Journal of Cancer最新文献

{"title":"Single-Cell-Derived Malignant Epithelial Programs Define Prognostic Risk and Therapeutic Vulnerability in Ovarian Cancer.","authors":"Jingwen Si, Hanbo Li, Han Zhang, Yan Shen","doi":"10.7150/jca.135548","DOIUrl":"10.7150/jca.135548","url":null,"abstract":"<p><strong>Background: </strong>Ovarian cancer (OV) is characterized by pronounced intratumoral heterogeneity and unfavorable clinical outcomes, yet clinically applicable biomarkers for risk stratification remain limited. Although bulk transcriptomic models have been widely proposed, they often overlook the cellular origins of prognostic signals. Advances in single-cell RNA sequencing (scRNA-seq) provide an opportunity to resolve malignant epithelial diversity and identify biologically meaningful predictors.</p><p><strong>Methods: </strong>Single-cell transcriptomic datasets were integrated to construct a comprehensive epithelial landscape of OV. Copy number variation profiles inferred by inferCNV were used to distinguish malignant epithelial cells, followed by subpopulation identification and trajectory inference using Slingshot and Monocle3. Subcluster-specific gene signatures were projected onto bulk RNA-seq cohorts, and prognostic genes were screened using Cox regression and LASSO modeling to establish a multigene risk score. The model was validated across multiple independent cohorts. Multi-omics analyses, including pathway enrichment, mutational profiling, tumor mutation burden, immune features, and drug sensitivity prediction, were performed to explore biological and clinical relevance. Functional assays were conducted to validate the role of the key gene PSMB1.</p><p><strong>Results: </strong>Malignant epithelial cells exhibited substantial transcriptional heterogeneity and distinct evolutionary trajectories, revealing subpopulations associated with differential clinical outcomes. A nine-gene risk model derived from these subpopulations demonstrated robust and consistent prognostic performance across multiple datasets. The risk score was closely associated with tumor progression pathways, immune suppression, genomic instability, and reduced therapeutic sensitivity. Notably, PSMB1 was identified as a critical oncogenic factor, and its knockdown significantly inhibited proliferation and colony formation in OV cells.</p><p><strong>Conclusions: </strong>This study establishes a single-cell-informed prognostic framework that links malignant epithelial heterogeneity to clinical outcomes and therapeutic response in OV. The proposed model provides biologically interpretable risk stratification and highlights PSMB1 as a potential therapeutic target, offering new insights for precision oncology.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"17 7","pages":"1274-1294"},"PeriodicalIF":3.4,"publicationDate":"2026-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13410796/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148620177","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":"Association of DNA damage response gene polymorphisms with treatment response and prognosis in acute myeloid leukemia.","authors":"Amin Zhang, Hanyang Wu, Wancheng Liu, Daoxin Ma","doi":"10.7150/jca.134391","DOIUrl":"10.7150/jca.134391","url":null,"abstract":"<p><p>The potential functional Single Nucleotide Polymorphism (SNPs) of DNA Damage Response (DDR)-related genes may influence AML aggressiveness and clinical outcomes through regulating genomic stability. However, systematic evaluation of functionally relevant SNPs across the entire DDR cascade in AML remains limited. In our study, significant associations were identified across multiple DDR modules. In the damage sensing module, <i>MRE11</i> rs2155209 TC/CC genotypes were protective against hyperleukocytosis and associated with longer OS, while <i>NBS1</i> rs1805794 CG/GG genotypes increased hyperleukocytosis risk. In the signal transduction module, <i>CHEK1</i> rs521102 AA genotype was a risk factor for thrombocytopenia but unexpectedly associated with prolonged OS; <i>CHEK2</i> rs738722 TT genotype increased hyperleukocytosis risk; <i>RAD17</i> rs1045051 GT/GG genotype conferred a higher relapse risk; and <i>BRCA1</i> rs1799949 GA/AA genotype as a protective factor for high BM blast percentage. In the DNA repair module, <i>LIG3</i> rs3744356 TT genotypes predicted higher WBC counts and lower complete remission rate. Both <i>LIG3</i> rs3744356 TT genotype and <i>MGMT</i> rs2296675 GA genotype were associated with shorter OS (HR = 1.719, 95% CI = 1.082 -2.741, <i>p</i> = 0.022; HR = 1.511, 95% CI = 1.046 - 2.182, <i>p</i> = 0.028). SNPs in effector genes <i>TP53</i> and <i>CDKN1A</i> showed no significant associations. In summary, SNPs across the DDR pathway-particularly in damage sensing, signal transduction, and DNA repair modules-are significantly associated with AML clinical features, treatment response, and survival. Our findings provide a foundation for developing DDR-based polygenic risk models and support the potential integration of germline SNP profiling into precision medicine strategies for AML.