Cancer Genomics & Proteomics最新文献

{"title":"Multi-level Transcriptomic and Machine-learning Analyses Identify <i>MZT1</i> as a Proliferation-associated Prognostic Marker in Lung Adenocarcinoma.","authors":"Dahlak Daniel Solomon, Hui-Ru Lin, Yung-Kuo Lee, Sachin Kumar, Ching-Chung Ko, Kai-Fu Chang, Chung-Hsien Lin, Ngoc Uyen Nhi Nguyen, DO Thi Minh Xuan, Neethu Palekkode, Chih-Yang Wang, Yun-Shih Lin","doi":"10.21873/cgp.20613","DOIUrl":"10.21873/cgp.20613","url":null,"abstract":"<p><strong>Background/aim: </strong>Lung adenocarcinoma (LUAD) exhibits substantial molecular heterogeneity and variable clinical outcomes, highlighting the need for biomarkers that reflect core tumor biological processes. Centrosome-associated proteins regulate mitotic fidelity and genome stability, yet their roles in LUAD remain incompletely defined. In this study, we systematically characterized mitotic spindle organizing protein 1 (<i>MOZART1</i>; <i>MZT1</i>) and related family members in LUAD.</p><p><strong>Materials and methods: </strong>We performed integrated analyses combining bulk transcriptomic datasets, survival modeling, gene set enrichment, immune deconvolution, machine-learning based prognostic modeling, and single-cell RNA sequencing. Expression patterns and clinical associations of <i>MZT</i> family genes were evaluated across pan-cancer and LUAD cohorts.</p><p><strong>Results: </strong><i>MZT</i> family genes were consistently upregulated in tumor tissues, with <i>MZT1</i> showing the most robust expression pattern. Elevated <i>MZT1</i> expression was significantly associated with reduced overall survival. Functional analyses revealed coordinated activation of proliferative and genome maintenance pathways, including G₂/M checkpoint regulation, E2F and MYC signaling, and DNA repair. A multivariable analysis indicated that the prognostic association of <i>MZT1</i> was reduced after adjusting for canonical proliferation markers, suggesting partial overlap with established proliferation signals. The LASSO-based Cox model demonstrated stable time-dependent predictive performance at 1-, 3-, and 5-year survival. Immune analyses indicated associations between <i>MZT1</i> expression and tumor microenvironmental features. Single-cell analysis showed that <i>MZT1</i> expression was predominantly enriched in malignant epithelial cells and associated with proliferative cellular states. Protein-level validation supported concordance with transcriptomic findings.</p><p><strong>Conclusion: </strong><i>MZT1</i> is a proliferation-associated marker that integrates clinical risk, transcriptional programs, cellular heterogeneity, and predictive modeling in LUAD, providing a potential framework for biomarker development and risk stratification.</p>","PeriodicalId":9516,"journal":{"name":"Cancer Genomics & Proteomics","volume":"23 5","pages":"996-1020"},"PeriodicalIF":2.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13531167/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863295","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":"CTGF/CCN2 Promotes Invasive Growth in Cervical Cancer Spheroids and Is Associated With Metastatic Cervical Cancer Tissue.","authors":"Linda VON DER Brelie, Nesibe Gökçe Kalyoncu, Julia Gallwas, Carsten Gründker","doi":"10.21873/cgp.20609","DOIUrl":"10.21873/cgp.20609","url":null,"abstract":"<p><strong>Background/aim: </strong>Metastatic spread defines the lethality of cervical cancer (CC). Connective tissue growth factor (CTGF/CCN2) regulates cell- extracellular matrix interactions but its role in CC is not well-defined. This study investigates the role of CTGF in driving CC invasive growth and its prevalence in patient tissues.</p><p><strong>Materials and methods: </strong>CC spheroids (C33A, HT3) were treated with recombinant human CTGF (rhCTGF) or a function-blocking antibody (IgG CTGF). Invasive growth was assessed via 3D spheroid assay using a Celigo imaging cytometer. Cancer stem cell (CD133, CD44) and epithelial-mesenchymal transition (EMT) markers (E-cadherin, N-cadherin) were analyzed by immunofluorescence. CTGF expression was evaluated using a tissue microarray containing 69 cases in triplicate from pre-invasive, invasive (FIGO I-III), and metastatic cervical lesions, quantified via immunofluorescence scoring.