Molecular medicine reports最新文献

{"title":"SPOCK: Master regulator of malignant tumors (Review).","authors":"Mingyuan Xiao, Jiancheng Xue, Enli Jin","doi":"10.3892/mmr.2024.13355","DOIUrl":"10.3892/mmr.2024.13355","url":null,"abstract":"<p><p>SPARC/osteonectin, CWCV and Kazal‑like domain proteoglycan (SPOCK) is a family of highly conserved multidomain proteins. In total, three such family members, <i>SPOCK1</i>, <i>SPOCK2</i> and <i>SPOCK3</i>, constitute the majority of extracellular matrix glycoproteins. The <i>SPOCK</i> gene family has been demonstrated to serve key roles in tumor regulation by affecting MMPs, which accelerates the progression of cancer epithelial‑mesenchymal transition. In addition, they can regulate the cell cycle via overexpression, inhibit tumor cell proliferation by inactivating PI3K/AKT signaling and have been associated with numerous microRNAs that influence the expression of downstream genes. Therefore, the SPOCK gene family are potential cancer‑regulating genes. The present review summarizes the molecular structure, tissue distribution and biological function of the SPOCK family of proteins, in addition to its association with cancer. Furthermore, the present review documents the progress made in investigations into the role of SPOCK, whilst also discussing prospects for the future of SPOCK‑targeted therapy, to provide novel ideas for clinical application and treatment.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 6","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11487499/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142400780","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] Tanshinone IIA regulates colorectal cancer apoptosis via attenuation of Parkin‑mediated mitophagy by suppressing AMPK/Skp2 pathways.","authors":"Lili He, Kebo Gu","doi":"10.3892/mmr.2024.13315","DOIUrl":"https://doi.org/10.3892/mmr.2024.13315","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 immunofluorescence assay data shown in Fig. 4A on p. 1698 were strikingly similar to data that had already been submitted for publication in different form in another article written by different authors at different research institutes. In addition, there was an instance of apparent duplication of western blot data comparing between Fig. 5A and 5G, and the reader also had concerns regarding the presentation of the flow‑cytometry cell‑count histograms in Fig. 2A. Owing to the fact that the contentious data in the above article had already been submitted for publication elsewhere prior to its submission to Molecular Medicine Reports, 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 18: 1692‑1703, 2018; DOI: 10.3892/mmr.2018.9087].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142109612","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Retracted] Salidroside mitigates hypoxia/reoxygenation injury by alleviating endoplasmic reticulum stress‑induced apoptosis in H9c2 cardiomyocytes.","authors":"Meng-Yao Sun, Da-Shi Ma, Song Zhao, Lei Wang, Chun-Ye Ma, Yang Bai","doi":"10.3892/mmr.2024.13320","DOIUrl":"10.3892/mmr.2024.13320","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 apoptotic assay data shown in Fig. 1D on p. 3763 were strikingly similar to data that had already been submitted for publication in Fig. 3A in different form in another article written by different authors at different research institutes. Owing to the fact that the contentious data in the above article had already been submitted for publication 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 18: 3760‑3768, 2018; DOI: 10.3892/mmr.2018.9403].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11391513/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142140571","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":"Extracellular vesicles derived from mesenchymal stem cells suppress breast cancer progression by inhibiting angiogenesis.","authors":"Manqian Zhou, Huifang Li, Jinglei Zhao, Qiaonan Zhang, Zhibo Han, Zhong-Chao Han, Lihong Zhu, Hui Wang, Zongjin Li","doi":"10.3892/mmr.2024.13316","DOIUrl":"10.3892/mmr.2024.13316","url":null,"abstract":"<p><p>Previous studies have highlighted the antitumor effects of mesenchymal stem cell‑derived extracellular vesicles (MSC‑EVs), positioning them as a promising therapeutic avenue for cancer treatment. However, some researchers have proposed a bidirectional influence of MSC‑EVs on tumors, determined by the specific tissue origin of the MSCs and the types of tumors involved. The present study aimed to elucidate the effects of human placenta MSC‑derived extracellular vesicles (hPMSC‑EVs) on the