Biomolecules & biomedicine最新文献

{"title":"Silencing CACYBP suppresses lung adenocarcinoma growth via CDK1 inhibition.","authors":"Ge Wen, Shaoqing Niu, Shiqi Mei, Senming Wang","doi":"10.17305/bb.2025.11849","DOIUrl":"https://doi.org/10.17305/bb.2025.11849","url":null,"abstract":"<p><p>Calcyclin-binding protein (CACYBP) is a multidomain adaptor protein implicated in the development of various cancers. However, its molecular and biological roles in lung adenocarcinoma (LUAD) remain unclear. In this study, we aimed to elucidate the biological impact of CACYBP in LUAD. Immunohistochemistry was used to assess CACYBP expression in LUAD tissues. Lentivirus-mediated CACYBP knockdown was established in LUAD cell lines, and target gene expression was analyzed via Western blotting and qRT-PCR. Cell proliferation, apoptosis, and migration were evaluated using flow cytometry, colony formation assays, cell counting kit-8 (CCK 8) assays, Celigo cell counting, wound healing assays, Transwell assays, and mouse xenograft models. Co-immunoprecipitation was performed to verify the interaction between CACYBP and cyclin-dependent kinase 1 (CDK1). Additionally, the phosphoinositide 3-kinase (PI3K) inhibitor LY294002 was used to investigate the involvement of CDK1 in the PI3K/AKT pathway. Our findings revealed that CACYBP was upregulated in LUAD tissues and correlated with advanced disease stages and poor prognosis. CACYBP knockdown inhibited LUAD progression and metastasis, promoted cell apoptosis in vitro, and reduced tumorigenicity in vivo. Mechanistically, we identified CDK1 as a direct interacting partner of CACYBP. CDK1 overexpression enhanced the malignant phenotype of LUAD cells and partially reversed the inhibitory effects of CACYBP knockdown. Furthermore, inhibition of the PI3K/AKT pathway using LY294002 significantly suppressed CDK1-mediated LUAD cell growth. In conclusion, CACYBP appears to function as a tumor promoter in LUAD, at least in part through CDK1-mediated activation of the PI3K/AKT pathway. These findings suggest that CACYBP could serve as a promising therapeutic target and a novel biomarker for LUAD prognosis.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143756201","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recent advances in stem cell-based therapies for type 1 diabetes: A glimpse into the future.","authors":"Ahmed Hassanein, Saghir Akhtar","doi":"10.17305/bb.2025.12222","DOIUrl":"https://doi.org/10.17305/bb.2025.12222","url":null,"abstract":"<p><p>Type 1 diabetes mellitus (T1DM) is a serious, chronic metabolic and autoimmune disease that affects millions globally. While insulin administration remains the most effective treatment, it is not a cure. Long-term therapies, such as immunotherapy, can be effective for some patients, but they have notable limitations and do not provide a permanent solution. As a result, current research has shifted towards stem cell-based therapies, which offer a potentially expandable and scalable source of pancreatic beta cells. These therapies aim to restore long-term endogenous β-cell function in all T1DM patients, provided they can avoid immune recognition and rejection by the host. In this review, we will discuss the latest first-in-human successes of stem cell therapies for T1DM. We will then explore stem cell-derived islet encapsulation technologies and hypoimmune stem cells, examining how they might overcome the need for immunosuppressive therapy. Additionally, we will provide a summary of recent and ongoing biopharmaceutical industry pipelines and clinical trials for stem cell therapies aimed at treating T1DM. These advances suggest that stem cell therapies offer a promising and highly effective approach to treating patients with this chronic disease. However, large-scale clinical trials over the long term are necessary to verify these early successes and assess the curative potential of stem cell therapy for T1DM.