Molecular medicine reports最新文献

{"title":"[Retracted] NG25, an inhibitor of transforming growth factor‑β‑activated kinase 1, ameliorates neuronal apoptosis in neonatal hypoxic‑ischemic rats.","authors":"Hua Wang, Zhong Chen, Yu Li, Qiaoyun Ji","doi":"10.3892/mmr.2024.13423","DOIUrl":"10.3892/mmr.2024.13423","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 TUNEL assay data shown in Fig. 4B were strikingly similar to data appearing in different form in another article written by different authors at different research institutes that had already been submitted for publication to the journal <i>Experimental and Therapeutic Medicine</i> (which has subsequently been retracted). Owing to the fact that these contentious data had already apparently been submitted for publication prior to the receipt of this paper 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 17: 1710-1716, 2018; DOI: 10.3892/mmr.2017.8024].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11715618/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142882555","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":"New insights into the role of complement system in colorectal cancer (Review).","authors":"Yuwen Xu, Jiaqi Zhou, Yuanyuan Wu, Jie Shen, Xiaoyan Fu, Meifang Liu, Shujuan Liang","doi":"10.3892/mmr.2025.13433","DOIUrl":"10.3892/mmr.2025.13433","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is one of the most common cancers worldwide. With the growing understanding of immune regulation in tumors, the complement system has been recognized as a key regulator of tumor immunity. Traditionally, the complement cascade, considered an evolutionarily conserved defense mechanism against invading pathogens, has been viewed as a crucial inhibitor of tumor progression. Complement components or activation products produced via cascade‑dependent or ‑independent processes are associated with the regulation of tumor‑associated inflammation. Various forms of complement activation products present in body fluids or inside cells, along with complement regulatory proteins and complement receptors, are involved in tumor cell growth and modulating the tumor microenvironment. In the present review, the role of the complement system in the tumor immunity of CRC is discussed. In addition, the contribution of the unconventional cascade‑independent pathway of complement activation in CRC progression is highlighted. A deeper understanding of the mechanism underlying the complement system in colitis‑associated colorectal cancer (CAC) may provide novel insights to assist the development of methods to prevent tumor progression and identify potential targets for the treatment of CAC.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11751662/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142951896","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":"Pin1 as a central node in oncogenic signaling: Mechanistic insights and clinical prospects (Review).","authors":"Shuning Lei, Min Luo, Yuxue Wang","doi":"10.3892/mmr.2025.13445","DOIUrl":"10.3892/mmr.2025.13445","url":null,"abstract":"<p><p>Peptidyl‑prolyl cis‑trans isomerase NIMA-interacting 1 (Pin1) is a specific phosphorylated serine/threonine-proline cis-trans isomerase, which is involved in the regulation of a variety of physiological and pathological processes, including cell cycle progression, proliferation and apoptosis. Pin1 plays a key role in tumorigenesis and tumor development and it promotes the proliferation and metastasis of cancer cells by regulating the cell cycle, signaling pathways and the function of tumor suppressors. Upregulated expression of Pin1 is closely associated with a poor prognosis in several types of cancers. Thus, Pin1 is may have potential as a novel potential biomarker for tumor diagnosis and prognosis, as well as a promising anticancer target. The aim of the present review was to discuss the mechanism of Pin1 in tumors and recent research progress in this field.