Molecular medicine reports最新文献

筛选
英文 中文
Water extract of Humulus japonicus improves age‑related cognitive decline by inhibiting acetylcholinesterase activity and the acetylcholine signaling pathway. 葎草水提物通过抑制乙酰胆碱酯酶活性和乙酰胆碱信号通路改善年龄相关性认知衰退。
IF 3.4 3区 医学
Molecular medicine reports Pub Date : 2025-05-01 Epub Date: 2025-03-21 DOI: 10.3892/mmr.2025.13496
Ju-Eun Kim, Kyeong-Seon Min, Jun Go, Hye-Yeon Park, Young-Keun Choi, In-Bok Lee, Jaewon Shin, Hyun-Ju Cho, Hong-Sik Kim, Dae Youn Hwang, Won-Keun Oh, Kyoung-Shim Kim, Chul-Ho Lee
{"title":"Water extract of <i>Humulus japonicus</i> improves age‑related cognitive decline by inhibiting acetylcholinesterase activity and the acetylcholine signaling pathway.","authors":"Ju-Eun Kim, Kyeong-Seon Min, Jun Go, Hye-Yeon Park, Young-Keun Choi, In-Bok Lee, Jaewon Shin, Hyun-Ju Cho, Hong-Sik Kim, Dae Youn Hwang, Won-Keun Oh, Kyoung-Shim Kim, Chul-Ho Lee","doi":"10.3892/mmr.2025.13496","DOIUrl":"10.3892/mmr.2025.13496","url":null,"abstract":"<p><p>The aging process is associated with a decline in certain cognitive abilities, including learning and memory. This age‑related cognitive decline is associated with a reduction in neurogenesis and alterations in the cholinergic system. <i>Humulus japonicus</i> (HJ), an ornamental plant in the family <i>Cannabaceae</i>, has been reported to exert beneficial effects against neurodegenerative pathophysiologies in mouse models of disorders such as Alzheimer's and Parkinson's disease. Despite the increasingly aging populations of numerous societies, no study has yet investigated the effects of HJ on cognitive decline associated with normal aging. The present study therefore aimed to examine the protective potential of HJ water (HJW) extract against age‑related cognitive decline and scopolamine‑induced cognitive impairment. The analyses revealed that the oral administration of HJW markedly improved novel objective recognition and spatial learning in the novel object recognition and Morris water maze tests, respectively, in aged mice. The administration of 600 mg/kg HJW further increased neurogenesis and CA1 thickness in the hippocampi of aged mice. In scopolamine‑induced cognitive impairment, administration of 400 or 600 mg/kg HJW markedly increased novel object recognition performance in scopolamine‑treated mice. The inhibitory effect of HJW on acetylcholinesterase (AChE) and the activation effects of HJW on the calcium/calmodulin‑dependent kinase (CaMK)IIα‑cAMP response element‑binding protein (CREB) and AKT‑glycogen synthase kinase‑3 β (GSK3β) pathways were further demonstrated. Overall, these results indicate that HJW administration improves cognitive function through the regulation of AChE activity and CaMKIIα‑CREB and AKT‑GSK3β pathways.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11938412/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143670484","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}
引用次数: 0
Fibrosis factor CTGF facilitates VCAM‑1‑dependent monocyte adhesion to osteoarthritis synovial fibroblasts via the FAK and JNK pathways. 纤维化因子CTGF通过FAK和JNK途径促进VCAM - 1依赖性单核细胞粘附到骨关节炎滑膜成纤维细胞。
IF 3.4 3区 医学
Molecular medicine reports Pub Date : 2025-05-01 Epub Date: 2025-03-14 DOI: 10.3892/mmr.2025.13489
Shan-Chi Liu, Yat-Yin Law, Yu-Ying Wu, Yuan-Li Huang, Chun-Hao Tsai, Wei-Cheng Chen, Chih-Hsin Tang
