BMC Cancer最新文献

{"title":"Prognostic values of intracellular cell-related genes in esophageal cancer and their regulatory mechanisms.","authors":"Wei Cao, Dacheng Jin, Weirun Min, Haochi Li, Rong Wang, Jinlong Zhang, Yunjiu Gou","doi":"10.1186/s12885-025-13483-8","DOIUrl":"https://doi.org/10.1186/s12885-025-13483-8","url":null,"abstract":"<p><p>Esophageal cancer is a grave malignant condition. While radiotherapy, often in conjunction with chemotherapy, serves as a cornerstone in the management of locally advanced or metastatic cases, patient tolerance and treatment resistance frequently hinder its efficacy. Cell-in-cell structures, prevalent in various tumors, have been linked to prognosis. Hence, investigating the prognostic significance and regulatory mechanisms of genes related to these intracellular structures in esophageal cancer is imperative. The Cancer Genome Atlas (TCGA) Esophageal Cancer (ESCA) dataset served as the training set for the analysis. Differentially expressed genes (DEGs) in ESCA samples were identified, with those related to intercellular structures designated cell-in-cell-related differential expression genes (CIC-related DEGs). Cox regression analysis was employed to identify prognostic genes, categorizing samples into high- and low-risk groups based on median risk scores. Validation was conducted using the GSE53624 risk model. Established methodologies included morphological mapping, enrichment analysis, immune infiltration analysis, prognostic gene expression validation, molecular docking, and Reverse Transcription Polymerase Chain Reaction (RT-PCR) validation. Thirty-eight intersecting genes were identified between the disease and normal groups in ESCA samples. Stepwise multivariate Cox analysis pinpointed three prognostic genes: androgen receptor (AR), C-X-C motif chemokine ligand 8 (CXCL8), and epidermal growth factor receptor (EGFR). The risk model's applicability was confirmed in the GSE53624 dataset, revealing eight significantly different immune-related gene sets. Prognostic gene expression validation demonstrated significant differences between the disease and normal groups in both datasets. The proteins corresponding to the three prognostic genes interacted with gefitinib and osimertinib. RT-PCR results corroborated the differential expression of prognostic genes in esophageal cancer tissues. This study identified AR, CXCL8, and EGFR as prognostic genes and demonstrated their molecular interactions with gefitinib and osimertinib, providing a foundation for ESCA diagnosis and treatment.</p>","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"25 1","pages":"105"},"PeriodicalIF":3.4,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000013","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Incidence and determinants of mortality among patients with colorectal cancer in oncology centers of Amhara region, Ethiopia, 2024: multicenter retrospective follow up study.","authors":"Getachew Tesfaw Walle, Tegene Atamenta Kitaw, Seteamlak Adane","doi":"10.1186/s12885-025-13462-z","DOIUrl":"https://doi.org/10.1186/s12885-025-13462-z","url":null,"abstract":"<p><strong>Introduction: </strong>Colorectal cancer is a significant cause of mortality globally, with several factors impacting patient outcomes, including access to healthcare, early detection, and treatment. Despite this, the specific factors affecting incidence of death among colorectal cancer patients in the Amhara region have not been thoroughly investigated. Thus, this study seeks to assess incidence and determinants of mortality among colorectal cancer patients in Amhara Region oncology centers.</p><p><strong>Results: </strong>The mean age of the participants was 48.6 years (SD ± 15). Median survival time was 23.8 months. The overall incidence rate or incidence density of a colorectal cancer mortality rate was 2.9 per 100 person-months (95% CI: 2.5-3.4). Survival rates of colorectal cancer patients 1and 5 year was 69.78% and 16.1%, respectively. The result of the multivariable analysis showed that colorectal cancer patients who had presenting symptoms [AHR = 2.67 (95% CI: 1.95, 3.67)], Base line HGB level < 12.5 mg/dl [AHR = 1.63 (95% CI: 1.12, 2.37)], WHO or ECOG poor performance status [AHR = 2.99 (95% CI: 2.17, 4.12), late stage of cancer [AHR = 2.32 (95% CI: 1.42, 3.79)] and location of tumor on colorectal [AHR = 1.76 (95% CI: 1.20, 2.55)] were significantly associated with mortality of colorectal cancer.