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143675036","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adefovir anticancer potential: Network pharmacology, anti-proliferative & apoptotic effects in HeLa cells.","authors":"Muzammal Mateen Azhar, Tahir Maqbool, Fatima Ali, Awais Altaf, Muhammad Atif, Zulfiqar Ali, Zahid Habib Qureshi, Muhammad Naveed, Tariq Aziz, Rania Ali El Hadi Mohamed, Fakhria A Al-Joufi, Maher S Alwethaynani","doi":"10.17305/bb.2025.12058","DOIUrl":"https://doi.org/10.17305/bb.2025.12058","url":null,"abstract":"<p><p>Cervical cancer presents a significant healthcare challenge due to recurrent disease and drug resistance, highlighting the urgent need for novel therapeutic strategies. Network pharmacology facilitates drug repurposing by elucidating multi-target mechanisms of action. Adefovir, an acyclic nucleotide analog, has shown promising potential in cervical cancer treatment, particularly in HeLa cells. In vitro studies have demonstrated that adefovir inhibits HeLa cell proliferation by enhancing apoptosis while maintaining a low cytotoxicity profile at therapeutic concentrations, making it an attractive candidate for further exploration. A combined network pharmacology and in vitro study was conducted to investigate the molecular mechanism of adefovir against cervical cancer. Potential gene targets for adefovir and cervical cancer were predicted using database analysis. Hub targets were identified, and protein-protein interaction (PPI) networks were constructed. Molecular docking assessed adefovir's binding affinity to key targets. In vitro cytotoxic assays, including 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and crystal violet assays, were performed using 96-well plates to evaluate anti-proliferative effects in HeLa cells. Apoptosis was assessed via p53 immunocytochemistry Enzyme-Linked Immunosorbent Assay (ELISA), while Vascular Endothelial Growth Factor ELISA (VEGF ELISA) was used to measure cell proliferation. Venn analysis identified 144 common targets between adefovir and cervical cancer. Network analysis revealed key hub targets involved in oncogenic pathways. Molecular docking demonstrated strong binding between adefovir and Mitogen-Activated Protein Kinase 3 (MAPK3) and SRC proteins. In vitro, adefovir significantly suppressed HeLa cell viability, with an Inhibitory Concentration 50 (IC50) of 7.8 μM, outperforming 5-Fluorouracil (5-FU). Additionally, it induced apoptosis via p53 activation and inhibited cell proliferation through VEGF suppression. These integrated computational and experimental findings suggest that adefovir exerts multi-targeted effects against cervical cancer. Its promising preclinical efficacy warrants further investigation as a potential alternative therapy.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143659794","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular aspects of Angelman Syndrome: Defining the new path forward.","authors":"Jacqueline Fátima Martins de Almeida, Ilaria Tonazzini, Simona Daniele","doi":"10.17305/bb.2025.11724","DOIUrl":"https://doi.org/10.17305/bb.2025.11724","url":null,"abstract":"<p><p>As a rare neuro-genetic disease, Angelman syndrome (AS) affects about 15 to 500 thousand people worldwide. The AS is an imprinting genomic disease characterized by the loss of function of the maternal UBE3A gene, located in the 15q11-q13. This gene encodes a ~100 kDa protein, the Ubiquitin-protein ligase E3A (UBE3A), that participates in the ubiquitination process, one of the post-translational protein modifications. In the brain, under normal conditions, the paternal allele of the UBE3A gene is silenced, with only the maternal allele being active. However, in individuals with AS, the maternal loss of function of this gene leads to the complete absence of UBE3A expression, resulting in multiple pathological features. Clinically, children diagnosed with AS exhibit a characteristic behavioral phenotype, including a happy demeanor, frequent and unmotivated laughter, movement, speech impairment, severe intellectual disability, and sleep problems. Since its discovery in 1965, significant progress has been made in understanding the genetic and pathophysiological aspects of AS. However, despite these advances, the molecular mechanisms underlying the disease remain incompletely understood, and no effective treatment currently exists. Current therapies focus solely on symptom management, and no approach has yet succeeded in reactivating the silenced paternal UBE3A allele. Therefore, this review highlights the epigenetic aspects involved in the AS in order to provide a better understanding and clarification of the mechanisms, hopefully paving the way for future research to improve the treatment of affected individuals.