{"title":"Fibrosis factor CTGF facilitates VCAM‑1‑dependent monocyte adhesion to osteoarthritis synovial fibroblasts via the FAK and JNK pathways.","authors":"Shan-Chi Liu, Yat-Yin Law, Yu-Ying Wu, Yuan-Li Huang, Chun-Hao Tsai, Wei-Cheng Chen, Chih-Hsin Tang","doi":"10.3892/mmr.2025.13489","DOIUrl":"10.3892/mmr.2025.13489","url":null,"abstract":"<p><p>Osteoarthritis (OA) is a long‑term, degenerative joint disease that presents significant clinical challenges and imposes considerable financial burdens. Fibrosis is closely intertwined with the pathogenesis of various degenerative diseases, including OA. Using data from the GDS5401 dataset, the present study determined that expression levels of the fibrosis factor connective tissue growth factor (CTGF) were significantly higher in OA patients than in normal individuals. The present study also identified CTGF elevated expression levels in both OA patients compared with healthy controls and in rats with anterior cruciate ligament transection‑induced OA versus controls. Stimulating OA synovial fibroblasts (OASFs) with CTGF was shown to promote vascular cell adhesion molecule‑1 (VCAM‑1) production, thereby facilitating monocyte adhesion to OASFs. Analysis of a large dataset revealed that monocytes are the only mononuclear cells with significantly elevated levels in OA patients. It also appeared that CTGF‑induced VCAM‑1 production and monocyte adhesion were mediated via the focal adhesion kinase and JNK pathways. These findings suggest that CTGF contributes to OA progression by enhancing monocyte adhesion to the synovial membrane.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11920775/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143625377","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}
引用次数: 0
Role of multi‑omics in advancing the understanding and treatment of prostate cancer (Review). 多组学在促进前列腺癌认识和治疗中的作用(综述)。
IF 3.4 3区 医学
Molecular medicine reports Pub Date : 2025-05-01 Epub Date: 2025-03-21 DOI: 10.3892/mmr.2025.13495
Li Yan, Pengxiao Su, Xiaoke Sun
{"title":"Role of multi‑omics in advancing the understanding and treatment of prostate cancer (Review).","authors":"Li Yan, Pengxiao Su, Xiaoke Sun","doi":"10.3892/mmr.2025.13495","DOIUrl":"10.3892/mmr.2025.13495","url":null,"abstract":"<p><p>The application of multi‑omics methodologies, encompassing genomics, transcriptomics, proteomics, metabolomics and integrative genomics, has markedly enhanced the understanding of prostate cancer (PCa). These methods have facilitated the identification of molecular pathways and biomarkers crucial for the early detection, prognostic evaluation and personalized treatment of PCa. Studies using multi‑omics technologies have elucidated how alterations in gene expression and protein interactions contribute to PCa progression and treatment resistance. Furthermore, the integration of multi‑omics data has been used in the identification of novel therapeutic targets and the development of innovative treatment modalities, such as precision medicine. The evolving landscape of multi‑omics research holds promise for not only deepening the understanding of PCa biology but also for fostering the development of more effective and tailored therapeutic interventions, ultimately improving patient outcomes. The present review aims to synthesize current findings from multi‑omics studies associated with PCa and to assess their implications for the improvement of patient management and therapeutic outcomes. The insights provided may guide future research directions and clinical practices in the fight against PCa.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11938414/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143670479","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}
引用次数: 0
Investigating the molecular mechanism of purslane‑based vitiligo treatment using network pharmacology, molecular docking and in vitro analyses. 运用网络药理学、分子对接、体外分析等方法探讨马齿苋类药物治疗白癜风的分子机制。
IF 3.4 3区 医学
Molecular medicine reports Pub Date : 2025-05-01 Epub Date: 2025-03-07 DOI: 10.3892/mmr.2025.13482
Xueying Zhang, Lele Meng, Xiaorong Ran, Shuang Li, Changhui Wen
