Cancer Genomics & Proteomics最新文献

{"title":"Knockdown of Derlin-1 Represses Cellular Oncogenic Activities in Uveal Melanoma, Enhances its Chemosensitivity to Cisplatin and Reduces Cancer Stem Cell Potential.","authors":"Ming-Yun Hsieh, Jiun-Rung Chen, Ping-Chung Tsai, Cheng-Yi Chen, An-Chi Liu, Hui-Ying Yeh, Wei-Ting Chen, Chang-Yi Wu, Sung-Chou Li","doi":"10.21873/cgp.20538","DOIUrl":"10.21873/cgp.20538","url":null,"abstract":"<p><strong>Background/aim: </strong>Uveal melanoma (UM) is the most common primary intraocular malignancy in adults, with a mean incidence of 5.1 cases per million people per year. At least 40% of uveal melanoma patients ultimately develop distant metastasis. But unlike cutaneous melanoma, targeted therapies and immune checkpoint blockers have shown limited effects. Investigating the metastasis-related pathogenesis mechanisms of uveal melanoma could facilitate the development of potential therapies.</p><p><strong>Materials and methods: </strong>For this purpose, we integrated microarray gene expression data (GSE22138) and an independent TCGA dataset to identify derlin-1 (DERL1) as our candidate gene. <i>In vitro</i> cellular assays were conducted to examine DERL1's role in the pathogenesis of uveal melanoma.</p><p><strong>Results: </strong>DERL1 up-regulation was identified in metastatic UM based on the microarray dataset, which was consistent with the TCGA dataset. However, the detailed mechanism has not yet been investigated. Therefore, we manipulated DERL1 expression with siRNA in a uveal melanoma cell line. After confirming the successful knockdown of DERL1, <i>in vitro</i> oncogenicity and chemosensitivity were assessed. Knockdown of DERL1 repressed cell proliferation and impaired cell migration and invasion. Furthermore, uveal melanoma cells with DERL1 knockdown had increased chemosensitivity to cisplatin and a decreased cancer stem cell potential determined by examining the intensity of CD133 and CD271.</p><p><strong>Conclusion: </strong>By analyzing GEO and TCGA datasets combined with <i>in vitro</i> cellular assays, DERL1 was found to be associated with metastasis in uveal melanoma and to be a possible target for further treatment.</p>","PeriodicalId":9516,"journal":{"name":"Cancer Genomics & Proteomics","volume":"22 5","pages":"809-823"},"PeriodicalIF":2.6,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12402717/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944145","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of <i>CXCL8, IL1A</i>, and <i>IL1B</i> as Hub Genes of Therapeutic Resistance in Glioblastoma Multiforme <i>via</i> Bioinformatics Analysis.","authors":"Sujin Lee, Jungwook Roh, Goeun Yoon, Jihoon Kang, Buhyun Youn, Wanyeon Kim","doi":"10.21873/cgp.20537","DOIUrl":"10.21873/cgp.20537","url":null,"abstract":"<p><strong>Background/aim: </strong>Glioblastoma multiforme (GBM) is a highly aggressive, treatment-resistant brain tumor with a dismal prognosis, and identifying key molecules involved in its therapeutic resistance is essential to improve patient outcomes. This study was undertaken to identify hub genes associated with the radioresistance and temozolomide (TMZ) resistance of GBM using bioinformatics analysis.</p><p><strong>Materials and methods: </strong>RNA-seq and microarray datasets from the GEO database were analyzed to identify differentially expressed genes (DEGs). GO and KEGG pathway enrichment analyses were performed using Enrichr. A protein-protein interaction (PPI) network was constructed using STRING and visualized with Cytoscape, and hub genes were identified by MCODE analysis. Expression and survival analyses were conducted on TCGA and GTEx datasets using GEPIA2.</p><p><strong>Results: </strong>Twenty-four DEGs were considered linked to radioresistance and 122 to TMZ resistance. Functional enrichment and PPI network analyses highlighted key therapeutic resistance pathways, including cytokine-mediated signaling and inflammatory response pathways. Notably, <i>CXCL8, IL1A</i>, and <i>IL1B</i> were identified as key hub genes significantly enriched in these pathways. Expression analysis confirmed their up-regulation in GBM, and survival analysis indicated their association with prognosis.