Molecular medicine reports最新文献

{"title":"Ameliorative effects of <i>Asiasarum</i> root and rhizome extract on high fat diet‑induced obesity in mice through regulation of the SIRT1/PGC1α/AMPK pathways in muscle and liver tissues.","authors":"Chenzi Lyu, Seok Yong Kang, Haifeng Shao, Dongeun Kim, Hyo Won Jung","doi":"10.3892/mmr.2025.13440","DOIUrl":"10.3892/mmr.2025.13440","url":null,"abstract":"<p><p>Asiasarum root and rhizome (<i>Asarum</i>) is commonly used as a diaphoretic. Due to its warm and pungent characteristics in traditional Chinese and Korean medicine, it is considered as having the potential to prevent disease. The present study investigated the effects of <i>Asarum</i> extract on the symptoms of obesity in mice, and the regulation of energy metabolism in the liver and skeletal muscle tissues. In addition, to identify the potential molecular targets and signaling pathways involved in the mechanism of action of <i>Asarum</i> extract in obesity, network pharmacological and molecular docking analysis was performed. <i>In vitro</i> studies demonstrated that <i>Asarum</i> extract significantly increased the expression of regulators of energy metabolism [sirtuin 1 (SIRT1), peroxisome proliferator‑activated receptor γ coactivator 1‑α (PGC1α), nuclear respiratory factor 1, AMP‑activated protein kinase (AMPK) and glucose transporter type 4 (GLUT4)] and myogenic regulatory factors (MyoD, myogenin and myosin heavy chain) in C2C12 myotubes. Furthermore, the in vivo studies demonstrated that <i>Asarum</i> extract could reduce increases in body weight, and the levels of blood glucose, insulin, total cholesterol, triglycerides and low‑density lipoprotein cholesterol in the sera of obese mice. <i>Asarum</i> extract also improved pathological changes in the liver and pancreatic tissues of obese mice, and significantly increased the ratio of brown fat mass to body weight. In addition, <i>Asarum</i> extract reversed the expression of energy metabolism regulators and myogenic regulatory factors in the gastrocnemius tissues of obese mice. <i>Asarum</i> extract also activated the expression of SIRT1, PGC1α and AMPK in the liver tissues of obese mice. These findings indicated that <i>Asarum</i> extract may exert anti‑obesity effects, such as body weight loss, decreases in lipid metabolite levels, and inhibition of pancreatic and liver damage. Using network pharmacological analysis, the mechanisms underlying the effects of <i>Asarum</i> extract on the regulation of energy metabolism were explored, particularly in skeletal muscle and liver tissues.</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/PMC11795245/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143066513","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":"Heat shock protein 22: A new direction for cardiovascular disease (Review).","authors":"Yi Chen, Meng Li, Yanqing Wu","doi":"10.3892/mmr.2025.13447","DOIUrl":"10.3892/mmr.2025.13447","url":null,"abstract":"<p><p>Small heat shock proteins (sHSPs) are common molecular chaperone proteins that function in various biological processes, and serve indispensable roles in maintaining cellular protein homeostasis and regulating the hydrolysis of unfolded proteins. HSP22 is a member of the sHSP family that is primarily expressed in the heart and skeletal muscle, as well as in various types of cancer. There have been important findings concerning the role of HSP22 in cardiovascular diseases. The aim of the present study was to provide insights into the various molecular mechanisms by which HSP22 functions in the heart, including oxidative stress, autophagy, apoptosis, the subcellular distribution of proteins and the promoting effect of proteasomes. In addition, drugs and cytokines, including geranylgeranylacetone, can exert protective effects on the heart by regulating the expression of HSP22. Based on increasingly abundant research, HSP22 may be considered a potential therapeutic target in cardiovascular diseases.</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/PMC11800183/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143066767","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":"Integrated transcriptomics and proteomics analysis of the impact of iodine‑125 in hepatocellular carcinoma.","authors":"Yang Yang, Wei Yang, Jie Shen, Enci Ding","doi":"10.3892/mmr.2025.13431","DOIUrl":"10.3892/mmr.2025.13431","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is a common cause of cancer‑related mortality and morbidity worldwide. While iodine‑125 (¹²⁵I) particle brachytherapy has been extensively used in the clinical treatment of various types of cancer, the precise mechanism underlying its effectiveness in treating HCC remains unclear. In the present study, MHCC‑97H cells were treated with ¹²⁵I, after which, cell viability and proliferation were assessed using Cell Counting Kit‑8, 