{"title":"Investigating the molecular mechanism of purslane‑based vitiligo treatment using network pharmacology, molecular docking and <i>in vitro</i> analyses.","authors":"Xueying Zhang, Lele Meng, Xiaorong Ran, Shuang Li, Changhui Wen","doi":"10.3892/mmr.2025.13482","DOIUrl":"10.3892/mmr.2025.13482","url":null,"abstract":"<p><p>Purslane is a traditional Chinese medicine with a long‑standing history of efficacy in the management of dermatological conditions such as vitiligo. However, the molecular mechanisms underlying its therapeutic effects on vitiligo remain unclear. Therefore, the present study explored these mechanisms using network pharmacology, molecular docking and <i>in vitro</i> experiments. Following the screening process, seven principal active components were identified, namely kaempferol, hesperetin, luteolin, quercetin, arachidonic acid, cycloartenol and β‑sitosterol. In addition, six key targets, namely AKT1, tumor protein p53, peroxisome proliferator‑activated receptor γ (PPARG), estrogen receptor 1, prostaglandin‑endoperoxidase synthase 2 and mitogen‑activated protein kinase 1, and eight pathways in purslane‑based vitiligo treatment were identified. Network pharmacology and molecular docking demonstrated that flavonoids are the key components of purslane likely to mitigate oxidative stress damage in vitiligo. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses revealed that the phosphatidylinositol 3‑kinase (PI3K)/AKT, p53 and PPARG signaling pathways are associated with purslane components and vitiligo. <i>In vitro</i> experiments revealed that purslane total flavones (PTF) increased cell viability, decreased ROS levels and increased antioxidant enzyme activities in H<sub>2</sub>O<sub>2</sub>‑induced B16F10 cells. In addition, PTF activated the PI3K/AKT signaling pathway in H<sub>2</sub>O<sub>2</sub>‑induced B16F10 cells, and the antioxidant effect of PTF was attenuated by a PI3K/AKT inhibitor. In conclusion, the findings of the present study suggest that the flavonoids of purslane contribute, at least in part, to its therapeutic effectiveness in vitiligo by mitigating oxidative stress in melanocytes through the PI3K/AKT signaling pathway.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11905198/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143573444","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}
引用次数: 0
LncPrep + 96kb inhibits ovarian fibrosis by upregulating prolyl oligopeptidase expression. LncPrep + 96kb 通过上调脯氨酰寡肽酶的表达抑制卵巢纤维化。
IF 3.4 3区 医学
Molecular medicine reports Pub Date : 2025-05-01 Epub Date: 2025-02-28 DOI: 10.3892/mmr.2025.13478
Hongdan Zhang, Jing Wang, Jianwei Liu, Xiang Fan, Yinuo Jia, Yingtong Huang, Qihui Han, Shimeng Wang, Li Xiao, Xiang Li, Chunping Zhang
{"title":"LncPrep + 96kb inhibits ovarian fibrosis by upregulating prolyl oligopeptidase expression.","authors":"Hongdan Zhang, Jing Wang, Jianwei Liu, Xiang Fan, Yinuo Jia, Yingtong Huang, Qihui Han, Shimeng Wang, Li Xiao, Xiang Li, Chunping Zhang","doi":"10.3892/mmr.2025.13478","DOIUrl":"10.3892/mmr.2025.13478","url":null,"abstract":"<p><p>LncPrep + 96kb is a long non‑coding RNA expressed in murine granulosa cells. The 2.2-kb fragment of lncPrep + 96kb inhibits aromatase expression and estrogen secretion in ovarian granulosa cells. In the present study, lncPrep + 96kb‑knockout (KO) mice were generated, and significant ovarian fibrosis and reduced female fertility through fertility monitoring and superovulation. The augmentation of ovarian fibrosis was observed by Sirius red staining and western blot and <i>RT‑qPCR</i>. Notably, lncPrep + 96kb was identified in conserved non‑coding sequences adjacent to the prolyl oligopeptidase (POP) gene. Furthermore, POP expression was shown to be reduced in lncPrep + 96kb‑KO mice, whereas overexpression of lncPrep + 96kb increased POP expression. Further studies revealed that POP regulated the expression levels of factors related to fibrosis, including matrix metalloproteinase 2 (MMP2), transforming growth factor β1 (TGF‑β1) and peroxisome proliferator activated receptor γ (PPAR‑γ). In conclusion, ovarian fibrosis was elevated in lncPrep + 96kb‑KO mice, and POP may act as a target of lncPrep + 96kb, which mediates ovarian fibrosis through the regulation of PPAR‑γ, MMP2 and TGF‑β1 expression.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11894593/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143523877","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}