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11795255/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143066695","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":"Insights into renal damage in hyperuricemia: Focus on renal protection (Review).","authors":"Hang Yang, Jie Ying, Tong Zu, Xiao-Ming Meng, Juan Jin","doi":"10.3892/mmr.2024.13424","DOIUrl":"10.3892/mmr.2024.13424","url":null,"abstract":"<p><p>The incidence of hyperuricemia has increased recently, posing a serious threat to public health. Hyperuricemia is associated with an increased risk of gout, chronic kidney disease (CKD), obesity, metabolic syndrome, type 2 diabetes mellitus, hypertension, hypertriglyceridaemia, metabolic dysfunction‑associated steatotic liver disease, acute kidney injury, coronary heart disease and cardiovascular disease (CVD). These diseases are commonly accompanied by varying degrees of kidney damage. A number of randomized controlled clinical trials have investigated the effectiveness of UA‑lowering therapies in preventing kidney disease progression. The present review provided fundamental insights into the pathogenesis, principles and therapeutic approaches for managing hyperuricemia in patients with aforementioned diseases and assesses the effect of uric acid‑lowering therapy on diabetic nephropathy, systemic lupus erythematosus, CKD, CVD and obesity progression.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11711934/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142882559","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":"Epigenetic downregulation of the proapoptotic gene <i>HOXA5</i> in oral squamous cell carcinoma.","authors":"Ying-Ju Chen, Shin-Wei Liao, Yen-Ling Lai, Yu-Fen Li, Yin-Che Lu, Chien-Kuo Tai","doi":"10.3892/mmr.2024.13421","DOIUrl":"10.3892/mmr.2024.13421","url":null,"abstract":"<p><p>Homeobox A5 (<i>HOXA5</i>) has been identified as a tumor suppressor gene in breast cancers, but its role in oral squamous cell carcinoma (OSCC) has not been confirmed. The Illumina GoldenGate Assay for methylation identified that DNA methylation patterns differ between tumorous and normal tissues in the oral cavity and that <i>HOXA5</i> is one of the genes that are hypermethylated in oral tumor tissues. The present study obtained more‑complete information on the methylation status of <i>HOXA5</i> by using the Illumina Infinium MethylationEPIC BeadChip and bisulfite sequencing assays. The results indicated that <i>HOXA5</i> hypermethylation has great potential as a biomarker for detecting OSCC. Comparing <i>HOXA5</i> RNA expression between normal oral tissue and OSCC tissue samples indicated that its median level was 2.06‑fold higher in normal tissues that in OSCC tissues. Moreover, treatment using the demethylating agent 5‑aza‑2'‑deoxycytidine can upregulate <i>HOXA5</i> expression in OSCC cell lines, verifying that the silencing of <i>HOXA5</i> is primarily regulated by its hypermethylation. It was also found that upregulation of <i>HOXA5</i> expression can not only increase OSCC cell death but that it can also enhance the therapeutic effect of cisplatin both <i>in vitro</i> and <i>in vivo</i>, suggesting that <i>HOXA5</i> is an epigenetically downregulated proapoptotic gene in OSCC.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11683450/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142864062","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":"Mitochondrial DNA copy number alterations: Key players in the complexity of glioblastoma (Review).","authors":"Abdul Aziz Mohamed Yusoff, Siti Zulaikha Nashwa Mohd Khair, Siti Muslihah Abd Radzak","doi":"10.3892/mmr.2025.13443","DOIUrl":"10.3892/mmr.2025.13443","url":null,"abstract":"<p><p>Renowned as a highly invasive and lethal tumor derived from neural stem cells in the central nervous system, glioblastoma (GBM) exhibits substantial histopathological variation and genomic complexity, which drive its rapid progression and therapeutic resistance. Alterations in mitochondrial DNA (mtDNA) copy number (CN) serve a crucial role in GBM development and progression, affecting various aspects of tumor biology, including energy production, oxidative stress regulation and cellular adaptability. Fluctuations in mtDNA levels, whether elevated or diminished, can impair mitochondrial function, potentially disrupting oxidative phosphorylation and amplifying reactive oxygen species generation, thereby fueling tumor growth and influencing treatment responses. Understanding the mechanisms of mtDNA‑CN variations, and their interplay with genetic and environmental elements in the tumor microenvironment, is essential for advancing diagnostic and therapeutic strategies. Targeting mtDNA alterations could strengthen treatment efficacy, mitigate resistance and ultimately enhance the prognosis of patients with this aggressive brain tumor. The present review summarizes the existing literature on mtDNA alterations, specifically emphasizing variations in mtDNA‑CN and their association with GBM by surveying articles published between 1996 and 2024, sourced from databases such as Scopus, PubMed and Google Scholar. In addition, the review provides a brief overview of mitochondrial genome architecture, knowledge regarding the regulation of mtDNA integrity and CN, and how mitochondria significantly impact GBM tumorigenesis. This review further presents information on therapeutic approaches for restoring mtDNA‑CN that contribute to optimized mitochondrial function and improved health outcomes.