5‑ethynyl‑2'‑deoxyuridine and colony formation assays, cell invasion and migration were evaluated using wound healing and Transwell assays, and cell apoptosis was determined using flow cytometry. Omics data were analyzed using Kyoto Encyclopedia of Genes and Genomes, Gene Ontology and STRING analyses to observe the key genes that exhibited significant changes at the transcriptional and protein levels in MHCC‑97H cells treated with ¹²⁵I particles. Finally, the expression levels of key genes (GPNMB, C4BPA, CTH, H1‑0 and MT2A) were verified through reverse transcription quantitative PCR. Following treatment with ¹²⁵I, the proliferation, invasion and migration of MHCC‑97H cells were inhibited, and apoptosis was enhanced. The results of omics data analysis indicated that the biological behavior of MHCC‑97H cells treated with ¹²⁵I was related to the expression levels of CTH and MT2A genes. These findings indicated that intervention with ¹²⁵I radiation particles may induce changes in gene expression, potentially influencing alterations in biological characteristics. In conclusion, these insights may shed light on the underlying mechanisms of ¹²⁵I radiation particle therapy in HCC and offer novel targets for HCC treatment.</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/PMC11736249/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142951893","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":"Multifaceted roles of insulin‑like growth factor 2 mRNA binding protein 2 in human cancer (Review).","authors":"Jianan Shen, Youxiang Ding","doi":"10.3892/mmr.2025.13441","DOIUrl":"10.3892/mmr.2025.13441","url":null,"abstract":"<p><p>Insulin‑like growth factor 2 mRNA binding protein 2 (IGF2BP2) is an RNA binding protein that functions as an N⁶‑methyladenosine reader. It regulates various biological processes in human cancers by affecting the stability and expression of target RNA transcripts, including coding RNAs and non‑coding RNAs (ncRNAs). Numerous studies have shown that IGF2BP2 expression is aberrantly increased in various types of cancer and plays multifaceted roles in the development and progression of human cancers. In the present review, the clinical importance of IGF2BP2 is summarized and its involvement in the regulation of biological processes, including proliferation, metastasis, chemoresistance, metabolism, tumor immunity, stemness and cell death, in human cancers is discussed. The chemical compounds that have been developed as IGF2BP2 inhibitors are also detailed. As ncRNAs are now important potential therapeutic agents for cancer treatment, the microRNAs that have been reported to directly target and inhibit IGF2BP2 expression in cancers are also described. In summary, by reviewing the latest literature, the present study aimed to highlight the clinical importance and physiological functions of IGF2BP2 in human cancer, with a focus on the great potential of IGF2BP2 as a target for inhibitor development. The present review may inspire new ideas for future studies on IGF2BP2, which may serve as a specific therapeutic target in cancer.</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/PMC11795254/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143066692","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":"RMRP variants inhibit the cell cycle checkpoints pathway in cartilage‑hair hypoplasia.","authors":"Jian Gao, Junge Zheng, Shiguo Chen, Sheng Lin, Shan Duan","doi":"10.3892/mmr.2025.13446","DOIUrl":"10.3892/mmr.2025.13446","url":null,"abstract":"<p><p>Cartilage‑hair hypoplasia (CHH) is an autosomal recessive form of metaphyseal chondrodysplasia caused by RNA component of mitochondrial RNA processing endoribonuclease (RMRP) gene variants; however, its molecular etiology remains unclear. Whole‑exome sequencing was performed to detect possible pathogenic variants in a patient with a typical short stature and sparse hair. A co‑segregation analysis was also conducted and variants in the family members of the patient were confirmed by Sanger sequencing. A novel compound heterozygous variant in RMRP (NR_003051.4: n.‑21_‑2dup and n.197C>T) was identified in the affected patient. Data from 2 years and 4 months of follow‑up showed a positive effect of growth hormone (GH) therapy on height. Subsequently, two gene expression profiles associated with CHH were obtained from the EMBL‑EBI ENA and ArrayExpress databases. Differentially expressed genes between patients with CHH and healthy controls were selected using R software and were subjected to core analysis using ingenuity pathway analysis (IPA) software. IPA core analysis showed that the 'cell cycle checkpoints' was the most prominent canonical pathway, and the top enriched diseases and functions included various types of cancer, immunological diseases, development disorders and respiratory diseases. The integrative analysis displayed that RMRP can regulate the aberrant expression of downstream targets mainly via the transcription factor TP53, which results in the inhibition of 'cell cycle checkpoints'; eventually, functions associated with the CHH phenotype, such as 'growth failure or short stature' are activated. In conclusion, novel disease‑causing genetic variants of RMRP expand the genetic etiology of CHH, which must be clinically differentiated from achondroplasia. The findings of the present study provide new insights into the mechanisms underlying CHH.