引用次数: 0
N‑methyladenosine reader YTHDF2‑mediated AC026691.1 degradation promotes gastric cancer cell proliferation, migration and M2 macrophage polarization. N -甲基腺苷读取器YTHDF2介导的AC026691.1降解促进胃癌细胞增殖、迁移和M2巨噬细胞极化。
IF 3.4 3区 医学
Molecular medicine reports Pub Date : 2025-05-01 Epub Date: 2025-03-07 DOI: 10.3892/mmr.2025.13485
Cong-Fei Ji, Jin-Feng Ji, Xiao-Bing Yu, Zhen-Xin Wang
{"title":"N‑methyladenosine reader YTHDF2‑mediated AC026691.1 degradation promotes gastric cancer cell proliferation, migration and M2 macrophage polarization.","authors":"Cong-Fei Ji, Jin-Feng Ji, Xiao-Bing Yu, Zhen-Xin Wang","doi":"10.3892/mmr.2025.13485","DOIUrl":"10.3892/mmr.2025.13485","url":null,"abstract":"<p><p>The present study aimed to explore the effects of key N6‑methyladenosine (m6A)‑related long non‑coding RNAs (lncRNAs) on the malignant behavior and macrophage polarization of gastric cancer cells, and their preliminary mechanisms. Gastric cancer‑related lncRNA datasets were downloaded from The Cancer Genome Atlas database, and m6A‑related differentially expressed lncRNAs (DElncRNAs) were analyzed. Subsequently, Cox regression and lasso regression analyses were used to screen the m6A‑related DElncRNAs associated with the prognosis of patients with gastric cancer. Additionally, reverse transcription‑quantitative polymerase chain reaction (qPCR) was employed to detect the expression levels of m6A‑related lncRNAs in normal gastric epithelial cells (GES‑1) and human gastric cancer cells (AGS and MKN‑45). In addition, the methylation levels of lncRNAs were measured using a methylated RNA immunoprecipitation qPCR assay kit, and the interaction between m6A‑related lncRNAs and m6A‑related proteins was observed by RNA pull‑down assay. Subsequently, m6A‑related lncRNAs and proteins were knocked down separately or simultaneously in gastric cancer cell lines. Bioinformatics analysis revealed that m6A‑related AC026691.1 was significantly associated with the prognosis of patients with gastric cancer and had a potential binding site for YT521‑B homology domain family member 2 (YTHDF2). The RNA pull‑down assay indicated that YTHDF2 not only had binding sites with AC026691.1 but could also markedly promote the degradation of m6A‑related AC026691.1. Furthermore, AC026691.1 was lowly expressed in gastric cancer cells, whereas YTHDF2 was highly expressed. Knockdown of YTHDF2 inhibited the proliferation, migration and epithelial‑mesenchymal transition of gastric cancer cells, and reduced M2 macrophage polarization. By contrast, knocking down AC026691.1 showed the opposite trend. Knockdown of YTHDF2 and AC026691.1 further confirmed the stable impact of YTHDF2 on AC026691.1. In conclusion, the degradation of AC026691.1 modified by YTHDF2‑mediated m6A may promote gastric cancer cell proliferation, migration, epithelial‑mesenchymal transition and M2 macrophage polarization.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11914866/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143573446","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}
引用次数: 0
Advances in research on the intestinal microbiota in the mechanism and prevention of colorectal cancer (Review). 肠道菌群在结直肠癌发病机制及预防中的研究进展(综述)。
IF 3.4 3区 医学
Molecular medicine reports Pub Date : 2025-05-01 Epub Date: 2025-03-21 DOI: 10.3892/mmr.2025.13498