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"17 7","pages":"1265-1273"},"PeriodicalIF":3.4,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13410339/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148620091","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":"Microfluidic Immunomagnetic Capture of Circulating Tumor Cells via On-Bead Antibody Conjugation.","authors":"Ming-Lin Tsai, Wen-Ching Hsieh, Sung-Chi Tsai, Yi-Chiung Hsu","doi":"10.7150/jca.134785","DOIUrl":"10.7150/jca.134785","url":null,"abstract":"<p><p>Microfluidic immunomagnetic platforms have been widely explored for circulating tumor cell (CTC) enrichment; however, operational complexity, unstable flow control, and limited real-time observation remain practical challenges for routine implementation. In this study, we developed an integrated microfluidic chip system for EpCAM-based immunomagnetic enrichment of tumor cells using antibody-functionalized magnetic beads. The platform incorporates a gas-liquid separation structure, pressure-regulated flow control, and a transparent chip design that enables real-time microscopic observation of bead-cell interactions during capture. Biotin loading on streptavidin-coated beads was optimized, with surface saturation observed at 6 nmol. Flow-rate optimization identified 0.4 μL/s as the selected flow rate, balancing capture efficiency and cell-bead interaction time. In whole-blood spike-in experiments using MCF-7 cells, the platform achieved recovery efficiencies ranging from approximately 57% to 91%, depending on the input cell number. Cells with Hoechst⁺/CD326⁺/CD45⁻ phenotypes were also observed in patient-derived blood samples, supporting the feasibility of detecting putative CTCs in clinical specimens. This study positions the system as an engineering-integrated, real-time-observable platform for CTC enrichment. Further validation using larger clinical cohorts, multi-marker capture strategies, quantitative purity analysis, and cell viability assays will be required before translational application.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"17 7","pages":"1256-1264"},"PeriodicalIF":3.4,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13410613/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148620228","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":"Association of NAP1L1 polymorphism with clinicopathological progression in oral squamous cell carcinoma.","authors":"Ming-Ju Hsieh, Hsin-Yu Ho, Yu-Sheng Lo, Min-Yun Kao, Chia-Chieh Lin, Yi-Ching Chuang, Mu-Kuan Chen","doi":"10.7150/jca.132751","DOIUrl":"10.7150/jca.132751","url":null,"abstract":"<p><strong>Objective: </strong>Nucleosome assembly protein 1-like 1 (NAP1L1) plays an important role in the development and progression of several types of cancer.</p><p><strong>Subject and methods: </strong>This study investigated the association between NAP1L1 polymorphisms, particularly rs11180813, and susceptibility to oral squamous cell carcinoma (OSCC).</p><p><strong>Results: </strong>Our study showed that betel quid chewing and cigarette smoking were significantly associated with OSCC risk (p < 0.001). No significant correlation was found between NAP1L1 SNPs and overall OSCC susceptibility. However, among OSCC patients, patients with rs11180813 variant genotypes (GC/CC) were associated with lymph node metastasis (adjusted OR = 1.565, 95% CI = 1.042-2.350, p = 0.031) and poor tumor differentiation (adjusted OR = 2.284, 95% CI = 1.126-4.635, p = 0.022). In buccal OSCC, the rs11180813 variant was associated with lymph node metastasis (adjusted OR = 2.349, 95% CI = 1.213-4.549, p = 0.011). TCGA analysis revealed that high NAP1L1 expression correlated significantly with lymph node metastasis and poor tumor differentiation (p < 0.0001).</p><p><strong>Conclusion: </strong>These findings suggest that NAP1L1 and its rs11180813 polymorphism may be associated with certain clinicopathological characteristics of OSCC, particularly lymph node metastasis and tumor differentiation. Further studies are required to validate their clinical significance.