</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/PMC11800184/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143066782","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":"SIRT1 regulates cigarette smoke extract‑induced alveolar macrophage polarization and inflammation by inhibiting the TRAF6/NLRP3 signaling pathway.","authors":"Fang Yang, Huiping Qin, Chaoqun Qin, Bing Huang, Feng Gao, Yi Liao, Yanping Tang, Yanju Mo, Qianjie Yang, Changming Wang","doi":"10.3892/mmr.2024.13408","DOIUrl":"10.3892/mmr.2024.13408","url":null,"abstract":"<p><p>M1 macrophages activated by cigarette smoke extract (CSE) serve a pro‑inflammatory role in chronic obstructive pulmonary disease (COPD). The expression of silent information regulator 1 (SIRT1) is decreased in the alveolar macrophages of patients with COPD. However, whether SIRT1 is involved in COPD by regulating macrophage polarization remains unknown. Rat Alveolar Macrophage NR8383 cells were exposed to CSE. Cell Counting Kit‑8 assay, western blot assay and ELISA showed that with increasing concentration of CSE, the activity of NR8383 cells and expression of SIRT1 gradually decreased, while the release of inflammatory cytokines TNFα, IL‑1β and IL‑6 increased. As shown in western blot or Immunofluorescence assays, exposure to CSE also increased expression levels of the M1 markers inducible nitric oxide synthase and CD86, whereas it downregulated expression of the M2 markers arginase 1 and CD206. In addition, CSE increased expression of TNF receptor associated factor 6 (TRAF6), NOD‑like receptor thermal protein domain associated protein 3 (NLRP3) and cleaved caspase‑1 protein in NR8383 cells. Overexpression plasmids of SIRT1 and TRAF6 significantly reversed the aforementioned changes induced by CSE. Moreover, immunoprecipitation demonstrated that TRAF6 could bind to NLRP3. The overexpression of TRAF6 notably attenuated the regulatory effects of overexpression of SIRT1 on polarization and inflammation in NR8383 cells. Conversely, overexpression of SIRT1 inhibited the TRAF6/NLRP3 signaling pathway, thereby suppressing CSE‑induced M1 polarization and release of inflammatory factors in NR8383 cells. The present study demonstrates that SIRT1 regulates CSE‑induced alveolar macrophage polarization and inflammation by inhibiting the TRAF6/NLRP3 signaling pathway.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 2","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11632293/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142786233","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":"Tissue factor signalling modifies the expression and regulation of G1/S checkpoint regulators: Implications during injury and prolonged inflammation.","authors":"Sophie J Featherby, Eamon C Faulkner, Camille Ettelaie","doi":"10.3892/mmr.2024.13404","DOIUrl":"10.3892/mmr.2024.13404","url":null,"abstract":"<p><p>Tissue factor (TF) possesses additional physiological functions beyond initiating the coagulation cascade. Cellular signals initiated by cellular TF or on contact with TF‑containing microvesicles, contribute to wound healing through regulating a number of cellular properties and functions. TF regulates the cell cycle checkpoints, however the underlying signalling mechanisms have not been determined. Endothelial (human dermal blood endothelial cells and human umbilical vein endothelial cells) and epithelial [human telomerase reverse transcriptase‑human pancreatic nestin‑expressing ductal cells (hTERT‑HPNE) and AsPC‑1] cells were exposed to different concentrations of recombinant TF, and the influence on G1/S checkpoint regulators examined. Short‑term exposure to a lower concentration of TF promoted increased p16^INKa and decreased p21^CIP1/WAF1 expression, together with higher early region 2 binding factor (E2F) transcriptional activity and increased phosphorylation of Thr821/826 within retinoblastoma protein, leading to cell proliferation. The increase in p16^INKa expression was prevented following inhibition of β1‑integrin, or blocking the exosite within TF with AIIB2 and 10H10 antibodies, respectively. Exposure of cells to higher concentrations of TF induced disproportionate increases in p16^INKa and p21^CIP1/WAF1 expression, reduced retinoblastoma protein phosphorylation and E2F activity. Prolonged treatment of the immortalised hTERT‑HPNE cells