malignant behavior of a mouse breast cancer model of 4T1 cells <i>in</i> <i>vitro</i> and <i>in</i> <i>vivo</i>. The findings revealed that hPMSC‑EVs significantly inhibited the proliferation, migration and colony formation of cultured 4T1 mouse breast cancer cells without inducing apoptosis. Exposure to conditioned medium from 4T1 cells pretreated with hPMSC‑EVs resulted in decreased angiogenic activity, accompanied by the downregulation of angiogenesis‑promoting genes in human umbilical vein endothelial cells. In murine xenograft models derived from the 4T1 cell line, local administration of hPMSC‑EVs substantially hindered tumor growth. Further results revealed that hPMSC‑EVs inhibited angiogenesis <i>in</i> <i>vivo</i>, as reflected by the use of a vascular growth factor receptor 2‑Fluc transgenic mouse model. In summary, the results confirmed that hPMSC‑EVs negatively modulated breast cancer growth by suppressing tumor cell proliferation and migration via an indirect antiangiogenic mechanism. These results underscored the therapeutic potential of EVs, suggesting a promising avenue for alternative anticancer treatments in the future.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142109615","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>ARID1A</i> overexpression inhibits colorectal cancer cell migration through the regulation of epithelial‑mesenchymal transition.","authors":"Sasithorn Wanna-Udom, Siripat Aluksanasuwan, Keerakarn Somsuan, Wariya Mongkolwat, Natthiya Sakulsak","doi":"10.3892/mmr.2024.13325","DOIUrl":"https://doi.org/10.3892/mmr.2024.13325","url":null,"abstract":"<p><p>The advancement of tumor cell metastasis is significantly influenced by epithelial‑to‑mesenchymal transition (EMT), and metastasis is a prominent contributor to the mortality of patients diagnosed with colorectal cancer (CRC). AT‑rich interactive domain‑containing protein 1A (ARID1A), which acts as a tumor suppressor, frequently exhibits a loss‑of‑function mutation in metastatic CRC tissues. However, the underlying molecular mechanisms of ARID1A relating to EMT remain poorly understood. The present study aimed to clarify the association between ARID1A and EMT regulation in human CRC cells. The investigation into the loss of ARID1A expression in tissues from patients with CRC was performed using immunohistochemistry. Furthermore, <i>ARID1A</i>‑overexpressing SW48 cells were established using lentiviruses carrying human full‑length <i>ARID1A</i>. The results revealed that overexpression of <i>ARID1A</i> induced cellular morphological changes by promoting the tight junction molecule zonula occludens 1 (ZO‑1) and the adherens junction molecule E‑cadherin, whereas it decreased the intermediate filament protein vimentin. The results of reverse transcription‑quantitative PCR also confirmed that <i>ARID1A</i> overexpression upregulated the mRNA expression levels of <i>TJP1</i>/ZO‑1 and <i>CDH1</i>/E‑cadherin, and downregulated VIM/vimentin and zinc finger E‑box binding homeobox 1 expression, which are considered epithelial and mesenchymal markers, respectively. In addition, the overexpression of <i>ARID1A</i> in CRC cells resulted in a suppression of cell motility and migratory capabilities. The present study also demonstrated that the tumor suppressor ARID1A was commonly absent in CRC tissues. Notably, <i>ARID1A</i> overexpression could reverse the EMT‑like phenotype and inhibit cell migration through alterations in EMT‑related markers, leading to the inhibition of malignant progression. In conclusion, ARID1A may serve as a biomarker and therapeutic target in the clinical management of metastatic CRC.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11406482/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142291513","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":"Copper ions: The invisible killer of cardiovascular disease (Review).","authors":"Yi-Ming Wang, Lan-Shuan Feng, Ao Xu, Xiao-Han Ma, Miao-Tiao Zhang, Jie Zhang","doi":"10.3892/mmr.2024.13334","DOIUrl":"10.3892/mmr.2024.13334","url":null,"abstract":"<p><p>Copper, a vital trace element, is indispensable for the maintenance of physiological functioning, particularly in the cardiac system. Unlike other forms of cell death such as iron death and apoptosis, copper‑induced cell death has gained increasing recognition as a significant process influencing the development of cardiovascular diseases. The present review highlights the significance of maintaining copper homeostasis in addressing cardiovascular diseases. This review delves into the crucial roles of copper in physiology, including the metabolic pathways and its absorption, transport and excretion. It provides detailed insights into the mechanisms underlying cardiovascular diseases resulting from both excess and deficient copper levels. Additionally, it summarizes strategies for treating copper imbalances through approaches such as copper chelators and ion carriers while discussing their limitations and future prospects.