</p><p><strong>Results: </strong>Functional blockade of CTGF significantly reduced 3D spheroid invasive growth in C33A and HT3 cells (<i>p</i><0.0001). Immunofluorescence revealed that CTGF modulation altered spatial distribution of key proteins: rhCTGF induced surface clustering of CD133 and peripheral N-cadherin enrichment, while CTGF blockade was associated with apparent nuclear/perinuclear enrichment of CD133 and E-cadherin and reduced N-cadherin signal. In patient tissue cores, metastatic samples exhibited the highest CTGF fluorescence intensity. High CTGF expression [immunoreactivity score (IRS) ≥ 6] was most prevalent in FIGO stage I (35.5%) compared to stage III (10.0%). Kaplan-Meier analysis revealed that high CTGF mRNA expression was associated with significantly reduced recurrence-free survival (log-rank <i>p</i>=0.0032).</p><p><strong>Conclusion: </strong>In 3D models of CC, CTGF appears to regulate an invasive phenotype, presumably by controlling aberrant localization of stemness and EMT markers. Its apparently elevated expression in early-stage cervical carcinomas and metastases, combined with its prognostic value for recurrence-free survival, suggests that CTGF may be involved in triggering the potential for metastasis and could therefore serve as an early prognostic biomarker.</p>","PeriodicalId":9516,"journal":{"name":"Cancer Genomics & Proteomics","volume":"23 5","pages":"934-947"},"PeriodicalIF":2.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13531173/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863098","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":"Integrative Cross-platform Analysis of Kinase Inhibitor Effects on Statin-relevant Cardioprotective Pathways in Human Cardiomyocytes.","authors":"Tai-Yu Kuo, Min-Chi Cheng, Hong-Jie Jhou, Cho-Hao Lee, Po-Huang Chen","doi":"10.21873/cgp.20612","DOIUrl":"10.21873/cgp.20612","url":null,"abstract":"<p><strong>Background/aim: </strong>Kinase inhibitors (KIs) can cause cardiotoxicity through mechanisms overlapping with statin cardioprotective pathways, yet their effects on these pathways in cardiomyocytes remain uncertain. We evaluated six literature-defined statin-relevant gene sets using transcriptomic and proteomic data.</p><p><strong>Materials and methods: </strong>Pre-ranked gene set enrichment analysis was performed for 23 KIs in primary cardiac cells (GSE146096; <i>n</i>=319) and iPSC-derived cardiomyocytes (GSE217421; <i>n</i>=541), with cross-platform analysis of 21 KIs by shotgun proteomics (PXD014791; <i>n</i>=300). Pathway-specific concordance was assessed by Spearman correlation with Benjamini-Hochberg correction; protein scores were estimated after adjustment for cell line.</p><p><strong>Results: </strong>KI effects were heterogeneous. The anti-fibrotic pathway showed nominal concordance across the two transcriptomic datasets (ρ=0.495, <i>p</i>=0.016, q=0.098; 91% direction concordance) and significant cell-line-adjusted transcriptomic-proteomic concordance (ρ=0.644, <i>p</i>=0.0016, q=0.0081). Nilotinib reproducibly upregulated NF-κB pathway genes [normalized enrichment score (NES)=+2.29 and +2.18 in discovery and validation], with targeted inter-gene-correlation-adjusted testing supporting higher NF-κB expression than under rosuvastatin (CAMERA <i>p</i>=3.54×10^-8). No global cross-omics summary remained significant after harmonizing pathway universes and accounting for repeated pathways.</p><p><strong>Conclusion: </strong>KI effects on statin-relevant pathways were pathway-specific. Anti-fibrotic concordance and nilotinib-associated NF-κB upregulation are hypothesis-generating candidates for experimental validation.</p>","PeriodicalId":9516,"journal":{"name":"Cancer Genomics & Proteomics","volume":"23 5","pages":"982-995"},"PeriodicalIF":2.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13531158/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863257","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":"ERP44 Is Associated With Poor Prognosis and Promotes Proliferation and Temozolomide Resistance in Lower-grade Glioma.","authors":"Lingmin Shao, Jia Liu, Mohammad Rohul Amin, Zhihong Jian","doi":"10.21873/cgp.20608","DOIUrl":"10.21873/cgp.20608","url":null,"abstract":"<p><strong>Background/aim: </strong>Endoplasmic reticulum resident protein 44 (ERP44), a protein disulfide isomerase family member, has been implicated in tumor biology, but its role in lower-grade glioma (LGG) remains unclear. This study investigated the prognostic significance and biological function of ERP44 in LGG, focusing on proliferation and temozolomide (TMZ) resistance.