</p><p><strong>Conclusion: </strong>This study identifies <i>CXCL8, IL1A</i>, and <i>IL1B</i> as potential therapeutic targets for overcoming the resistance of GBM to radiotherapy and chemotherapy. In addition, these genes might serve as prognostic biomarkers and key regulators of GBM malignancy. Future studies are warranted to explore their functional roles <i>in vivo</i> and assess their potential use as therapeutic intervention targets.</p>","PeriodicalId":9516,"journal":{"name":"Cancer Genomics & Proteomics","volume":"22 5","pages":"791-808"},"PeriodicalIF":2.6,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12402718/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944123","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Programmatically Efficient Separation of Immune Infiltrate and Tumor Gene Expression Overlap Potentials in a Big Data Setting: FASLG Gene Expression-related Survival Distinctions.","authors":"Elizabeth A Fletcher, Toriana R Dabkowski, Mallika Varkhedi, George Blanck","doi":"10.21873/cgp.20531","DOIUrl":"10.21873/cgp.20531","url":null,"abstract":"<p><strong>Background/aim: </strong>Typically expressed on T-cells and NK cells, FASLG induces apoptosis in target cells upon binding Fas. However, assessing potential FASLG expression in tumor cells with convenient genomics approaches has been challenging.</p><p><strong>Materials and methods: </strong>This study applied a novel assessment of FASLG copy numbers (CNs) and gene expression levels, applicable to bulk exome and RNAseq files.</p><p><strong>Results: </strong>Analyses indicated high FASLG CN associated with worse survival outcomes. Interestingly, higher FASLG gene expression was found to be associated with better survival outcomes, which led to a determination of whether this result was due to FASLG expression from tumor-infiltrating lymphocytes (TILs) instead of cancer cells demonstrating the higher CNs. In fact, T-cell markers CD4 and CD8A highly correlated with FASLG expression, consistent with the hypothesis that the high FASLG expression was associated with the TILs. Subsequent analyses confirmed that CN increases led to increased gene expression in the genomic region of the FASLG gene, particularly with an assessment of the expression of the neighboring PRRC2C gene. In sum, FASLG CN assessments, even independently of a corresponding gene expression correlation, may provide important characterizations of tumor cells.</p><p><strong>Conclusion: </strong>This study indicates that FASLG CN increases could represent a mechanism of tumor escape from TILs and a prognostic indicator; and tumor FASLG may be a suitable drug target for reducing tumor evasion of T-cells.</p>","PeriodicalId":9516,"journal":{"name":"Cancer Genomics & Proteomics","volume":"22 5","pages":"716-724"},"PeriodicalIF":2.6,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12402715/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944141","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LOC100506691 Is an Oncogenic Long Noncoding RNA that Promotes Growth and Motility of Lung Cancer Cells.","authors":"Yu-Hsuan Chen, Chih-Yun Yang, Pei-Jung Liu, Wan-Chung Hu, Kuo-Cheng Lu, Ching-Feng Cheng, Kuo-Wang Tsai","doi":"10.21873/cgp.20536","DOIUrl":"10.21873/cgp.20536","url":null,"abstract":"<p><strong>Background/aim: </strong>Lung cancer is the most prevalent type of cancer and the leading cause of cancer-related mortality worldwide. Understanding the detailed mechanisms of lung carcinogenesis can improve the survival rates of patients with lung cancer. Long noncoding RNAs (lncRNAs) are large (>200 nucleotides) noncoding RNAs that play a key role in various types of human cancer by regulating the proliferation, apoptosis, and metastasis of cancer cells. LOC100506691 is an oncogene that promotes the growth and metastasis of cancer cells. However, its biological role in lung cancer remains unknown.</p><p><strong>Materials and methods: </strong>The expression levels and clinical significance of LOC100506691 in lung cancer were analyzed using public databases. The biological function of LOC100506691 was investigated in lung cancer cell lines following siRNA-mediated knockdown, with assessments of cell proliferation, colony formation, motility, apoptosis, and cell cycle progression. Potential signaling pathways affected by LOC100506691 knockdown were examined through western blotting and pathway enrichment analysis.