing through an undetermined mechanism. In the present study, RNA sequencing was performed on wound granulation tissue from 3 patients with DFU before and after 1 week of NPWT. The fused in sarcoma (FUS) and interleukin enhancer binding factor 2 (ILF2) encoding RNA‑binding proteins (RBPs) were screened from the sequencing data, and wound tissue samples from 24 patients with DFU were validated and analyzed before and after receiving NPWT by reverse transcription‑quantitative PCR, western blotting and immunohistochemistry. In addition, <i>in vitro</i> and <i>in vivo</i> experiments were conducted to determine the effect of the expression of FUS and ILF2 on the function of human epidermal keratinocyte cells (HaCaT cells) and the healing of diabetic skin wounds. The results indicated that NPWT induced the upregulation of 101 genes and the downregulation of 98 genes in DFU wound granulation tissue. After NPWT, the expression of FUS and ILF2 was significantly upregulated (P<0.05). Pearson's correlation coefficient showed that the changes in FUS and ILF2 before and after NPWT were negatively correlated with changes in white blood cells, the neutrophil percentage, C‑reactive protein, tumor necrosis factor‑α, reactive oxygen species, lipid peroxides, matrix metalloproteinase (MMP) 2 and MMP9 (P<0.05), but positively correlated with the anti‑inflammatory factor, IL‑4 (P<0.01). There was also a positive correlation (P<0.05) with the 4‑week ulcer healing rate. Additionally, the knockdown of FUS and ILF2 expression inhibited the proliferation and migration of HaCaT cells, while increasing cell apoptosis. <i>In vivo</i>, the knockdown of FUS and ILF2 significantly reduced the rate of skin wound healing in diabetic mice. The results of the present study therefore provide new insights into the mechanism by which NPWT promotes DFU wound healing. In conclusion, the RBPs, FUS and ILF2, promoted DFU wound healing by regulating the function of keratinocytes and reducing the inflammatory response and oxidative stress.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":null,"pages":null},"PeriodicalIF":5.7,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11414528/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142286465","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of mesenchymal stem cells in sepsis and their therapeutic potential in sepsis‑associated myopathy (Review).","authors":"Dongfang Wang, Ligang Xu, Yukun Liu, Chuntao Wang, Siyuan Qi, Zhanfei Li, Xiangjun Bai, Yiliu Liao, Yuchang Wang","doi":"10.3892/ijmm.2024.5416","DOIUrl":"10.3892/ijmm.2024.5416","url":null,"abstract":"<p><p>Sepsis‑induced myopathy (SIM) is one of the leading causes of death in critically ill patients. SIM mainly involves the respiratory and skeletal muscles of patients, resulting in an increased risk of lung infection, aggravated respiratory failure, and prolonged mechanical ventilation and hospital stay. SIM is also an independent risk factor associated with increased mortality in critically ill patients. At present, no effective treatment for SIM has yet been established. However, mesenchymal stem cells (MSCs) have emerged as a promising therapeutic approach and have been utilized in the treatment of various clinical conditions. A significant body of basic and clinical research supports the efficacy of MSCs in managing sepsis and muscle‑related diseases. This literature review aims to explore the relationship between MSCs and sepsis, as well as their impact on skeletal muscle‑associated diseases. Additionally, the present review discusses the potential mechanisms and therapeutic benefits of MSCs in the context of SIM.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":null,"pages":null},"PeriodicalIF":5.7,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11374154/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142107177","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Retracted] Ubiquitin‑specific protease 4 inhibits breast cancer cell growth through the upregulation of PDCD4.","authors":"Yang Li, Daqing Jiang, Qi Zhang, Xiaoli Liu, Zhengang Cai","doi":"10.3892/ijmm.2024.5417","DOIUrl":"10.3892/ijmm.2024.5417","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that certain of the colony formation assay data shown in Fig. 4D on p. 807 and western blot assay data shown in Fig. 7A on p. 809 were strikingly similar to data appearing in different form other articles written by different authors at different research institutes that had already been published elsewhere prior to the submission of this paper to International Journal of Molecular Medicine.  In view of the fact that the abovementioned data had already apparently been published previously, the Editor of <i>International Journal of Molecular Medicine</i> has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Molecular Medicine 38: 803‑811, 2016; DOI: 10.3892/ijmm.2016.2685].</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":null,"pages":null},"PeriodicalIF":5.7,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11374156/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142107173","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Histone methylation modification and diabetic kidney disease: Potential molecular mechanisms and therapeutic approaches (Review).","authors":"Peng Qu, Lanfang Li, Qi Jin, Donghai Liu, Yuan Qiao, Yijia Zhang, Qiuyue Sun, Shuman Ran, Zecheng Li, Tongtong Liu, Liang Peng","doi":"10.3892/ijmm.2024.5428","DOIUrl":"https://doi.org/10.3892/ijmm.2024.5428","url":null,"abstract":"<p><p>Diabetic kidney disease (DKD) is the leading cause of chronic kidney disease and end‑stage renal disease, and is characterized by persistent proteinuria and decreased glomerular filtration rate. Despite extensive efforts, the