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143733429","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A deep learning model based on chest CT to predict benign and malignant breast masses and axillary lymph node metastasis.","authors":"Jingxiang Sun, Xiaoming Xi, Mengying Wang, Menghan Liu, Xiaodong Zhang, Haiyan Qiu, Youxin Zhang, Taian Fu, Yanan Du, Wanqing Ren, Dawei Wang, Guang Zhang","doi":"10.17305/bb.2025.12010","DOIUrl":"https://doi.org/10.17305/bb.2025.12010","url":null,"abstract":"<p><p>Differentiating early-stage breast cancer from benign breast masses is crucial for radiologists. Additionally, accurately assessing axillary lymph node metastasis (ALNM) plays a significant role in clinical management and prognosis for breast cancer patients. Chest computed tomography (CT) is a commonly used imaging modality in physical and preoperative evaluations. This study aims to develop a deep learning model based on chest CT imaging to improve the preliminary assessment of breast lesions, potentially reducing the need for costly follow-up procedures such as magnetic resonance imaging (MRI) or positron emission tomography-CT and alleviating the financial and emotional burden on patients. We retrospectively collected chest CT images from 482 patients with breast masses, classifying them as benign (n = 224) or malignant (n = 258) based on pathological findings. The malignant group was further categorized into ALNM-positive (n = 91) and ALNM-negative (n = 167) subgroups. Patients were randomly divided into training, validation, and test sets in an 8:1:1 ratio, with the test set excluded from model development. All patients underwent non-contrast chest CT before surgery. After preprocessing the images through cropping, scaling, and standardization, we applied ResNet-34, ResNet-50, and ResNet-101 architectures to differentiate between benign and malignant masses and to assess ALNM. Model performance was evaluated using sensitivity, specificity, accuracy, receiver operating characteristic (ROC) curves, and the area under the curve (AUC). The ResNet models effectively distinguished benign from malignant masses, with ResNet-101 achieving the highest performance (AUC: 0.964; 95% CI: 0.948-0.981). It also demonstrated excellent predictive capability for ALNM (AUC: 0.951; 95% CI: 0.926-0.975). In conclusion, these deep learning models show strong diagnostic potential for both breast mass classification and ALNM prediction, offering a valuable tool for improving clinical decision-making.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143659790","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The influence of sodium-glucose co-transporter-2 inhibitors on the risk of cancer therapy-related cardiac dysfunction: A meta-analysis.","authors":"Zhitao Yan, Xiaona Xing, Jinmei Huang","doi":"10.17305/bb.2025.11847","DOIUrl":"https://doi.org/10.17305/bb.2025.11847","url":null,"abstract":"<p><p>Cancer therapy-related cardiac dysfunction (CTRCD) is a major concern for patients undergoing cardiotoxic cancer treatments. Sodium-glucose co-transporter-2 (SGLT2) inhibitors have shown cardioprotective effects in both diabetic and non-diabetic populations. However, their impact on CTRCD risk remains uncertain. This meta-analysis aimed to assess the association between SGLT2 inhibitor use and CTRCD in cancer patients receiving cardiotoxic treatments. A systematic search of PubMed, Embase, and Web of Science was conducted to identify relevant studies. Cohort studies comparing CTRCD incidence in cancer patients with and without SGLT2 inhibitor use were included. Risk ratios (RRs) were pooled using a random-effects model, and subgroup and meta-regression analyses were performed to explore potential effect modifiers. Ten cohort studies involving 34,847 cancer patients met the inclusion criteria. Overall, SGLT2 inhibitor use was associated with a significantly reduced risk of CTRCD (RR: 0.47, 95% confidence interval: 0.33-0.68, P < 0.001), though significant heterogeneity was observed (I² = 70%). Subgroup analysis indicated a stronger protective effect in patients receiving anthracyclines (RR: 0.26) compared to those undergoing other treatments (RR: 0.73, P for subgroup difference = 0.001). Additionally, the cardioprotective effect was more pronounced in cohorts with a lower proportion of men (<55%, RR: 0.27) compared to those with a higher proportion (≥55%, RR: 0.75, P < 0.001). Sensitivity analyses, conducted by excluding one study at a time, consistently supported these findings, reinforcing their robustness. In conclusion, SGLT2 inhibitor use is associated with a lower risk of CTRCD in cancer patients, particularly those receiving anthracyclines. These findings highlight the potential role of SGLT2 inhibitors in mitigating cardiotoxicity during cancer therapy.