</p><p><strong>Results: </strong>According to public databases, the expression of LOC100506691 is significantly higher in lung cancer cells than in adjacent normal tissues. These high expression levels of LOC100506691 are strongly associated with poor survival outcomes in patients with lung cancer. Knockdown of LOC100506691 significantly suppresses the proliferation, colony formation ability, and metastasis of lung cancer cells. In lung cancer cells, LOC100506691 knockdown impairs the cell cycle progression and induces apoptosis by modulating the PI3K/AKT signaling pathway.</p><p><strong>Conclusion: </strong>Our findings indicate that LOC100506691 is a novel lncRNA that promotes the growth and metastasis of lung cancer cells and therefore provide valuable insights that can aid in the development of lung cancer therapy.</p>","PeriodicalId":9516,"journal":{"name":"Cancer Genomics & Proteomics","volume":"22 5","pages":"775-790"},"PeriodicalIF":2.6,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12402720/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944143","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Insights from Tissue Inhibitor of Metalloproteinase-2 Genotypes to Decipher the Genetic Architecture of Childhood Acute Lymphocytic Leukemia Risk.","authors":"Pei-Chen Hsu, Chung-Lin Tsai, Jen-Sheng Pei, Chao-Chun Chen, Huey-En Tzeng, Te-Chun Hsia, Yun-Chi Wang, Hou-Yu Shih, Chia-Wen Tsai, DA-Tian Bau, Wen-Shin Chang","doi":"10.21873/cgp.20532","DOIUrl":"10.21873/cgp.20532","url":null,"abstract":"<p><strong>Background/aim: </strong>Acute lymphoblastic leukemia (ALL) is the most common pediatric hematologic malignancy, particularly affecting children aged 2~5 years. Tissue inhibitor of metalloproteinase-2 (TIMP-2), a key regulator of MMP-2 activity, has been implicated in several cancers, yet its genetic role in childhood ALL remains unexplored.</p><p><strong>Materials and methods: </strong>This study investigated four <i>TIMP-2</i> polymorphic genotypes, rs8179090, rs4789936, rs2009196, and rs7342880, in 266 Taiwanese children with ALL and 266 matched controls using polymerase chain reaction-restriction fragment length polymorphism methodology.</p><p><strong>Results: </strong><i>TIMP-2</i> rs8179090 exhibited a significant association with ALL risk. Individuals with the CC genotype had a markedly increased risk [odds ratio (OR)=4.01, 95% confidence interval (CI)=1.46-11.04, <i>p</i>=0.0076], particularly under a recessive model (OR=3.79, 95%CI=1.39-10.36, <i>p</i>=0.0105). The C allele frequency was also elevated in cases (20.7%) <i>versus</i> controls (14.5%) (<i>p</i>=0.0100). Stratified analysis showed stronger risk association in children aged ≤3.5 years (CC genotype: OR=5.06, <i>p</i>=0.0084) and in boys (CC genotype: OR=5.53, <i>p</i>=0.0046). Moreover, CG+CC genotypes were associated with higher clinical risk classification (OR=2.25, <i>p</i>=0.0031) and shorter survival (<5 years) (OR=3.68, <i>p</i>=0.0003), though no correlation was found with immunophenotypic subtypes. No significant associations were identified for rs4789936, rs2009196, or rs7342880.</p><p><strong>Conclusion: </strong><i>TIMP-2</i> rs8179090, particularly the CC genotype, may serve as a novel biomarker for childhood ALL susceptibility and prognosis, especially in younger and male patients. Genotyping of this polymorphism could support early risk assessment and personalized clinical management in childhood ALL.</p>","PeriodicalId":9516,"journal":{"name":"Cancer Genomics & Proteomics","volume":"22 5","pages":"725-737"},"PeriodicalIF":2.6,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12402721/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944168","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gene Expression Insights into Cytarabine Resistance in Acute Myeloid Leukemia: The Role of Cytokines.","authors":"Chieh-Ming Lee, Yin-Hwa Shih, I-Chen Chen, Tzong-Ming Shieh, Chung-Yu Yeh, Yu-Hsin Tseng","doi":"10.21873/cgp.20533","DOIUrl":"10.21873/cgp.20533","url":null,"abstract":"<p><strong>Background/aim: </strong>Cytarabine is the main chemotherapy agent used to treat acute myeloid leukemia (AML), but drug resistance remains a major challenge. Imbalances in cytokine secretion are known to play a role in the survival and proliferation of AML blast cells. While numerous studies have investigated cytokine secretion in AML, the precise role of cytokines in the pathogenesis of AML remains unclear. This study aimed to compare cytokine-related gene expression in parental and resistant HL60 cells and assess their prognostic relevance in AML.