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11425066/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142291514","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":"Exploring the therapeutic potential of rabdoternin E in lung cancer treatment: Targeting the ROS/p38 MAPK/JNK signaling pathway.","authors":"Jinghui Jin, Juan Nan, Yanpo Si, Xiaohui Chen, Haibo Wang, Xiaowei Wang, Jingwang Huang, Tao Guo","doi":"10.3892/mmr.2024.13330","DOIUrl":"10.3892/mmr.2024.13330","url":null,"abstract":"<p><p>Lung cancer has the highest incidence and mortality rates of all cancer types in China and therefore represents a serious threat to human health. In the present study, the mechanism of rabdoternin E against the proliferation of the lung cancer cell line A549 was explored. It was found that rabdoternin E caused the accumulation of large amounts of reactive oxygen species (ROS), promoted cell S phase arrest by reducing the expression of CDK2 and cyclin A2, induced apoptosis by increasing the Bax/Bcl‑2 ratio and promoted the phosphorylation of proteins in the ROS/p38 MAPK/JNK signaling pathway, which is associated with apoptosis and ferroptosis. In addition, it was also found that Z‑VAD‑FMK (an apoptosis inhibitor), ferrostatin‑1 (ferroptosis inhibitor) and N‑acetylcysteine (a ROS inhibitor) could partially or greatly reverse the cytotoxicity of rabdoternin E to A549 cells. Similarly, NAC (N‑acetylcysteine) treatment notably inhibited the rabdoternin E‑stimulated p38 MAPK and JNK activation. Furthermore, <i>in vivo</i> experiments in mice revealed that Rabdoternin E markedly reduced tumor volume and weight and regulated the expression levels of apoptosis and ferroptosis‑related proteins (including Ki67, Bcl‑2, Bax, glutathione peroxidase 4, solute carrier family 7 member 11 and transferrin) in the tumor tissues of mice. Histopathological observation confirmed that the number of tumor cells decreased markedly after administration of rabdoternin E. Taken together, rabdoternin E induced apoptosis and ferroptosis of A549 cells by activating the ROS/p38 MAPK/JNK signaling pathway. Therefore, the results of the present study showed that rabdoternin E is not toxic to MCF‑7 cells (normal lung cells), had no significant effect on body weight and was effective and therefore may be a novel therapeutic treatment for lung cancer.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11420865/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142291515","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":"Construction and validation of a bioinformatics‑based screen for cuproptosis‑related genes and risk model for Alzheimer's disease.","authors":"Rui Hu, Zhen Xiao, Mingyu Qiao, Chaoyu Liu, Guiyou Wu, Yunyi Wang, Mingyou Dong, Zhongshi Huang","doi":"10.3892/mmr.2024.13318","DOIUrl":"10.3892/mmr.2024.13318","url":null,"abstract":"<p><p>The present study aimed to validate the association between core cuproptosis genes (CRGs) and Alzheimer's disease (AD) from both bioinformatics and experimental perspectives and also to develop a risk prediction model. To this end, 78 human‑derived temporal back samples were analyzed from GSE109887, and the biological functions of the resulting CRGs were explored by cluster analysis, weighted gene co‑expression network analysis and similar methods to identify the best machine model. Moreover, an external dataset GSE33000 and a nomogram were used to validate the model. The mRNA and protein expression of CRGs were validated using the SH‑SY5Y cell model and the Sprague‑Dawley rat animal model. The RT‑qPCR and western blotting results showed that the mRNA and protein expression content of dihydrolipoamide dehydrogenase, ferredoxin 1, glutaminase and pyruvate dehydrogenase E1 subunit β decreased, and the expression of dihydrolipoamide branched chain transacylase E2 increased in AD, which supported the bioinformatic analysis results. The CRG expression alterations affected the aggregation and infiltration of certain immune cells. The present study also confirmed the accuracy and validity of AD diagnostic models and nomograms, and validated the association between five CRGs and AD, indicating a significant difference between patients with AD and healthy individuals. Therefore, CRGs are expected to serve as relevant biomarkers for the diagnosis and prognostic monitoring of AD.