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143617681","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Invasive pulmonary aspergillosis evaluation in hematology patients: Three years results of tertiary hospital.","authors":"Mine Aydın Kurc, Betül Günaydın, Seval Akpınar, Birol Safak, Nuri Kiraz","doi":"10.17305/bb.2024.10766","DOIUrl":"10.17305/bb.2024.10766","url":null,"abstract":"<p><p>Invasive pulmonary aspergillosis (IPA) is the most frequent invasive fungal disease occurring in patients with hematological malignancies. Serum galactomannan (GM) antigen monitoring is thought to be helpful in the diagnosis of IPA. The aim of this study was to determine the role of a GM assay in serum samples for the diagnosis of IPA in patients with hematological disease. The data of 366 immunosuppressed patients that were hospitalized and followed up in the hematology clinic from January 2017 to December 2019 were retrospectively analyzed. The clinical and radiological findings of the patients and the GM results, requested twice a week, were evaluated. In this study, the incidence of probable and possible IPA was determined to be 15.3% (56/366). Of the cases detected, 28 (50.0%) were patients diagnosed with acute myeloid leukemia (AML), and 34 (60.7%) patients who had compatible clinical and examination findings were started on antifungal treatment. Additionally, area under the curve (AUC) values were calculated by receiver operating characteristic (ROC) analysis, and it was determined that the diagnostic efficiency was more predictive when the cut-off was 0.5 in the GM test for IPA disease. The detection of GM antigen in serum is a very useful and rapid method for diagnosing IPA disease in immunosuppressed hematology patients. However, GM results should be evaluated together with clinical and radiological findings for early diagnosis, and the treatment approach should be determined accordingly.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"850-856"},"PeriodicalIF":0.0,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11959390/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141735837","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Total glucosides of paeony inhibit NLRP3/caspase-1/GSDMD-mediated inflammation and pyroptosis in C3H/HeJ mice with alopecia areata.","authors":"Jingfang Zhang, Zhiquan Li, Kunpeng Liu, Xueyuan Du, Tao Yao, Jianzhou Ye","doi":"10.17305/bb.2024.10907","DOIUrl":"10.17305/bb.2024.10907","url":null,"abstract":"<p><p>One of the most prominent causes of alopecia areata (AA) is chronic inflammation of the hair follicles. Inhibiting cellular pyroptosis, a form of inflammatory programmed cell death, is crucial for reducing follicular inflammation in the skin. Total glucosides of paeony (TGP) possess anti-inflammatory properties across a broad range of illnesses. However, the role of TGP in AA and its relationship to pyroptosis remain unclear. A chronic unpredictable mild stress (CUMS) approach was used to create an AA mouse model. TGP suspension and MCC950 were administered to AA mice via gavage. HE staining, ELISA, immunohistochemistry, immunofluorescence, RT-qPCR, and Western blotting were performed to detect pathological changes in the skin and investigate the levels of inflammatory factors and pyroptosis-related proteins, as well as the potential mechanisms of TGP's effects. TGP reduced hair loss, increased the number of hair follicles in skin tissues, and decreased inflammatory markers (IL-6, TNF-α, IL-18, and IL-1β) in AA mice. MCC950 significantly reduced the levels of NLRP3/caspase-1/Gasdermin D (GSDMD)-mediated pyroptosis-related proteins (NLRP3, ASC, caspase-1 p10, and GSDMD-N), as well as inflammatory factors. TGP markedly inhibited NLRP3/caspase-1/GSDMD-mediated cellular pyroptosis in a concentration-dependent manner. TGP suppresses the NLRP3/caspase-1/GSDMD signaling cascade in the skin tissues of AA mice, thereby reducing cellular pyroptosis and inflammation. TGP may be a potential therapeutic agent for AA.