</p><p><strong>Materials and methods: </strong>ERP44 expression, clinicopathological associations, and prognostic value were analyzed using The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression (GTEx), and Chinese Glioma Genome Atlas (CGGA) datasets. Time-dependent receiver operating characteristic (ROC) curves, Cox regression, and a prognostic nomogram were constructed. Differential expression, Gene Set Enrichment Analysis (GSEA), Gene Ontology (GO) enrichment, immune infiltration, and drug sensitivity analyses were performed. Functional validation was conducted in SW1088 and SW1783 cells using shRNA-mediated ERP44 knockdown, followed by RT-qPCR, western blotting, CCK-8, colony formation, and TMZ IC₅₀ assays. Subcutaneous xenograft models with or without TMZ treatment were used for <i>in vivo</i> validation.</p><p><strong>Results: </strong>ERP44 was markedly upregulated in LGG and associated with higher WHO grade, IDH wildtype status, 1p/19q non-codeletion, and poor survival in TCGA and CGGA cohorts. ERP44 showed strong prognostic performance and improved risk stratification in a multivariable nomogram. Enrichment analyses linked high ERP44 expression to immune/inflammatory pathways and reduced neuronal functional signatures. ERP44 positively correlated with immune infiltration, proliferation/stemness markers, and predicted TMZ resistance, while its knockdown inhibited proliferation and colony formation, reduced TMZ IC₅₀, suppressed xenograft growth, enhanced TMZ efficacy, and decreased Ki67 positivity.</p><p><strong>Conclusion: </strong>ERP44 is a prognostic biomarker that promotes LGG proliferation and TMZ resistance, suggesting its potential as a therapeutic target.</p>","PeriodicalId":9516,"journal":{"name":"Cancer Genomics & Proteomics","volume":"23 5","pages":"914-933"},"PeriodicalIF":2.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13531103/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863219","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":"Tumor Mutational Landscape and Its Correlation With Histopathological Characteristics in Breast Cancer.","authors":"Eirini Papadopoulou, Maroulio Stathoulopoulou, Maria Matiatou, Panagiotis Karathanasis, Xenofon Xenakis, Grigorios Pesmatzoglou, Ioannis Fyssas, Konstantinos Louis, Dimitrios Maniatis, Anastasia Ekmektzoglou, Dimitrios Alexandrou, Christos Kalivopoulos, Christos Kanistras, Nikolaos Katsiakis, Ioanna Konstantiadou, Christos Kavazis, Athanasios Kokolakis, Nikolaos Papaioannou, Anna Sachoulidou, Eleftherios Sfakianakis, Sofia Triantafyllidou, Sofia Filippidou, Christos Damaskos, George Lazaridis, Filippos Koinis, Eirini Biziota, Angelos Koutras, Aikaterini Kotsori, Vassileios Venizelos","doi":"10.21873/cgp.20616","DOIUrl":"10.21873/cgp.20616","url":null,"abstract":"<p><strong>Background/aim: </strong>In breast cancer, knowledge of the associations between clinicopathologic characteristics, genetic changes, and subtype-specific patterns is expanding. This study investigated how pathological and clinical variables affect the actionability of Next Generation Sequencing (NGS)-based tumor molecular data.</p><p><strong>Materials and methods: </strong>227 breast cancer patients referred to Genekor's laboratory for tumor molecular profile analysis were included in the study. Pathology records were used to assess critical clinicopathological features, including HER2, ER, PR, Ki67, grade, metastatic site, and age. A 1021-gene NGS-based multigene panel was utilized to assess tumor biology alongside tumor mutational burden (TMB) and microsatellite instability (MSI).