Molecular medicine reports最新文献

{"title":"Zinc in psychosis (Review).","authors":"Christos Theleritis, Marina Demetriou, Maria-Ioanna Stefanou, Evangelos Alevyzakis, Michael Makris, Vassilios Zoumpourlis, Melpomeni Peppa, Nikolaos Smyrnis, Demetrios A Spandidos, Emmanouil Rizos","doi":"10.3892/mmr.2025.13566","DOIUrl":"10.3892/mmr.2025.13566","url":null,"abstract":"<p><p>Zinc (Zn) may be associated with schizophrenia (SCH), since its altered homeostasis can contribute to abnormal glutamatergic neurotransmission, inflammation, neurodegeneration and autoimmune abnormalities. It has been proposed that a number of patients with SCH could benefit from the use of Zn, either on its own or along with vitamins C, E and B6, and prenatal supplementation of Zn during the gestation period can mitigate the lipopolysaccharide‑induced rat model of maternal immune activation. The aim of the present review was to summarize the various effects of Zn dyshomeostasis on patients with psychosis and to clarify in what ways they could benefit from Zn supplementation.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12105465/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144079132","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":"CDK5 targets p21^CIP1 to regulate thyroid cancer cell proliferation and malignancy in patients.","authors":"Min-Che Tung, Muhammet Oner, Shiuan-Woei Soong, Pang-Ting Cheng, Yu-Hsuan Li, Mei-Chih Chen, Chen-Kai Chou, Hong-Yo Kang, Frank Cheau-Feng Lin, Stella Chin-Shaw Tsai, Ho Lin","doi":"10.3892/mmr.2025.13547","DOIUrl":"https://doi.org/10.3892/mmr.2025.13547","url":null,"abstract":"<p><p>Cyclin‑dependent kinase 5 (CDK5), known for its role in neuronal function, has emerged as a key player in cancer biology, particularly in thyroid cancer. The present study explored the interaction between CDK5 and the cyclin‑dependent kinase inhibitor p21^CIP1 in thyroid cancer (TC). Bioinformatic tools and immunoprecipitation assays were used to confirm that CDK5 targets p21 for ubiquitin‑mediated degradation, reducing its stability and tumor‑suppressive effects. Data from The Cancer Genome Atlas revealed a significant inverse correlation between CDK5 and p21 expression, with higher CDK5 levels linked to increased tumor malignancy and worse survival outcomes; conversely, higher p21 expression was correlated with an improved prognosis. Immunohistochemistry analysis of TC samples further confirmed that increased CDK5 and reduced p21 expression were associated with more advanced tumor stages and aggressive phenotypes. These findings suggested that CDK5‑mediated degradation of p21 contributes to TC progression and malignancy, highlighting the potential of targeting the CDK5‑p21 axis as a therapeutic strategy for management of TC.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12059462/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143990580","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":"Action and mechanisms of neferine in inflammatory diseases (Review).","authors":"Qin Zhang, Qiaoling Zhou, Huihui Li","doi":"10.3892/mmr.2025.13539","DOIUrl":"https://doi.org/10.3892/mmr.2025.13539","url":null,"abstract":"<p><p>Neferine is a bisbenzylisoquinoline alkaloid derived from the seed embryo of <i>Nelumbo nucifera</i>, a traditional Chinese medicine. It has been extensively studied for its therapeutic potential in various disease models. Extensive research has highlighted its diverse pharmacological activities, including antitumor, anti‑inflammatory, anti‑fibrosis, anti‑oxidative stress, anti‑platelet aggregation and anti‑arrhythmic effects. The present review, however, focuses on the anti‑inflammatory properties of neferine, emphasizing its fundamental mechanisms as demonstrated in both <i>in vivo</i> and <i>in vitro</i> studies. By critically evaluating its effect on inflammation and the underlying pathways, this review aims to provide a comprehensive understanding of the potential of neferine in the management of inflammatory diseases. Furthermore, it seeks to establish a foundational framework for the future development of neferine as a novel therapeutic agent for inflammatory conditions.