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"17 7","pages":"1248-1255"},"PeriodicalIF":3.4,"publicationDate":"2026-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13410463/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148620202","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":"Emerging Oncolytic Viruses: Beyond Adenoviruses and Herpes Simplex Virus.","authors":"Santosh Chokkakula, Chengliang Yin, Bing Yang, Siomui Chong, Balaji Pathakumari, Yi-Quan Zhang, Pangi Vijaya Nirmala, Khin Wee Lai, Bommireddy Naveen, Quan Tang","doi":"10.7150/jca.134550","DOIUrl":"10.7150/jca.134550","url":null,"abstract":"<p><p>Oncolytic virotherapy represents an innovative therapeutic modality in oncology, exploiting the selective tropism of viruses to target and eradicate malignant cells. Unlike conventional cancer treatments such as chemotherapy and radiotherapy, oncolytic viruses (OVs) exhibit a dual mechanism of action: direct tumor cell lysis and potent immune activation. This approach transforms tumors into <i>in situ</i> vaccines, generating durable anti-tumor immune memory. The field has garnered substantial attention following the regulatory approval of talimogene laherparepvec (T-VEC), a genetically engineered herpes simplex virus, for metastatic melanoma treatment-a watershed moment in oncolytic virotherapy. Recent advances in genetic engineering have significantly enhanced OV specificity and efficacy, addressing critical challenges including tumor-selective targeting and immune evasion. This review comprehensively examines the complex mechanisms underlying OV therapeutic action, clinical applications, and recent developments that position oncolytic virotherapy as a transformative strategy in contemporary cancer treatment.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"17 6","pages":"1229-1247"},"PeriodicalIF":3.4,"publicationDate":"2026-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13280627/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148295018","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":"Assessing the Association Between Genetic Variants in ACE, SOD1, and PER3 and their Role in Breast Cancer Risk among Jordanian Women.","authors":"Laith N Al-Eitan, Fouad A Almomani, Mohammed S Alorjani, Maryam K Alasmar, Haneen O Ali, Mansour A Alghamdi","doi":"10.7150/jca.133243","DOIUrl":"10.7150/jca.133243","url":null,"abstract":"<p><strong>Background: </strong>Genetic and environmental factors regulate many physiological processes in the human body, and alterations in these processes may contribute to the development of various diseases, including breast cancer (BC), which is considered the most prevalent cancer among women and a leading cause of cancer-related mortality in the Jordanian population. Genes such as <i>ACE</i>, <i>SOD1</i> and <i>PER3</i> play important roles in regulating essential biological functions. These genes are involved in key physiological pathways, including blood pressure regulation, oxidative stress response and circadian rhythm maintenance, and genetic variants within them may influence susceptibility to cancer. Therefore, this study investigates the association between polymorphisms in the <i>ACE</i>, <i>SOD1</i> and <i>PER3</i> genes and the risk of breast cancer, with the aim of evaluating how these genetic variations relate to breast cancer susceptibility and clinical outcomes in Jordanian women.</p><p><strong>Methods: </strong>Blood samples of 300 women diagnosed with breast cancer, along with 300 healthy participants, were collected, and DNA was extracted from them. Genetic variants in the <i>ACE</i> (rs1799752), <i>SOD1</i> (rs36232792) and <i>PER3</i> (rs57875989) genes are examined through employing direct PCR to amplify the target regions.</p><p><strong>Results: </strong>The <i>ACE</i> (rs1799752) variant was observed to be associated with breast cancer susceptibility, with the I/I genotype increasing risk of breast cancer (OR = 5.138, 95% CI = 1.38-19.03, p = 0.014). No associations were observed for <i>SOD1</i> (rs36232792) and <i>PER3</i> (rs57875989) variants.</p><p><strong>Conclusion: </strong>The rs1799752 polymorphism is suggested to have the potential of serving as a biomarker for breast cancer susceptibility in Jordanian women, as it is associated with elevating the risk.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"17 6","pages":"1195-1205"},"PeriodicalIF":3.4,"publicationDate":"2026-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13280626/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148294986","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":"<i>GALNT14</i>-rs9679162 Genotypes Predict Post-immunotherapy Side Effect and Survival in Patients with Hepatitis B Virus-related Hepatocellular Carcinoma.","authors":"Po-Ting Lin, Wei Teng, Wei-Ting Chen, Yu-De Chu, Chung-Wei Su, Yi-Chung Hsieh, Chen-Chun Lin, Yung-Chang Lin, Chun-Yen Lin, Chau-Ting Yeh, Shi-Ming Lin","doi":"10.7150/jca.133473","DOIUrl":"10.7150/jca.133473","url":null,"abstract":"<p><strong>Introduction: </strong>Genomic alterations have been reported to correlate with patients' response to immune checkpoint inhibitor (ICI) therapy in hepatocellular carcinoma (HCC). The present study aimed to examine whether single nucleotide polymorphism (SNP) is associated with ICI treatment-related side effects and progression-free survival (PFS) in HCC patients.