</p><p><strong>Results: </strong>Comprehensive genomic profiling revealed that 95.6% of the patients harbored at least one oncogenic or likely oncogenic alteration, highlighting the high diagnostic yield of NGS-based testing. Distinct subtype-specific patterns were observed: HR+/HER2- tumors were enriched for <i>PIK3CA</i> and <i>ESR1</i> gene alterations, whereas triple-negative breast cancer (TNBC) was dominated by <i>TP53</i> alterations. Clinically actionable alterations were most common in HR+/HER2- tumors (~60% on-label), whereas TNBC more often harbored off-label or trial-associated targets. The inclusion of tumor-agnostic biomarkers (TMB/MSI) increased on-label actionability up to 64.5% in HR+/HER2- tumors, primarily driven by TMB-high cases. Median TMB values were low, and age was the only independent predictor. Furthermore, the presence of actionable alterations was significantly higher in metastatic tumors, and <i>TP53</i> alterations were associated with aggressive tumor characteristics.</p><p><strong>Conclusion: </strong>Comprehensive NGS-based genomic profiling identifies clinically actionable alterations in over half of breast cancer patients, with substantial variability across molecular subtypes. The HR+/HER2- subtype demonstrates the highest prevalence of on-label actionable biomarkers. These findings support the routine implementation of comprehensive genomic profiling, especially in metastatic HER2-negative breast cancer, to guide precision oncology strategies and enable enrollment in biomarker-driven clinical trials.</p>","PeriodicalId":9516,"journal":{"name":"Cancer Genomics & Proteomics","volume":"23 5","pages":"1061-1081"},"PeriodicalIF":2.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13531161/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863593","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":"Integrated Immunotherapy Target Atlas for Ewing Sarcoma.","authors":"Corey Goldman","doi":"10.21873/cgp.20605","DOIUrl":"10.21873/cgp.20605","url":null,"abstract":"<p><strong>Background/aim: </strong>Ewing sarcoma is a fusion-driven malignancy with low tumor mutational burden, making recurrent tumor-associated antigens with favorable tumor-to-normal contrast central to immunotherapy development. We converted the Deng <i>et al.</i>-defined 32-gene Ewing Sarcoma Specific Signature (ESS32) into a practical target atlas by integrating tumor RNA expression with normal-tissue context, protein evidence, subcellular localization, and therapeutic accessibility.</p><p><strong>Materials and methods: </strong>A 38-gene set was analyzed, including ESS32 and six comparator antigens (STEAP1, LINGO1, PRAME, CD99, CD276/B7-H3, and ENPP1). Eight Gene Expression Omnibus datasets (<i>n</i>=854 samples) were assigned predefined roles spanning tumor-<i>versus</i>-skeletal-muscle comparison, broad normal-organ context, EWSR1::FLI1 perturbation, tumor-only support cohorts, cell-line models, and cross-sarcoma comparison. Results were overlaid with Human Protein Atlas and published proteomic/surfaceome evidence.</p><p><strong>Results: </strong>In GSE17674, the strongest tumor-enriched transcripts included NKX2-2, NPY1R, STEAP1, RBM11, RNF182, LIPI, CD99, STEAP2, LOXHD1, and DCDC2. Normal-tissue and compartment data substantially reordered RNA-only ranking. NKX2-2 showed the strongest Ewing-associated signal but encodes a nuclear transcription factor, favoring peptide-HLA/T-cell receptor (TCR) or vaccine development. RBM11 and LIPI emerged as high-interest intracellular/secretome-associated candidates, with an explicit epididymal/male reproductive caveat for LIPI. CD99 and NPY1R illustrated normal-cell reservoir and receptor-distribution constraints.</p><p><strong>Conclusion: </strong>ESS32 should be interpreted as an EWSR1::FLI1-associated RNA discovery set, not as a pre-validated target panel. Practical nomination requires integration of RNA enrichment, normal-tissue distribution, protein evidence, cellular compartment, and modality compatibility before nomination of TCR, vaccine, antibody-drug conjugate (ADC), chimeric antigen receptor (CAR), radioligand, or validation-first candidates.</p>","PeriodicalId":9516,"journal":{"name":"Cancer Genomics & Proteomics","volume":"23 5","pages":"856-879"},"PeriodicalIF":2.