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"954-964"},"PeriodicalIF":0.0,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11959395/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142333653","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Screening and validating genes associated with cuproptosis in systemic lupus erythematosus by expression profiling combined with machine learning.","authors":"Zhongbin Xia, Ruoying Cheng, Qi Liu, Yuxin Zu, Shilu Liao","doi":"10.17305/bb.2024.10996","DOIUrl":"10.17305/bb.2024.10996","url":null,"abstract":"<p><p>Cell death has long been a focal point in life sciences research, and recently, scientists have discovered a novel form of cell death induced by copper, termed cuproptosis. This paper aimed to identify genes associated with cuproptosis in systemic lupus erythematosus (SLE) through machine learning, combined with single-cell RNA sequencing (scRNA-seq), to screen and validate related genes. The analytical results were then experimentally verified. Two published microarray gene expression datasets (GSE65391 and GSE61635) from SLE and control peripheral blood samples were downloaded from the GEO database. The GSE65391 dataset was used as the training group, while the GSE61635 dataset served as the validation group. Differentially expressed genes from GSE65391 identified 12 differential genes. Nine diagnostic genes, considered potential biomarkers, were selected using the least absolute shrinkage and selection operator and support vector machine recursive feature elimination analysis. The receiver operating characteristic (ROC) curves for both the training and validation groups were used to calculate the area under the curve to assess discriminatory properties. CIBERSORT was used to assess the relationship between these diagnostic genes and a reference set of infiltrating immune cells. scRNA-seq data (GSE162577) from SLE patients were also obtained from the GEO database and analyzed. Experimental validation of the most important SLE biomarkers was performed. Twelve significantly different cuproptosis-related genes were identified in the GSE65391 training set. Immune cell analysis revealed 12 immune cell types and identified nine signature genes, including PDHB, glutaminase (GLS), DLAT, LIAS, MTF1, DLST, DLD, LIPT1, and FDX1. In the GSE61635 validation set, seven genes were weakly expressed, and two genes were strongly expressed in the treatment group. According to the ROC curves, PDHB and GLS demonstrated significant diagnostic value. Additionally, correlation analysis was conducted on the nine characteristic genes in relation to immune infiltration. The distribution of key genes in immune cells was determined using scRNA-seq data. Finally, the mRNA expression of the nine diagnostic genes was validated using qPCR.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"965-975"},"PeriodicalIF":0.0,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11959400/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142402195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bioinformatics analysis and experimental validation of <i>C6orf120</i> as a potential prognostic marker and therapeutic target for liver hepatocellular carcinoma.","authors":"Yingying Lin, Xin Wang, Yanyan Li, Xinyu Cui, Na Zhu, Xin Li","doi":"10.17305/bb.2024.11246","DOIUrl":"10.17305/bb.2024.11246","url":null,"abstract":"<p><p>The C6orf120 gene is a novel gene whose function has not been fully defined. Previous studies have associated it with various liver pathologies, but its specific role in hepatocellular carcinoma (LIHC) remains unclear. This study aimed to investigate the diagnostic and prognostic value of C6orf120 in LIHC, as well as its potential biological functions. In this preliminary research, we utilized data from various databases and bioinformatics tools, including TCGA, GEO, TIMER2, HPA, GEPIA, Linkeomics, Metascape, CIBERSORT, TargetScan, DIANA-microT, RNAinter, and ENCORI, to analyze the expression patterns and mechanisms of C6orf120 in LIHC. Our bioinformatics analysis revealed that C6orf120 is upregulated in LIHC and may serve as a diagnostic and prognostic biomarker. The aberrant expression of C6orf120 in LIHC was further supported by clinical samples and cell lines. In vitro experiments demonstrated that the knockdown of C6orf120 in HepG2 cells significantly reduced migration capacity without affecting proliferation. Additionally, the downregulation of C6orf120 in LIHC cells appeared to inhibit endothelial cell migration and angiogenesis, which are critical in tumorigenesis and development. In conclusion, our findings suggest that C6orf120 could serve as a novel diagnostic and prognostic biomarker for LIHC and is expected to be a prognostic marker and a potential therapeutic target in the clinical management of LIHC.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"925-939"},"PeriodicalIF":0.0,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11959399/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142402172","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}