</p><p><strong>Materials and methods: </strong>This study compared gene expression profiles of parental HL60 and R-HL60 cells by analyzing gene expression arrays. Further, the correlation between the differential expression genes (DEGs) and overall survival in patients with AML was obtained from the Cancer Genome Atlas (TCGA) database, and the expression of genes was validated by quantitative PCR (QPCR).</p><p><strong>Results: </strong>Our results showed that twenty-six genes involved in cytokine regulation were significantly different between HL60 and R-HL60 cells. The DEGs associated with cytokine production between parental HL60 and R-HL60 was subjected to a functional enrichment analysis by ShinyGO. The expression of <i>BCL3, OAS3, RELB, AIM2, NFKB2, CLEC9A</i>, and <i>OAS2</i> involved in the regulation of cytokine production was associated with survival probability of AML patient in the TCGA database. Among them, the expression of <i>BCL3, OAS3, RELB, AIM2</i>, and <i>NFKB2</i> genes in R-HL60 cells was higher than that in HL-60 cells.</p><p><strong>Conclusion: </strong>This study identified key genes involved in cytokine dysregulation in cytarabine-resistant HL60 cells, providing potential targets for overcoming drug resistance in AML. These findings offer new avenues for the development of more effective therapies for relapsed or refractory AML patients.</p>","PeriodicalId":9516,"journal":{"name":"Cancer Genomics & Proteomics","volume":"22 5","pages":"738-749"},"PeriodicalIF":2.6,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12402712/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944106","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High-Resolution aCGH Analysis of the Jurkat Cell Line: Copy Number Alterations and Their Association With Cancer Hallmarks.","authors":"Layssa Mota DA Costa, Wallax Augusto Silva Ferreira, Caio Bezerra Machado, Carolina Koury Nassar Amorim, Ana Virgínia VAN DEN Berg, Manoel Odorico DE Moraes Filho, Maria Elisabete Amaral DE Moraes, Lucas Eduardo Botelho DE Souza, André Salim Khayat, Edivaldo Herculano Correa DE Oliveira, Caroline Aquino Moreira-Nunes","doi":"10.21873/cgp.20539","DOIUrl":"10.21873/cgp.20539","url":null,"abstract":"<p><strong>Background/aim: </strong>Cell lines serve as valuable <i>in vitro</i> models to study altered cellular signaling pathways, to identify mutations in key oncogenic genes, and to test potential antitumor drugs. The Jurkat cell line, for example, has provided important information about various signaling pathways in lymphoblastic leukemia, establishing most of what is currently known about T-cell receptor (TCR) signaling. However, many aspects of the genome modification of this cell line have not yet been analyzed. To identify genes of potential biological and clinical relevance in acute T-lymphoblastic leukemia (T-ALL), we performed an array comparative genomic hybridization (aCGH) approach on the widely used Jurkat cell line and examined the association of the detected copy number alterations (CNAs) with cancer hallmarks and T-ALL pathogenesis.</p><p><strong>Materials and methods: </strong>Cells were harvested by using trypsin/EDTA from culture flasks to extract genomic DNA. aCGH experiments were performed on an Agilent microarray platform using the SurePrint G3 Cancer CGH + SNP Microarray 4×180 K. Functional enrichment analysis of all CNAs was performed with the R package g:Profiler2. The association of these alterations with key cancer hallmarks was analyzed using the Cancer Hallmarks web-tool.</p><p><strong>Results: </strong>Our analysis revealed several novel CNAs, including losses at 5p15.2, 6q27, 10q22.2, 14q11.2, 18q11.2-q12.1, and Xp22.33, as well as gains at 2p11.2, 7p21.2, 7q21.2 and 18p11.32. Genes within these regions were associated with important oncogenic pathways, including 'sustained proliferative signaling', 'tumor suppressor evasion', and 'angiogenesis promotion'.