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142109614","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tetraspanins in digestive‑system cancers: Expression, function and therapeutic potential (Review).","authors":"Kexin Chen, Qiuhong Li, Yangyi Li, Donghui Jiang, Ligang Chen, Jun Jiang, Shengbiao Li, Chunxiang Zhang","doi":"10.3892/mmr.2024.13324","DOIUrl":"10.3892/mmr.2024.13324","url":null,"abstract":"<p><p>The tetraspanin family of membrane proteins is essential for controlling different biological processes such as cell migration, penetration, adhesion, growth, apoptosis, angiogenesis and metastasis. The present review summarized the current knowledge regarding the expression and roles of tetraspanins in different types of cancer of the digestive system, including gastric, liver, colorectal, pancreatic, esophageal and oral cancer. Depending on the type and context of cancer, tetraspanins can act as either tumor promoters or suppressors. In the present review, the importance of tetraspanins in serving as biomarkers and targets for different types of digestive system‑related cancer was emphasized. Additionally, the molecular mechanisms underlying the involvement of tetraspanins in cancer progression and metastasis were explored. Furthermore, the current challenges are addressed and future research directions for advancing investigations related to tetraspanins in the context of digestive system malignancies are proposed.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11411235/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142140575","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":"High‑fat diet‑induced LCN2 exacerbates myocardial ischemia‑reperfusion injury by enhancing platelet activation.","authors":"Peng Li, Juhai Chen, Mingdong Wang, Qi Wang, Xingde Liu","doi":"10.3892/mmr.2024.13329","DOIUrl":"10.3892/mmr.2024.13329","url":null,"abstract":"<p><p>Following acute myocardial infarction, the recovery of blood flow leads to myocardial ischemia‑reperfusion (MI/R) injury, which is primarily characterized by the activation of inflammatory signals, microvascular obstruction, increased oxidative stress and excessive Ca²⁺ overload. It has also been demonstrated that platelets can exacerbate MI/R injury by releasing reactive oxygen species, inflammatory factors and chemokines, while also obstructing microvessels through thrombus formation. As a bioactive molecule with proinflammatory and chemotactic properties, lipocalin 2 (LCN2) exhibits a positive correlation with obesity, hyperglycemia, hypertriglyceridemia and insulin resistance index, which are all significant risk factors for ischemic cardiomyopathy. Notably, the potential role of LCN2 in promoting atherosclerosis may be related to its influence on the function of macrophages, smooth muscle cells and endothelial cells, but its effect on platelet function has not yet been reported. In the present study, the effect of a high‑fat diet (HFD) on LCN2 expression was determined by detecting LCN2 expression levels in the liver and serum samples of mice through reverse transcription‑quantitative PCR and enzyme linked immunosorbent assay, respectively. The effect of LCN2 on platelet function was evaluated by examining whether LCN2 affected platelet activation, aggregation, adhesion, clot retraction and P‑selectin expression. To determine whether LCN2 aggravated MI/R injury in HFD‑fed mice by affecting platelet and inflammatory cell recruitment, wild‑type and LCN2 knockout mice fed a HFD were subjected to MI/R injury, then hearts were collected for hematoxylin and eosin staining and 2,3,5‑triphenyltetrazolium chloride staining, and immunohistochemistry was employed to detect the expression of CD42b, Ly6G, CD3 and B220. Based on observing the upregulation of LCN2 expression in mice fed a HFD, the present study further confirmed that LCN2 could accelerate platelet activation, aggregation and adhesion. Moreover, <i>in vivo</i> studies validated that knockout of LCN2 not only mitigated MI/R injury, but also inhibited the recruitment of platelets and inflammatory cells in myocardial tissue following ischemia‑reperfusion. In conclusion, the current findings suggested that the effect of HFD‑induced LCN2 on aggravating MI/R injury may totally or partially dependent on its promotion of platelet function.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11420867/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142291517","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}