Weitong Sun, Shize Ma, Dongdong Meng, Chaoxing Wang, Jinbo Zhang
{"title":"Advances in research on the intestinal microbiota in the mechanism and prevention of colorectal cancer (Review).","authors":"Weitong Sun, Shize Ma, Dongdong Meng, Chaoxing Wang, Jinbo Zhang","doi":"10.3892/mmr.2025.13498","DOIUrl":"10.3892/mmr.2025.13498","url":null,"abstract":"<p><p>The intestinal microbiota represents a diverse population that serves a key role in colorectal cancer (CRC) and its treatment outcomes. Advancements in sequencing have revealed notable shifts in microbial composition and diversity among individuals with CRC. Concurrently, animal models have elucidated the involvement of specific microbes such as <i>Lactobacillus fragilis</i>, <i>Escherichia coli</i> and <i>Fusobacterium nucleatum</i> in the progression of CRC. The present review aimed to highlight contributions of intestinal microbiota to the pathogenesis of CRC, the effects of traditional treatments on intestinal microbiota and the potential for microbiota modulation as a therapeutic strategy for CRC.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11948985/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143670510","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}
引用次数: 0
Effects of natural killer cell‑conditioned medium on UVB‑induced photoaging in human keratinocytes and a human reconstructed skin model. 自然杀伤细胞调节培养基对紫外线诱导的人类角质细胞光老化和人类重建皮肤模型的影响
IF 3.4 3区 医学
Molecular medicine reports Pub Date : 2025-05-01 Epub Date: 2025-03-14 DOI: 10.3892/mmr.2025.13488
Jung Ok Lee, Jung Min Lee, Yujin Kim, A Yeon Park, Daewon Yoon, Su Young Kim, Jihye Heo, Seungryel Han, Hyungjin Nam, Hye Jin Shin, Kyeongsoo Jeong, Minju Im, Beom Joon Kim
{"title":"Effects of natural killer cell‑conditioned medium on UVB‑induced photoaging in human keratinocytes and a human reconstructed skin model.","authors":"Jung Ok Lee, Jung Min Lee, Yujin Kim, A Yeon Park, Daewon Yoon, Su Young Kim, Jihye Heo, Seungryel Han, Hyungjin Nam, Hye Jin Shin, Kyeongsoo Jeong, Minju Im, Beom Joon Kim","doi":"10.3892/mmr.2025.13488","DOIUrl":"10.3892/mmr.2025.13488","url":null,"abstract":"<p><p>Natural killer (NK) cells produce various cytokines, including interleukin (IL)‑1β, IL‑6, IL‑10, IL‑12, interferon γ, tumor necrosis factor α and transforming growth factor β, which are critical in modulating immune responses. NK cell‑conditioned medium (NK‑CdM), rich in cytokines, has potential applications in therapy and healing. The present study aimed to investigate the protective effect of NK‑CdM against ultraviolet B (UVB)‑mediated photoaging using <i>in vitro</i> and <i>ex vivo</i> models. In human keratinocyte cell line (HaCaT cells), NK‑CdM mitigated UVB‑induced cytotoxicity and suppressed the production of reactive oxygen species. NK‑CdM enhanced the mRNA expression levels of superoxide dismutase 1 (SOD1) and catalase (CAT) and inhibited the reduction in SOD1 and CAT expression levels caused by UVB irradiation. Furthermore, NK‑CdM inhibited the UVB‑mediated nuclear translocation of nuclear factor erythroid 2‑related factor 2. NK‑CdM also prevented UVB‑induced downregulation of filaggrin and involucrin and attenuated the UVB‑induced reduction in hyaluronan synthase (HAS)1, HAS2, HAS3, aquaporin‑3 and hyaluronan levels. Notably, NK‑CdM upregulated the expression of elongation of very long chain fatty acids (ELOVL) enzymes, including ELOVL1, ELOVL5 and ELOVL6, as well as ceramide synthases (CerS), specifically CerS2 and CerS3. Furthermore, NK‑CdM inhibited the UVB‑induced reduction in the levels of these proteins. Overall, these findings suggested that NK‑CdM has the potential to prevent UVB‑mediated photoaging and promote skin health.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11920773/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143625347","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}