increasing incidence highlights the urgent need for more effective treatments. Histone methylation is a crucial epigenetic modification, and its alteration can destabilize chromatin structure, thereby regulating the transcriptional activity of specific genes. Histone methylation serves a substantial role in the onset and progression of various diseases. In patients with DKD, changes in histone methylation are pivotal in mediating the interactions between genetic and environmental factors. Targeting these modifications shows promise in ameliorating renal histological manifestations, tissue fibrosis and proteinuria, and represents a novel therapeutic frontier with the potential to halt DKD progression. The present review focuses on the alterations in histone methylation during the development of DKD, systematically summarizes its impact on various renal parenchymal cells and underscores the potential of targeted histone methylation modifications in improving DKD outcomes.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":null,"pages":null},"PeriodicalIF":5.7,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11414529/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142286475","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Retracted] Long non‑coding RNA SNHG3 promotes the development of non‑small cell lung cancer via the miR‑1343‑3p/NFIX pathway.","authors":"Lijun Zhao, Xue Song, Yesong Guo, Naixin Ding, Tingting Wang, Lei Huang","doi":"10.3892/ijmm.2024.5421","DOIUrl":"https://doi.org/10.3892/ijmm.2024.5421","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that certain of the Transwell cell migration and invasion assay data shown in Fig. 3B were strikingly similar to data appearing in different form in a pair of other articles written by different authors at different research institutes, one of which had already been published elsewhere prior to the submission of this paper to <i>International Journal of Molecular Medicine</i>, and one of which was under consideration for publication at around the same time. In view of the fact that the abovementioned data had already apparently been published previously, the Editor of <i>International Journal of Molecular Medicine</i> has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a satisfactory reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Molecular Medicine 48: 147, 2021; DOI: 10.3892/ijmm.2021.4980].</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":null,"pages":null},"PeriodicalIF":5.7,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11410307/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142286463","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lipid metabolic rewiring in glioma‑associated microglia/macrophages (Review).","authors":"Yixuan Ma, Yimin Huang, Feng Hu, Kai Shu","doi":"10.3892/ijmm.2024.5426","DOIUrl":"10.3892/ijmm.2024.5426","url":null,"abstract":"<p><p>Gliomas are the most prevailing brain malignancy in both children and adults. Microglia, which are resident in the central nervous system (CNS), are distributed throughout the brain and serve an important role in the immunity of the CNS. Microglial cells exhibit varying phenotypic and metabolic properties during different stages of glioma development, making them a highly dynamic cell population. In particular, glioma‑associated microglia/macrophages (GAMs) can alter their metabolic characteristics and influence malignancies in response to the signals they receive. The significance of macrophage metabolic reprogramming in tumor growth is becoming increasingly acknowledged in recent years. However, to the best of our knowledge, there is currently a scarcity of data from investigations into the lipid metabolic profiles of microglia/macrophages in the glioma setting. Therefore, the present review aims to provide a thorough review of the role that lipid metabolism serves in tumor‑associated macrophages. In addition, it outlines potential targets for therapy based on lipid metabolism. The present review aims to serve as a reference source for future investigations into GAMs.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":null,"pages":null},"PeriodicalIF":5.7,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11414527/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142286476","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Retracted] Jumonji AT‑rich interactive domain 1B overexpression is associated with the development and progression of glioma.","authors":"Liping Fang, Jiuhan Zhao, Dan Wang, Liyu Zhu, Jian Wang, Kui Jiang","doi":"10.3892/ijmm.2024.5425","DOIUrl":"https://doi.org/10.3892/ijmm.2024.5425","url":null,"abstract":"<p><p>Following the publication of this paper, and subsequently to the publication of a corrigendum (DOI: 10.3892/ijmm.2016.2682) that was intended to address the issue of misassembled data in Figs. 3, 5 and 8, it was drawn to the Editor's attention by a concerned reader that certain of the scratch‑wound assay data shown in Fig. 5B were strikingly similar to data appearing in different form in an article written by different authors at different research institutes that had already been published in the journal <i>Cancer Research</i>. In view of the fact that the abovementioned data had already apparently been published prior to its submission to International <i>Journal of Molecular Medicine</i>, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Journal of Molecular Medicine 38: 172‑182, 2016; DOI: 10.3892/ijmm.2016.2614].</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":null,"pages":null},"PeriodicalIF":5.7,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11414524/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142286462","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}