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12046375/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144034460","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":"CXCL9 is a dual‑role biomarker in colorectal cancer linked to mitophagy and modulated by ALKBH5.","authors":"Geng Hu, Shijun Shen, Mingchao Zhu","doi":"10.3892/mmr.2025.13553","DOIUrl":"10.3892/mmr.2025.13553","url":null,"abstract":"<p><p>Colorectal cancer (CRC), the third most prevalent cancer globally, shows a diminished 5‑year survival rate compared with patients at early stages of the disease, underscoring the urgency for early diagnostic biomarker identification. The C‑X‑C motif chemokine ligand (CXCL) family plays a significant role in immune modulation and cancer progression. the present study constructed a prognostic model for CXCL family in CRC and conducted an in‑depth investigation of the hub gene CXCL9 within the model. CXCL9 is highly expressed in CRC while high expression levels of CXCL9 in patients with CRC often indicates an improved prognosis. Through Gene Ontology, Kyoto Encyclopedia of Genes and Genomes and gene set enrichment analysis enrichment analysis, it was discovered that CXCL9 is not only associated with immune modulation but also closely related to pathways that affect the occurrence and development of cancer. CXCL9 is closely related to mitophagy and blocks autophagy flow by altering the expression of autophagy‑related genes. Additionally, it was found that CXCL9 is a downstream gene modified by ALKBH5 and can partially restore the tumor‑suppressive effects induced by the knockdown of ALKBH5. These studies indicated that CXCL9 is a prognostic marker in CRC and plays a dual role in cancer progression: It activates immune responses on one hand and promotes the malignant characteristics of cancer on the other hand.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12076282/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144018625","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] MicroRNA‑195 suppresses rectal cancer growth and metastasis via regulation of the PI3K/AKT signaling pathway.","authors":"Yeli Wang, Linsong Mu, Miaoling Huang","doi":"10.3892/mmr.2025.13543","DOIUrl":"https://doi.org/10.3892/mmr.2025.13543","url":null,"abstract":"<p><p>Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, regarding the scratch wound assay experiments shown in Fig. 2A and the cell invasion assay experiments shown in Figs. 2B and 7A, a large number of data panels showed evidence of overlapping data, both within the same figure parts and comparing between Figs. 2 and 7.  Owing to the large number of data duplication events that have been identified in this paper, the Editor of <i>Molecular Medicine Reports</i> has decided that it should be retracted from the Journal on account of a lack of confidence in the presented data. 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. [Molecular Medicine Reports 20: 4449‑4458, 2019; DOI: 10.3892/mmr.2019.10717].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12046938/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144028418","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":"NLRP3 inflammasome expression affects immune cell infiltration and clinical prognosis in <i>Helicobacter pylori</i> infection‑associated gastric cancer.","authors":"Chuandan Wan, Yeqiong Xu, Yanping Zhu, Xuexian Cao, Ping Wang, Yulan Gu","doi":"10.3892/mmr.2025.13550","DOIUrl":"10.3892/mmr.2025.13550","url":null,"abstract":"&lt;p&gt;&lt;p&gt;High &lt;i&gt;Helicobacter pylori&lt;/i&gt; infection rates contribute to high gastric cancer (GC) incidence. While &lt;i&gt;H.&lt;/i&gt; &lt;i&gt;pylori&lt;/i&gt; infection is associated with GC development its mechanisms are still being studied. The aim of the present study was to examine the differences between &lt;i&gt;H. pylori&lt;/i&gt; infection‑induced GC and non‑infected tissues, and to investigate the correlation between nucleotide‑binding oligomerization domain, leucine rich repeat and pyrin domain containing 3 (NLRP3) inflammasome expression and immune cell infiltration in GC, thus providing a theoretical basis for clinical prognosis and immunotherapy. High‑throughput RNA‑sequencing expression data from The Cancer Genome Atlas (TCGA) were analyzed. Additionally, TIMER2.0 and Kaplan‑Meier Plotter were used to analyze the differential expression of NLRP3 mRNA in various tumors, the effect of &lt;i&gt;H. pylori&lt;/i&gt; infection on gene expression, and the association between NLRP3 and clinical prognosis among patients with GC. Immunohistochemistry (IHC) was used to assess the effects of NLRP3 protein expression on immune cell infiltration in clinical tissues with or without &lt;i&gt;H. pylori&lt;/i&gt; infection. R software was used for data visualization and statistical analysis. TCGA data revealed that the expression levels of NLRP3 in GC tissues were increased compared with those in normal tissues (P&lt;0.05), which was further validated in clinical samples. Furthermore, NLRP3 mRNA expression was significantly