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13531131/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863243","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":"An Update on Selected Giant Cell-Rich Tumors of Soft Tissue.","authors":"Jun Nishio, Mikiko Aoki","doi":"10.21873/cgp.20607","DOIUrl":"10.21873/cgp.20607","url":null,"abstract":"<p><p>Giant cell-rich tumors of soft tissue present a significant diagnostic challenge due to pronounced morphological overlap, particularly in limited tissue samples. This review provides a streamlined update on the clinicopathological and molecular features of nine distinct entities: nodular fasciitis, juvenile xanthogranuloma, phosphaturic mesenchymal tumor, tenosynovial giant cell tumor, giant cell fibroblastoma, giant cell-rich solitary fibrous tumor, giant cell tumor of soft tissue, keratin-positive giant cell-rich tumor, and undifferentiated pleomorphic sarcoma. While these neoplasms are unified by a prominence of multinucleated giant cells, recent genomic insights have identified signature, diagnostically defining molecular drivers. We highlight characteristic gene fusions, including USP6, NTRK1, FN1, CSF1, COL1A1-PDGFB, NAB2-STAT6, and HMGA2-NCOR2, as well as entities characterized by non-recurrent or highly complex genomic alterations. Synthesizing these data, this review underscores the critical role of advanced molecular testing in resolving diagnostic ambiguities, refining tumor classification, and guiding targeted therapeutic strategies.</p>","PeriodicalId":9516,"journal":{"name":"Cancer Genomics & Proteomics","volume":"23 5","pages":"899-913"},"PeriodicalIF":2.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13531115/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863017","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":"A Functionally Constrained Immune Ecosystem in Microsatellite-stable Colorectal Cancer Resolved by Single-cell and Exome Profiling.","authors":"Wenxu Liu, Yipan Zheng, Hao Wang, Feng Qi, Xiulan Zhao, Zhenyi Ma, Zhe Liu","doi":"10.21873/cgp.20615","DOIUrl":"10.21873/cgp.20615","url":null,"abstract":"<p><strong>Background/aim: </strong>Microsatellite-stable (MSS) colorectal cancer (CRC) generally responds poorly to immune checkpoint blockade, but some MSS tumors are T-cell rich. We examined whether such infiltration reflected effective immunity or functional immune constraint.</p><p><strong>Case report: </strong>A 77-year-old woman underwent resection of a mismatch repair-proficient (pMMR), MSS, low-mutational-burden CRC with a synchronous adenoma. Whole-exome sequencing of tumor, adenoma and adjacent normal tissue detected no shared high-confidence somatic mutations between tumor and adenoma within the sensitivity of this WES analysis and identified tumor-specific APC, KRAS and TP53 alterations. Tumor single-cell RNA sequencing yielded 7,569 cells, with T-lineage populations comprising 83.5%. Cytotoxic T cells showed cytolytic and dysfunction-associated features, regulatory T cells (Tregs) showed suppressive remodeling, and Th17 cells showed inflammatory/profibrotic programs. CellChat nominated stromal MIF/FN1-CD74/CD44 and extracellular-matrix communication with T-cell compartments.</p><p><strong>Conclusion: </strong>This molecular case report shows that T-cell abundance and immune effectiveness can be uncoupled in MSS CRC.</p>","PeriodicalId":9516,"journal":{"name":"Cancer Genomics & Proteomics","volume":"23 5","pages":"1043-1060"},"PeriodicalIF":2.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13531133/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863752","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":"Tumor Suppressive Role of Hsa-miR-328-3p in Colon Cancer by Regulating <i>EN2</i>.","authors":"Yun Ju Lee, DU Hyeong Lee, Hyeon-Su Jeong, Hyun-Young Roh, Ga-Ram Jeong, Heui-Soo Kim","doi":"10.21873/cgp.20610","DOIUrl":"10.21873/cgp.20610","url":null,"abstract":"<p><strong>Background/aim: </strong>Colon cancer is a prevalent and life-threatening malignancy worldwide. Recent studies have focused on how microRNAs (miRNAs) act as post-transcriptional modulators in colon cancer progression. Herein, this study aimed to identify the impact of miRNAs that are decreased in colon cancer and to investigate their regulatory mechanisms.</p><p><strong>Materials and methods: </strong>Differentially expressed miRNAs (DEmiRNAs) and genes (DEGs) were identified through analysis of miRNA sequencing and RNA sequencing data from normal and tumor tissues in The Cancer Genome Atlas (TCGA). Expression levels were validated by quantitative polymerase chain reaction (qPCR) in both tissues and cell lines. Functional effects of miRNAs were evaluated by assessing cell viability, proliferation, migration, and invasion following transfection with miRNA mimics.