</p><p><strong>Methods: </strong>This retrospective study included 96 patients with HBV-related HCC receiving ICI (atezolizumab plus bevazizumab) therapy between 2020 and 2023. Five SNPs derived from a previous genome-wide association study linking to chemotherapy responses in HCC patients were included. Their predictive values for PFS and side effects were examined.</p><p><strong>Results: </strong>After ICI therapy, patients with <i>GALNT14</i>-rs9679162 \"GG\" genotype (median PFS = 19.7 months, 95% confidence interval [CI]: 12.3-35.7; p = 0.032) had a longer PFS, whereas <i>GALNT14</i>-rs675230, <i>BMP7</i>-rs6025211, <i>WWOX</i>-rs13338697 or <i>WWOX</i>-rs13333314 were not associated with PFS (all p > 0.05). <i>GALNT14</i>-rs9679162 \"GG\" genotype (odds ratio [OR] = 0.298, 95% CI: 0.096-0.926; p = 0.036) was also associated with a decreased risk of post-treatment high-grade aspartate aminotransferase (AST) elevation. Multivariate analysis showed that <i>GALNT14</i>-rs9679162 \"GG\" genotype (hazard ratio [HR] = 0.433, 95% CI: 0.212-0.886; p = 0.022) and high initial albumin-bilirubin (ALBI) grade (HR = 2.053, 95% CI: 1.153-3.590; p = 0.014) were independently associated with PFS.</p><p><strong>Conclusions: </strong>Genetic variant of an SNP, <i>GALNT14</i>-rs9679162, predicts post-treatment PFS and side effect in HBV-related HCC patients receiving ICIs therapy.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"17 6","pages":"1220-1228"},"PeriodicalIF":3.4,"publicationDate":"2026-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13280630/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148295052","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":"Association between obesity, sex, medical comorbidities, and survival in cancer patients treated with immune checkpoint inhibitors.","authors":"Mingjia Li, Daniel J Spakowicz, Songzhu Zhao, Hyunwoo Kwon, Kenneth Chian, Adam Khorasanchi, Yizhen Guo, Lai Wei, Lingbin Meng, Yuanquan Yang, Asrar Alahmadi, Regan M Memmott, Jacob Kaufman, Kai He, Peter G Shields, Thomas A Mace, Mitch A Phelps, Christopher C Coss, Zihai Li, Kari L Kendra, David P Carbone, Gregory A Otterson, Carolyn J Presley, Dwight H Owen","doi":"10.7150/jca.130032","DOIUrl":"10.7150/jca.130032","url":null,"abstract":"<p><strong>Background: </strong>Obesity's impact on cancer treatment outcomes is poorly understood, especially in the context of immuno-oncology. This study explores how obesity and medical comorbidities are associated with overall survival in cancer patients receiving immune checkpoint inhibitors (ICIs). Additionally, considering the influence of sex on body composition in obesity, this study examines the relationship between sex, obesity, medical comorbidities, and survival.</p><p><strong>Methods: </strong>This cohort study involved 688 patients with metastatic cancer received ICIs as first- or second-line therapy. Obesity was assessed using body mass index (BMI). Cox proportional hazard models and Kaplan-Meier survival analysis were used to examine associations between predictors and overall survival.</p><p><strong>Results: </strong>Patients with higher BMI had longer overall survival, and hazard ratio (HR) for death was 0.83 (95% CI 0.73-0.95) for every 10 units increased in BMI. Additionally, patients belonged to the highest BMI group (≥ 40) had the lowest risk of death when comparing to patients with BMI 18.5 to < 30 with HR 0.58 (95% CI 0.37-0.90). In subgroup analysis, a significant association between high BMI and decreased HR for death was predominantly observed in the male cohort. In multivariate analysis, the prognostic value of BMI remained significant after adjusting for performance status, line of therapy, age-adjusted medical comorbidities, and cancer type.</p><p><strong>Conclusions: </strong>Obesity was associated with decreased mortality risk for cancer patients who had received ICIs. There could be a sex-dependent association between survival benefit and obesity.