</p><p><strong>Conclusion: </strong>These findings suggest that Jurkat cells may serve as a valuable model for identifying new targets for cancer research. Further studies are required to confirm the phenotypic implications of these variants, which may open new avenues for exploring the functional impact of these alterations and their potential role in the development of therapies.</p>","PeriodicalId":9516,"journal":{"name":"Cancer Genomics & Proteomics","volume":"22 5","pages":"824-835"},"PeriodicalIF":2.6,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12402711/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944130","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of <i>FOXP3</i> rs3761548 With Cancer: Systematic Review and Two Approaches of X-chromosome Genotypic Meta-analysis.","authors":"Charoula Achilla, Lefteris Angelis, Theodosios Papavramidis, Angeliki Chorti, Anthoula Chatzikyriakidou","doi":"10.21873/cgp.20529","DOIUrl":"10.21873/cgp.20529","url":null,"abstract":"<p><strong>Background/aim: </strong>Cancer development involves complex interactions between immune mechanisms and the tumor microenvironment, with regulatory T cells (Tregs) being implicated in suppressing anti-tumor immunity. The X-linked gene Forkhead Box P3 (<i>FOXP3</i>), which regulates Tregs' function, and its promoter variant rs3761548 C>A have been widely studied for their role in tumorigenesis. This meta-analysis aims to re-evaluate the association between rs3761548 and cancer risk using two statistical approaches to account for sex-based genotypic differences and X-chromosome statistical challenges.</p><p><strong>Materials and methods: </strong>A systematic search of PubMed, Google Scholar, and Scopus identified seventeen eligible case-control studies, including 6719 cancer patients and 6879 healthy controls. The statistical analyses employed an X-linked Generalized Linear Regression Model (GLRM) and a sex-stratified meta-analysis calculating odds ratios with 95% confidence intervals.</p><p><strong>Results: </strong>The results indicated that the presence of the A allele increases cancer risk in White and Asian populations. Furthermore, the A allele and the AA genotype were associated with breast cancer in Asians, while the AC genotype appeared protective against acute lymphoblastic leukemia in Whites possibly through non-random X-chromosome inactivation. The GLRM proved more robust, identifying additional associations and accounting for risk factors.</p><p><strong>Conclusion: </strong>The present study suggests a new statistical approach for analyzing X-linked genotypic data. Additionally, it underscores that the <i>FOXP3</i> gene could be either oncogenic or tumor suppressor depending on ethnicity, cancer type and genotype distribution among the studied groups since its expression is subject to epigenetic changes related to the rs3761548 C allele.</p>","PeriodicalId":9516,"journal":{"name":"Cancer Genomics & Proteomics","volume":"22 5","pages":"683-697"},"PeriodicalIF":2.6,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12402714/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944125","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Analysis of Peroxisomal ABCD3 Transporter as a Prognostic Factor in Clear Cell Renal Cell Carcinoma.","authors":"Simone Heyliger, Tamiel N Turley, Tracoyia Roach, Marilyn D Saulsbury, Equar Taka, Jordan P Reynolds, John A Copland, Adam M Kase, R Renee Reams","doi":"10.21873/cgp.20530","DOIUrl":"10.21873/cgp.20530","url":null,"abstract":"<p><strong>Background/aim: </strong>Clear cell renal cell carcinoma (ccRCC) is among the 10 most common cancers diagnosed in the United States. Despite its severity and aggressive nature, biomarkers that can serve as prognostic and predictive factors for ccRCC are lacking. ABCD3, a peroxisomal long-chain fatty acid transporter, has been shown to serve as a prognostic factor in both prostate and colon cancers. Thus, this study aimed to ascertain if ABCD3, which is highly expressed in kidney tissues, may also serve as a biomarker for renal cancer.