</p><p><strong>Conclusion and recommendation: </strong>The study highlights significant findings on the survival and mortality of colorectal cancer patients. The overall mortality rate was 2.9 per 100 person-months. Multivariable analysis identified presenting symptoms, low baseline hemoglobin levels, poor performance status, late-stage cancer, and tumor location as significant predictors of mortality. Highlighting the need for early detection and targeted care strategies.</p>","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"25 1","pages":"102"},"PeriodicalIF":3.4,"publicationDate":"2025-01-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000047","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pan-cancer analysis shows that TNFSF4 is a potential prognostic and immunotherapeutic biomarker for multiple cancer types including liver cancer.","authors":"Zhaoda Deng, Lincheng Li, Zihe Meng, Guineng Zeng, Rui Cao, Rong Liu","doi":"10.1186/s12885-025-13479-4","DOIUrl":"https://doi.org/10.1186/s12885-025-13479-4","url":null,"abstract":"<p><strong>Background: </strong>As a member of the tumor necrosis factor (TNF) superfamily, tumor necrosis factor superfamily member 4 (TNFSF4) is expressed on antigen-presenting cells and activated T cells by binding to its receptor TNFRSF4. However, tumorigenicity of TNFSF4 has not been studied in pan-cancer. Therefore, comprehensive bioinformatics analysis of pan-cancer was performed to determine the mechanisms through which TNFSF4 regulates tumorigenesis.</p><p><strong>Methods: </strong>RNA-seq data for 33 cancers were analyzed from UCSC XENA database. Online websites and databases were used to investigate TNFSF4's biological function, epigenetic modifications, genetic alterations, and tumor immunity. Furthermore, cell phenotype experiment and tumor xenotransplantation experiment were performed to determine the biological functions of TNFSF4.</p><p><strong>Results: </strong>The pan-cancer analysis showed that TNFSF4 was upregulated in several tumors. Significant relationships between TNFSF4 expression and single-cells data were also observed in numerous cancer types. TNFSF4 expression correlated with the expression of immune checkpoint genes and could influence various drug sensitivity. Vitro and vivo experiments showed that TNFSF4 could promote the development and progression of Hepatocellular Carcinoma (HCC).</p><p><strong>Conclusions: </strong>TNFSF4 was upregulated in multiple cancer types and promoted the development and progression of cancers through several mechanisms including regulation of the tumor-infiltration of immune cells. Our study shows that TNFSF4 is a promising prognostic and immunotherapeutic biomarker in some malignant tumors.</p>","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"25 1","pages":"100"},"PeriodicalIF":3.4,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11740393/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000011","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Enhanced spatial analysis assessing the association between PFAS-contaminated water and cancer incidence: rationale, study design, and methods.","authors":"Resa M Jones, Erin R Kulick, Ryan Snead, Robin Taylor Wilson, John Hughes, Ted Lillys","doi":"10.1186/s12885-025-13508-2","DOIUrl":"https://doi.org/10.1186/s12885-025-13508-2","url":null,"abstract":"<p><strong>Background: </strong>Cancer is a complex set of diseases, and many have decades-long lag times between possible exposure and diagnosis. Environmental exposures, such as per- and poly-fluoroalkyl substances (PFAS) and area-level risk factors (e.g., socioeconomic variables), vary for people over time and space. Evidence suggests PFAS exposure is associated with several cancers; however, studies to date have various limitations. Few studies have used rigorous spatiotemporal approaches, and, to our knowledge, none have assessed cumulative exposures given residential histories or incorporated chemical mixture modeling. Thus, spatiotemporal analysis using advanced statistical approaches, accounting for spatially structured and unstructured heterogeneity in risk, can be a highly informative strategy for addressing the potential health effects of PFAS exposure.</p><p><strong>Methods: </strong>Using population-based incident cancer cases and cancer-free controls in a 12-county area of southeastern Pennsylvania, we will apply Bayesian spatiotemporal analysis methods using historically reconstructed PFAS-contaminated water exposure given residential histories, and other potential cancer determinants over time. Bayesian group index models enable assessment of various mixtures of highly correlated PFAS chemical exposures incorporating mobility/residential history, and contextual factors to determine the association of PFAS-related exposures and cancer incidence.</p><p><strong>Discussion: </strong>The purpose of this paper is to describe the Enhanced PFAS Spatial Analysis study rationale, study design, and methods.