with recombinant TF, resulted in significant downregulation of p16^INKa protein, which was partially due to reduced mRNA expression, together with increased E2F activity, and cyclin E mRNA expression. Although an increase in the methylation of the p16^INKa promoter was detected, the reduction in p16^INKa protein was concurrent with, and partly attributed to increased p14^ARF expression. TF appears early at the site of trauma, and its concentration is an ideal gauge for determining the extent of cellular damage, initiating clearance and repair. It is hypothesised that the balance of this signal is also dependent on the ability of cells to moderate the TF, and therefore on the level of damage. However, prolonged exposure of cells for example due to inflammation, leads to the dysregulation of the G1/S checkpoint by the tumour suppressors, leading to aberrant growth.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 2","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11626423/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142750987","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 II A stabilizes vulnerable plaques by suppressing RAGE signaling and NF‑κB activation in apolipoprotein‑E‑deficient mice.","authors":"Dong Zhao, Lufang Tong, Lixin Zhang, Hong Li, Yingxin Wan, Tiezhong Zhang","doi":"10.3892/mmr.2024.13410","DOIUrl":"10.3892/mmr.2024.13410","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 western blotting data shown in Fig. 4B on p. 4988 had already appeared in an article written by different authors at different research institutes that had already been published. In addition, it appeared as if some of the control β‑actin protein bands had been re‑used in Fig. 3 on p. 4987, comparing between Fig. 3A and C.  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 14: 4983‑4990, 2016; DOI: 10.3892/mmr.2016.5916].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 2","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11632302/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142786224","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 combination of serum lncRNA PTTG3P and mRNA PTTG1 serves as a diagnostic and prognostic marker for hepatocellular carcinoma.","authors":"Shunwang Cao, Fei Zhong, Xueying Chen, Sikai Ke, Xiangrong Zhong, Tingting Li, Yanhua Sha, Chunmin Kang, Sheng Qin, Hongmei Wang, Yi Wang, Shuzhi Liao, Peifeng Ke","doi":"10.3892/mmr.2024.13409","DOIUrl":"10.3892/mmr.2024.13409","url":null,"abstract":"<p><p>Long noncoding RNA (lncRNA) PTTG3P has been demonstrated to participate in the development of hepatocellular carcinoma (HCC) by targeting the mRNA PTTG1. The present study aimed to investigate the diagnostic efficacy of serum lncRNA PTTG3P, mRNA PTTG1 and their combination for the diagnosis and prognosis of HCC. A total of 373 participants were enrolled in the present study, including 73 patients with HCC, 100 patients with chronic hepatitis B (CHB), 100 patients with liver cirrhosis (LC) and 100 healthy controls (HCs). The expression levels of serum RNAs were quantified by reverse transcription‑quantitative PCR. The association between serum lncRNA PTTG3P and clinical characteristics was further analyzed. Receiver operating characteristic (ROC) curve and area under curve (AUC) analyses were performed to estimate the diagnostic ability of serum lncRNA PTTG3P, PTTG1 and their combinations with other biomarkers for HCC. The results revealed that the expression levels of lncRNA PTTG3P and mRNA PTTG1 were markedly increased in the serum of patients with HCC and CHB compared with in the serum of HCs. Additionally, the postoperative levels of lncRNA PTTG3P and mRNA PTTG1 were significantly lower than the preoperative concentrations in 36 paired patients with HCC. Spearman's correlation coefficient analysis showed that serum lncRNA PTTG3P was correlated with aspartate transaminase (AST). ROC analysis showed that both lncRNA PTTG3P and mRNA PTTG1 had a significant predictive value for HCC. The AUC values of lncRNA PTTG3P and mRNA PTTG1 alone were 0.636 and 0.634, respectively. Furthermore, combining lncRNA PTTG3P, mRNA PTTG1, α‑fetoprotein (AFP), alanine aminotransferase (ALT), AST, γ‑glutamyl transpeptidase (GGT) and alkaline phosphatase (ALP) significantly increased the AUC value. The best performance was the combination of PTTG3P, PTTG1, AFP, ALT, AST, GGT and ALP with an AUC of 0.959, a sensitivity of 90.4% and a specificity of 98.0%. In conclusion, the combination of serum lncRNA PTTG3P, mRNA PTTG1 and AFP appeared to be a noninvasive biomarker with comparatively high specificity and sensitivity for the diagnosis of HCC.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 2","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11632297/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142786249","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}