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11795256/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143066771","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":"Calycosin‑7‑O‑β‑D‑glucoside downregulates mitophagy by mitigating mitochondrial fission to protect HT22 cells from oxygen‑glucose deprivation/reperfusion‑induced injury.","authors":"Xiangli Yan, Siqi Quan, Roujia Guo, Zibo Li, Ming Bai, Baoying Wang, Pan Su, Erping Xu, Yucheng Li","doi":"10.3892/mmr.2025.13436","DOIUrl":"10.3892/mmr.2025.13436","url":null,"abstract":"<p><p>Calycosin‑7‑O‑β‑D‑glucoside (CG), a major active ingredient of Astragali Radix, exerts neuroprotective effects against cerebral ischemia; however, whether the effects of CG are associated with mitochondrial protection remains unclear. The present study explored the role of CG in improving mitochondrial function in a HT22 cell model of oxygen‑glucose deprivation/reperfusion (OGD/R). The Cell Counting Kit‑8 assay, flow cytometry, immunofluorescence and western blotting were performed to investigate the effects of CG on mitochondrial function. The results demonstrated that mitochondrial function was restored after treatment with CG, as indicated by reduced mitochondrial reactive oxygen species levels, increased mitochondrial membrane potential and improved mitochondrial morphology. Overactivated mitophagy was revealed to be inhibited by the regulation of proteins involved in fission [phosphorylated‑dynamin‑related protein 1 (Drp1) and Drp1] and mitophagy (LC3, p62 and translocase of outer mitochondrial membrane 20), and mitochondrial biogenesis was demonstrated to be enhanced by increased levels of sirtuin 1 (SIRT1) and peroxisome proliferator‑activated receptor γ coactivator‑1α (PGC‑1α). In addition, neuronal apoptosis was ameliorated by CG, as determined by a decreased rate of apoptosis, and levels of caspase‑3 and Bcl‑2/Bax. In conclusion, the present study demonstrated that CG may alleviate OGD/R‑induced injury by upregulating SIRT1 and PGC‑1α protein expression, and reducing excessive mitochondrial fission and overactivation of mitophagy.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11751592/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143008524","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":"Exosomal SphK1 from colorectal cancer cells promotes cancer cell migration and activates hepatic stellate cells.","authors":"Wenlu Zhang, Chunyan Xu","doi":"10.3892/mmr.2025.13438","DOIUrl":"10.3892/mmr.2025.13438","url":null,"abstract":"<p><p>Exosomes are small extracellular vesicles that are naturally released into body fluids by cells. They are rich in bioactive molecules such as proteins. Sphingosine kinase 1 (SphK1) is an important potential drug target for the treatment of cancer due to its functions to regulate cancer cell migration, growth, apoptosis and angiogenesis. Tumor exosomes abundantly surround primary tumors, exchanging and transferring information between cells and modulating cancer progression. Given the importance of exosomes, the involvement of exosomal SphK1 from colorectal cancer (CRC) cells in the migration of these cells and the activation of hepatic stellate cells was investigated. Firstly, the plasma exosomal SphK1 protein expression, tested by ELISA, was compared between patients with CRC without metastasis and those with liver metastasis. The results revealed that plasma exosomal SphK1 levels were significantly upregulated in patients with liver metastasis of CRC. Secondly, exosomes with different expression levels of SphK1, which were regulated by cell transfection, were isolated from CRC cells to evaluate their effect on the expression levels of E‑cadherin and vimentin in these cells, as assessed by western blotting. The results demonstrated that depletion of exosomal SphK1 partially reversed the exosome‑induced migration of CRC cells, and caused decreased vimentin and increased E‑cadherin levels. Thirdly, the effects of exosomes from CRC cells, with different expression levels of SphK1, on hepatic stellate cell activation were investigated, with α‑SMA, TNF‑α and TGF‑β levels assessed by western blotting in LX‑2 cells. Moreover, AKT and phosphorylated (p‑)AKT levels were also assessed by western blotting. The results revealed that exosomes activated hepatic