引用次数: 0
Spliceosome protein EFTUD2: A potential pathogenetic factor in tumorigenesis and some developmental defects (Review). 剪接体蛋白 EFTUD2:肿瘤发生和某些发育缺陷的潜在致病因素(综述)。
IF 3.4 3区 医学
Molecular medicine reports Pub Date : 2025-05-01 Epub Date: 2025-03-21 DOI: 10.3892/mmr.2025.13499
Ankang Yin, Qiuyu Zhu, Yi Chen, Juan Wang
{"title":"Spliceosome protein EFTUD2: A potential pathogenetic factor in tumorigenesis and some developmental defects (Review).","authors":"Ankang Yin, Qiuyu Zhu, Yi Chen, Juan Wang","doi":"10.3892/mmr.2025.13499","DOIUrl":"10.3892/mmr.2025.13499","url":null,"abstract":"<p><p>The formation of mature mRNA is inseparable from the processing of RNA precursors and splicing by the spliceosome. The spliceosome is a multi‑protein complex composed of five small nuclear ribonucleoproteins. Elongation factor Tu GTP binding domain containing 2 (EFTUD2) is a component of spliceosome complex that is involved in the reorganization of the spliceosome complex, thereby promoting the removal of introns from precursor mRNA. Therefore, EFTUD2 can regulate embryonic development and innate immunity by modulating the splicing of various mRNAs. The mutations in EFTUD2 itself also lead to developmental defects and clinical manifestations in mandibulofacial dysostosis, the nervous system, the circulatory system, the digestive system and the reproductive system. Furthermore, the overexpression of EFTUD2 promotes the progression of hepatocellular carcinoma, breast cancer and colorectal cancer. The present review discussed the molecular mechanisms by which EFTUD2 exerts its physiological functions, focusing on EFTUD2 mutations and their corresponding clinical manifestations. It aimed to provide insight for the diagnosis and treatment of EFTUD2‑related diseases.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11948986/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143670481","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}
引用次数: 0
[Retracted] lncRNA MNX1‑AS1 promotes prostate cancer progression through regulating miR‑2113/MDM2 axis. lncRNA MNX1‑AS1通过调节miR‑2113/MDM2轴促进前列腺癌进展。
IF 3.4 3区 医学
Molecular medicine reports Pub Date : 2025-05-01 Epub Date: 2025-03-07 DOI: 10.3892/mmr.2025.13480
Dong Liang, Chuanjie Tian, Xiaowen Zhang
{"title":"[Retracted] lncRNA MNX1‑AS1 promotes prostate cancer progression through regulating miR‑2113/MDM2 axis.","authors":"Dong Liang, Chuanjie Tian, Xiaowen Zhang","doi":"10.3892/mmr.2025.13480","DOIUrl":"10.3892/mmr.2025.13480","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the cell migration assay data shown in Fig. 2D on p. 5 were strikingly similar to data that had already been published in different form in the journal <i>OncoTargets and Therapy</i> in an article written by different authors at different research institutes (which has subsequently been retracted). In addition, there were instances of overlapping data panels identified comparing the data in Fig. 2E and F with those in Fig. 5E and F, such that data which were intended to show the results from differently performed experiments had apparently been derived from the same original sources. Owing to the fact that the contentious data in the above article had already been published prior to its submission to <i>Molecular Medicine Reports</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. [Molecular Medicine Reports 26: 231, 2022; DOI: 10.3892/mmr.2022.12747].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11905196/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143573507","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}
引用次数: 0
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
相关产品
×
本文献相关产品
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信