</p><p><strong>Results: </strong>Analysis of miRNA-seq data from the TCGA database identified hsa-miR-328-3p as a miRNA consistently downregulated across all stages of colon cancer. This downregulation was independently validated in colon cancer patient tissues by qPCR. Functional assays demonstrated that enforced expression of hsa-miR-328-3p significantly reduced cell viability, proliferation, migration, and invasion in colon cancer cell lines, supporting its tumor-suppressive role. To elucidate the molecular mechanism underlying these inhibitory effects, target gene analysis was performed. Engrailed homeobox 2 (<i>EN2</i>) was identified as a potential target of hsa-miR-328-3p, and a dual-luciferase assay confirmed that <i>EN2</i> is directly regulated by hsa-miR-328-3p.</p><p><strong>Conclusion: </strong>Collectively, these findings indicate that hsa-miR-328-3p is frequently downregulated in colon cancer and functions as a tumor suppressor by negatively regulating its target gene, <i>EN2</i>, thereby contributing to colon cancer malignancy. <i>EN2</i> may serve as a potential diagnostic biomarker for colon cancer, while restoration of hsa-miR-328-3p expression represents a promising therapeutic strategy. Further studies are needed to clarify the precise molecular mechanisms linking the hsa-miR-328-3p/<i>EN2</i> axis to colon cancer progression.</p>","PeriodicalId":9516,"journal":{"name":"Cancer Genomics & Proteomics","volume":"23 5","pages":"948-963"},"PeriodicalIF":2.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13531123/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863598","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":"Mutual Information-based Prognostic Biomarker Discovery in Cancer Genomics: Conceptual Framework and Representative Applications of MI-POG.","authors":"Kazunori Akimoto, Shoma Tamori, Keiko Sato","doi":"10.21873/cgp.20606","DOIUrl":"10.21873/cgp.20606","url":null,"abstract":"<p><p>Mutual information (MI)-based approaches have increasingly been applied to cancer genomics; however, their use for genome-wide prognostic biomarker discovery remains relatively underexplored. The present article summarizes the conceptual workflow of Mutual Information-based Prognostic Omics Gene (MI-POG) based on previously published applications in breast cancer, lower-grade glioma, and other cancer datasets. The framework consists of clinical endpoint discretization, genome-wide MI-based screening, candidate ranking, and downstream validation using conventional survival-analysis approaches. Previous MI-POG applications identified solute carrier family 20 member 1 (<i>SLC20A1</i>) as a prognostic biomarker in hormone receptor-positive breast cancer. Elevated <i>SLC20A1</i> expression was associated with unfavorable survival outcomes and was independently validated in the Molecular Taxonomy of Breast Cancer International Consortium (METABRIC) cohort. Methodological analyses demonstrated how survival endpoints can be integrated into an information-theoretic framework through fixed-time outcome discretization, enabling model-independent assessment of molecular-clinical dependencies. Applications across multiple cancer datasets suggested the potential applicability of the framework across biologically distinct tumor types, although further validation will be required to establish its robustness and generalizability. In conclusion, MI-POG can be formalized as an information-theoretic framework for genome-wide identification of prognostic biomarkers by quantifying molecular-clinical dependencies using mutual information. Representative applications from previously published studies suggest that MI-POG may complement conventional survival-analysis approaches and provide a useful strategy for biomarker discovery, although additional benchmarking and prospective validation will be required.</p>","PeriodicalId":9516,"journal":{"name":"Cancer Genomics & Proteomics","volume":"23 5","pages":"880-898"},"PeriodicalIF":2.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13531165/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863639","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}