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"17 6","pages":"1117-1124"},"PeriodicalIF":3.4,"publicationDate":"2026-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13280536/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148295010","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":"Exosomes in Cancer Biology: Emerging Biomarkers and Therapeutic Targets.","authors":"Marriam Ahmed, Chieh-Wei Chang, Sundas Ijaz, Abdul Qadeer, Khalid J Alzahrani, Khalaf F Alsharif, Fuad M Alzahrani, Abdulwahab Abuderman, Chien-Chin Chen, Shahid Hussain","doi":"10.7150/jca.132498","DOIUrl":"10.7150/jca.132498","url":null,"abstract":"<p><p>Exosomes are small extracellular vesicles (EVs) that play an important role in intercellular communication among multiple cell types. In recent years, they have emerged as a novel and promising class of cancer biomarkers, offering significant potential to increase diagnostic and therapeutic strategies. These bilayer nano-vesicles are actively secreted by living cells into various biological fluids and carry a diverse cargo of proteins, nucleic acids, and other biomolecules that reflect the physiological and pathological state of their cells of origin. The molecular composition of exosomes mirrors the dynamic processes and unique cargo of molecular and genetic data, reflecting the complex activities within cancer cells, making them a promising alternative for cancer detection and treatment monitoring. Although the mechanisms underlying exosome biogenesis, secretion, and cargo selection in cancer remain incompletely understood, growing evidence highlights their importance in tumor progression and therapeutic response. Exosomal proteins have gained considerable attention as potential therapeutic targets. These proteins can regulate immune responses, reshape the tumor microenvironment, and influence cancer cell proliferation and survival. Consequently, targeting exosome-associated proteins represents a promising strategy for developing innovative anticancer therapies. Advances in exosomal protein analysis have provided a promising approach for unraveling the complex molecular networks underlying cancer biology. A wide range of analytical techniques is available to identify and quantify exosomal proteins, enabling characterization of cancer-specific molecular signatures. As an expanding field in cancer research, exosomes have the potential to revolutionize both therapies and diagnostics. By deciphering the diverse molecular and functional cargos of exosomes, exosomes offer new insights that may lead to more precise, effective, and personalized approaches to cancer management.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"17 6","pages":"1206-1219"},"PeriodicalIF":3.4,"publicationDate":"2026-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13280628/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148295062","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 Emerging Role of CACNA1E in Cancer: Molecular Mechanisms and Therapeutic Implications.","authors":"Wei Hou","doi":"10.7150/jca.133409","DOIUrl":"10.7150/jca.133409","url":null,"abstract":"<p><p>Voltage-gated calcium channels (VGCCs) are crucial membrane proteins that mediate calcium influx. The CACNA gene family, which encodes the alpha subunits of VGCC complexes, is essential for forming functional calcium channels and plays significant roles in various cancers. This review focuses on the CACNA1E gene, which encodes the Cav2.3 channel α1E subunit, and systematically elaborates its role in cancer. Studies have identified CACNA1E as a key prognostic stemness-related gene in bladder cancer. Its somatic mutations are associated with the development of air pollution-related lung cancer and non-small cell lung cancer. In breast cancer, genetic variations and DNA methylation differences in CACNA1E have also been reported. Functionally, CACNA1E drives tumor progression by regulating calcium signaling. For example, in osteosarcoma, METTL3-mediated m⁶A modification stabilizes CACNA1E mRNA, activating the WNT7B/Ca²⁺ signaling pathway and thereby promoting tumor progression and chemoresistance. The expression of CACNA1E is closely linked to patient prognosis, with its amplification and overexpression correlating with relapse in favorable histology Wilms' tumor. Additionally, CACNA1E is involved in therapy resistance, as evidenced by its downregulation being associated with temozolomide resistance in glioblastoma. Collectively, this evidence suggests that CACNA1E, along with other VGCC members, may serve as a potential prognostic biomarker and therapeutic target in cancer. Future research should further explore their molecular mechanisms, interactions with the tumor microenvironment, and clinical translation potential.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"17 6","pages":"1155-1164"},"PeriodicalIF":3.4,"publicationDate":"2026-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13280633/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148295123","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}