stellate cells by upregulating p‑AKT, and depletion of exosomal SphK1 partially reversed this effect. Furthermore, the application of an AKT agonist reversed the inhibition of hepatic stellate cell activation, which was induced by the depletion of exosomal SphK1. Finally, investigation of cell viability, analyzed by CCK‑8 assay, and assessment of PCNA as a proliferation marker, analyzed by western blot, revealed that the culture supernatant of the activated hepatic stellate cells promoted the viability of CRC cells. Overall, these results demonstrated that exosomal SphK1 increased the migration of CRC cells, and activated hepatic stellate cells by regulating p‑AKT. This suggests that exosomal SphK1 may serve a key role in the migration of CRC cells and potentially the liver metastasis of CRC.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11795250/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143391268","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] Limb remote ischemic post‑conditioning reduces injury and improves long‑term behavioral recovery in rats following subarachnoid hemorrhage: Possible involvement of the autophagic process.","authors":"Xiang Hu, Tao Lv, Shao-Feng Yang, Xiao-Hua Zhang, Yi-Feng Miao","doi":"10.3892/mmr.2024.13419","DOIUrl":"10.3892/mmr.2024.13419","url":null,"abstract":"<p><p>Following the publication of the above paper, a concerned reader drew to the attention of the Editorial Office that the 'Sham' brain image featured in Fig. 1B on p. 23 was strikingly similar to an image that was published subsequently in the journal <i>Scientific Reports</i>, whereas the control TUNEL assay data shown in Fig. 4A on p. 25 were similarly strikingly similar to data shown in a paper published previously in the journal <i>Mediators of Inflammation</i>, even though the overall experiments portrayed in the other journals were different. As the three affected articles did hold at least one author in common, we asked the authors to provide an explanation to account for the sharing of these data among these papers, but no reply was forthcoming from them; therefore, in the absence of a reply from these authors, the Editor of <i>Molecular Medicine Reports</i> has decided that this paper should be retracted from the Journal on account of a lack of confidence in the presented data. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 17: 21‑30, 2018; DOI: 10.3892/mmr.2017.7858].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11683449/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142864060","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":"NEDD4 enhances bone‑tendon healing in rotator cuff tears by reducing fatty infiltration.","authors":"Jian Li, Ying Peng, Dong Zhen, Caifen Guo, Wuxun Peng","doi":"10.3892/mmr.2024.13420","DOIUrl":"10.3892/mmr.2024.13420","url":null,"abstract":"<p><p>Rotator cuff tears (RCT) can cause shoulder pain, weakness and stiffness, significantly affecting daily life. Analysis of the GSE103266 dataset revealed significant changes in the mTOR/PI3K/Akt signaling pathway and lipid metabolism‑related pathways, suggesting that fatty infiltration may affect RCT. The analysis indicated that the ubiquitin ligase NEDD4 plays a critical role in RCT. NEDD4 was found to be highly associated with the mTOR/PI3K/Akt signaling pathway. An RCT model in Sprague‑Dawley (SD) rats was established to study the role of NEDD4 in regulating the mTOR pathway and investigate its effects on fatty infiltration. SD rats were divided into NEDD4 overexpression and knockout groups. Tissue recovery, apoptosis and fat deposition were measured through histological staining, reverse transcription‑quantitative PCR and western blotting. Additionally, cell culture of fibro‑adipogenic progenitors and lentiviral transfection were conducted to investigate the effect of NEDD4 on adipocyte differentiation. NEDD4 overexpression significantly reduced lipid accumulation, whereas NEDD4 knockdown enhanced lipid accumulation. NEDD4 was found to regulate the mTOR pathway and the expression of adipogenesis‑related genes, promoting fat metabolism and inhibiting adipocyte differentiation. Histological analysis indicated that NEDD4 overexpression improved tissue recovery and reduced apoptosis. Targeting NEDD4 offers a potential therapeutic strategy to improve the clinical outcomes of patients with RCT by modulating the mTOR pathway and fat metabolism.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11683452/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142864073","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}