elevated in clinical GC tissues infected with &lt;i&gt;H. pylori&lt;/i&gt;. Notably higher relative levels of NLRP3 mRNA were observed in tumor tissues with a tumor size ≥5 cm, lymph node metastasis, Tumor‑Node‑Metastasis stage III + IV or poor differentiation compared with the respective controls (P&lt;0.05). IHC confirmed a significant increase in NLRP3 expression within &lt;i&gt;H. pylori&lt;/i&gt;‑infected GC tissues compared with that in non‑infected tissues. In GC immune infiltration, NLRP3 expression was revealed to be associated with natural killer cell, whereas it was negatively correlated with regulatory T cells and CD8&lt;sup&gt;+&lt;/sup&gt; T cells. These findings indicated that NLRP3 may promote the polarization of tumor‑associated macrophages towards the M2 phenotype. High NLRP3 expression also promoted the infiltration of CD3&lt;sup&gt;+&lt;/sup&gt; and CD206&lt;sup&gt;+&lt;/sup&gt; cells, which significantly affected the survival rate of patients with GC. The immune infiltration of regulatory T lymphocytes was associated with better survival benefits for patients with GC; however, M2 macrophage infiltration was not conducive to the survival of patients with GC. Furthermore, survival analysis showed that high expression of NLRP3 was associated with a poorer 5‑year overall survival, progression‑free survival and post‑progression survival rates. In conclusion, elevated NLRP3 expression, which may be induced by &lt;i&gt;H. pylori&lt;/i&gt; infection, could promote immune cell infiltration potentially by regulating cancer cell proliferation and migration,","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12059518/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143982291","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":"The role of m6A methylation in abdominal aortic aneurysms: Mechanisms, progress and future perspectives (Review).","authors":"Keyu Wang, Ziqiang Sun","doi":"10.3892/mmr.2025.13564","DOIUrl":"10.3892/mmr.2025.13564","url":null,"abstract":"<p><p>Abdominal aortic aneurysm (AAA) is a type of cardiovascular disease. Sudden aortic rupture and subsequent bleeding are the main causes of mortality due to AAA. N6‑methyladenosine (m6A) methylation, the most common epitranscriptomic modification in eukaryotic mRNAs, has a key role in the regulation of gene expression. m6A methylation markedly influences the development and progression of AAA. The present review highlights the mechanism of m6A methylation in AAA, including current research progress and future prospects. From a mechanistic perspective, m6A methylation exerts its influence on AAA‑related genes by modulating the post‑transcriptional levels of RNA, thereby impacting the pathological process of AAA. In terms of clinical applications, the mechanisms by which m6A methylation regulators influence their development and progression in AAA involve multiple target genes and signaling pathways. These regulatory factors affect inflammatory immunomodulation, cell proliferation, apoptosis and endogenous processes by modulating the m6A modification status of target genes and the activity of immune‑related signaling pathways. Therefore, for the prevention and treatment of AAA, current therapeutic strategies should comprehensively consider the interactions and synergistic regulation among m6A methylation regulators to reveal the integrated effects of the entire regulatory network in AAA development. Consequently, a more comprehensive understanding of the precise mechanisms of m6A methylation in AAA should be attained, which will support the development of innovative therapeutic strategies aimed at m6A methylation and establish a basis for the early diagnosis and treatment of AAA.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12105455/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144079130","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] Triptolide inhibits migration and proliferation of fibroblasts from ileocolonic anastomosis of patients with Crohn's disease via regulating the miR‑16‑1/HSP70 pathway.","authors":"Min Chen, Jin-Min Wang, Dong Wang, Rong Wu, Hong-Wei Hou","doi":"10.3892/mmr.2025.13549","DOIUrl":"https://doi.org/10.3892/mmr.2025.13549","url":null,"abstract":"<p><p>Following the publication of the above article, a concerned reader drew to the authors' attention that, regarding the western blot data shown in Fig. 1, the Col‑I protein bands were strikingly similar to the bands that were featured in the third and fourth lanes of Fig. 5G to represent the α‑SMA data. In addition, the protein bands shown for the Col‑I and α‑SMA experiments in the first and second lanes of the respective gels in Fig. 5G also appeared to be strikingly similar. Upon examining these data independently in the Editorial Office, the Editor of <i>Molecular Medicine Reports</i> has determined that this article should be retracted from the Journal on the basis of a lack of confidence in the presented data. Upon contacting the authors, they accepted the decision to retract this article. The Editor apologizes to the readership of the Journal for any inconvenience caused. [Molecular Medicine Reports 19: 4841‑4851, 2019; DOI: 10.3892/mmr.2019.10117].