</p><p><strong>Materials and methods: </strong>Bioinformatics and immunohistochemical staining were employed to systematically investigate the relationship between the ABCD3 gene and protein expression, the immune microenvironment, and survival outcomes in ccRCC. We extensively harnessed data from publicly available databases, including The Cancer Genome Atlas (TGCA), UALCAN, Gene Set Cancer Analysis, UCSC Xena, and various other databases.</p><p><strong>Results: </strong><i>In silico</i> analyses of the TCGA database revealed that ABCD3 transcripts and protein levels were significantly reduced (<i>p</i><0.001) across all tumors and stages. Moreover, decreased ABCD3 expression was associated with poorer patient survival [hazard ratio=0.45 (0.33-0.61), <i>p</i><0.001]. Immunohistochemical and CPTAC database analyses revealed that ABCD3 was significantly downregulated in ccRCC patients (<i>p</i><0.05). Multivariate Cox regression analysis revealed that ABCD3 expression is an independent factor for overall survival [HR=0.4534 (0.2859-0.7189), <i>p</i><0.001].</p><p><strong>Conclusion: </strong>Our findings suggest that ABCD3 is a novel biomarker for ccRCC and that the downregulation of ABCD3 expression, and other members of the peroxisomal VLCFA oxidation pathway may represent a unique molecular feature of ccRCC.</p>","PeriodicalId":9516,"journal":{"name":"Cancer Genomics & Proteomics","volume":"22 5","pages":"698-715"},"PeriodicalIF":2.6,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12402713/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944133","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Serum Proteomic Signatures of Pregnancy-associated Breast Cancer.","authors":"Anna-Maria Korakiti, Eleni Zografos, Stavros C Proikakis, Alkistis-Maria Papatheodoridi, Kleoniki Apostolidou, Constantinos G Zografos, Dimitrios Maniatis, Christos Stefanou, Spyridon Marinopoulos, Constantine Dimitrakakis, Grigorios Xepapadakis, George T Tsangaris, Meletios-Athanasios Dimopoulos, Flora Zagouri","doi":"10.21873/cgp.20524","DOIUrl":"10.21873/cgp.20524","url":null,"abstract":"<p><strong>Background/aim: </strong>Pregnancy-associated breast cancer (PABC) is one of the most frequently diagnosed pregnancy-related malignancies, characterized by a notably rising incidence. Data remain scarce in the literature regarding the molecular nature and pathophysiology of PABC. Proteomic analyses are known to reflect cellular functions more accurately when compared to genomic or transcriptomic studies.</p><p><strong>Materials and methods: </strong>In the present study, two-dimensional gel electrophoresis and matrix-assisted laser desorption ionization time-of-flight mass spectrometry were employed to identify differentially expressed serum proteins among five patients with PABC, five matched (according to age, histological type and stage) non-pregnant patients diagnosed with BC, and five healthy pregnant controls.</p><p><strong>Results: </strong>A panel of 53 differentially expressed (>1.5-fold) proteins with diverse biological roles and various functional interactions was identified among the three groups examined in our study. Of the 53 differentially expressed proteins, 23 proteins were identified in the PABC group, 8 proteins in the non-PABC group, and 22 proteins in healthy pregnant controls. Many of the proteins differentially expressed in patients with PABC were involved in biological processes known to be deregulated in carcinogenesis, such as metabolism (<i>e.g</i>., apolipoprotein-E, and apolipoprotein-A1) and immune system regulation (<i>e.g</i>., complement factor B, and defensin-5).</p><p><strong>Conclusion: </strong>Differential proteomic expression was detected in PABC-derived serum samples, implying distinct PABC molecular features that require further investigation. The identification of PABC proteomic signatures provides significant insight into PABC pathophysiology and offers novel targets for early diagnosis and optimal treatment.</p>","PeriodicalId":9516,"journal":{"name":"Cancer Genomics & Proteomics","volume":"22 4","pages":"592-610"},"PeriodicalIF":2.6,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12216577/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144504907","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}