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12059459/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144018436","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":"Understanding the role of iron/heme metabolism in the anti‑inflammatory effects of natural sulfur molecules against lipopolysaccharide‑induced inflammation.","authors":"Dong Young Kang, Se Won Bae, Kyoung-Jin Jang","doi":"10.3892/mmr.2025.13542","DOIUrl":"https://doi.org/10.3892/mmr.2025.13542","url":null,"abstract":"<p><p>Iron transport and heme synthesis are essential processes in human metabolism, and any dysregulation in these mechanisms, such as inflammation, can have deleterious effects. Lipopolysaccharide (LPS)‑induced inflammatory responses can result in a number of adverse effects, including cancer. Natural mineral sulfur, methylsulfonylmethane (MSM) and nontoxic sulfur (NTS) suppress inflammatory responses. The present study hypothesized that MSM and NTS may inhibit LPS‑induced inflammatory responses in THP‑1 human monocytes. Reverse transcription‑quantitative PCR and western blotting assays were performed to analyze the molecular signaling pathways associated with sulfur‑treated and untreated cells. A comet assay was used to evaluate DNA damage, flow cytometry was performed to analyze cell surface receptors and chromatin immunoprecipitation was used to examine molecular interactions. Notably, LPS‑induced inflammation increased iron/heme metabolism, whereas MSM and NTS inhibited this effect. Furthermore, LPS treatment activated the Toll‑like receptor 4/NF‑κB signaling axis, which was downregulated by NTS and MSM. These sulfur compounds also suppressed the nuclear accumulation of LPS‑induced NF‑κB, which could induce the production of proinflammatory cytokines, such as TNF‑α, IL‑1β and IL‑6. Finally, MSM and NTS inhibited LPS‑induced reactive oxygen species generation and DNA damage in THP‑1 monocytic leukemia cells. These results suggested that natural sulfur molecules may be considered promising candidates for anti‑inflammation studies.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12046942/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144035713","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":"[Corrigendum] Heat shock protein 22: A new direction for cardiovascular disease (Review).","authors":"Yi Chen, Meng Li, Yanqing Wu","doi":"10.3892/mmr.2025.13535","DOIUrl":"https://doi.org/10.3892/mmr.2025.13535","url":null,"abstract":"<p><p>Subsequently to the publication of this paper, the authors were contacted by an interested reader who was concerned that they had reported some erroneous information regarding the structure and properties of small heat‑shock protein Hsp22, and its participation in different aspects of cardiovascular diseases. After having considered the reader's comments (with which the authors agree), they have proposed the following change should be made to the text of the paper: The opening sentence of the section <b>\"2. Protective effect of HSP22 on myocardial cells\"</b> in the left‑hand column of p. 2, instead of reading \"HSP22 is a transmembrane protein with a stable tertiary structure, which contains long α‑helices and short β‑curls that result in a high degree of stability (9,14).\", should be replaced by the following text: <b>\"HSP22 has an α‑crystallin domain next to the C‑terminus and is mainly found in the cytoplasm</b> (9,14). The authors regret that erroneous information that was included in the published review, and are grateful to the Editor of <i>Molecular Medicine Reports</i> for granting them the opportunity to publish this corrigendum. Furthermore, they thank the interested reader for drawing this matter to our attention, and apologize to the readership for any inconvenience caused. [Molecular Medicine Reports 31: 82, 2025; DOI: 10.3892/mmr.2025.13447].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12020347/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144028263","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}