</p>","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"25 1","pages":"101"},"PeriodicalIF":3.4,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000006","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of mast cell in locally advanced rectal cancer treated with neoadjuvant chemoradiotherapy.","authors":"Masaaki Nishi, Shoko Yamashita, Chie Takasu, Yuma Wada, Kozo Yoshikawa, Takuya Tokunaga, Toshihiro Nakao, Hideya Kashihara, Toshiaki Yoshimoto, Mitsuo Shimada","doi":"10.1186/s12885-025-13458-9","DOIUrl":"https://doi.org/10.1186/s12885-025-13458-9","url":null,"abstract":"<p><p>The pro-tumor effects of mast cell (MC) in the tumor microenvironment (TME) are becoming increasingly clear. Recently, MC were shown to contribute to tumor malignancy by supporting the migration of tumor-associated macrophages (TAMs), suggesting a relationship with tumor immunity. In the current study, we aimed to examine the correlation between MC infiltration and neoadjuvant chemoradiotherapy (nCRT) response for locally advanced rectal cancer (LARC). Ninety-five LARC patients who recieved nCRT were enrolled in this study. Protein levels of the MC marker tryptase and TAM marker CD206 were evaluated with immunohistochemistry (IHC). The correlation between MC infiltration and prognostic factors was evaluated. The effects of MCs on the malignant potential were examined using in vitro proliferation and invasion assays with a colorectal cancer (CRC) cell line (HCT-116). Following nCRT, 31.6% of resected LARC patient specimens were positive for MC infiltration by tryptase IHC analysis. MC infiltration was significantly correlated with nCRT response. The 5-year disease-free survival (DFS) rate was significantly lower in the MC-positive group compared with the MC-negative group (52.3% vs. 76.8%). Univariate and multivariate analyses revealed that MC infiltration was the independent prognostic indicator for DFS. MC infiltration was significantly correlated with CD206 expression, and therefore TAMs. In vitro experiments suggested that tumor activated mast cells could promote CRC cell malignant behavior via production of macrophage inhibitory factor. MC infiltration in LARC patients was positively correlated with TAM infiltration and resistance to nCRT, and was also an independent poor prognostic indicator.</p>","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"25 1","pages":"99"},"PeriodicalIF":3.4,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11740561/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142999999","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Factors associated with health-related quality of life in women with paid work at breast cancer diagnosis: a German repeated cross-sectional study over the first five years after primary surgery.","authors":"Batoul Safieddine, Siegfried Geyer, Stefanie Sperlich, Johannes Beller, Dorothee Noeres","doi":"10.1186/s12885-025-13491-8","DOIUrl":"https://doi.org/10.1186/s12885-025-13491-8","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Evidence suggests a deterioration of health-related quality of life (HRQL) after breast cancer diagnosis and therapy. This study examines sociodemographic and health-related factors that could be associated with the HRQL of working women with breast cancer during the first five years after primary surgery. Second, it explores potential vulnerable groups with respect to HRQL using decision tree analyses.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Women diagnosed with breast cancer who had paid work at diagnosis were recruited at 11 breast cancer centers in the Hannover region, Germany, after primary surgery. Assessments took place four times. 455 patients completed mailed questionnaires at 3 weeks after primary surgery. Women were followed up at 6 months, 1 year and on average 5 years after primary surgery. The physical and mental wellbeing dimensions of HRQL were examined through the Short-Form health survey-12. Potential associations between HRQL and health and sociodemographic factors were examined using multiple linear regression. Classification tree analyses were applied to define specific vulnerable groups.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Mastectomy (ß=-2.49; CI:-4.67, -0.30) and chemotherapy (ß=-4.25; CI:-7.04, -1.46) as health related factors were significantly associated with poorer physical wellbeing at 3 weeks and 6 months after primary surgery, respectively. Returning to work (RTW) after having been on sick leave was strongly associated with better HRQL as illustrated by higher sum scores for physical (at 3 weeks: ß=6.21; CI:3.36, 9.05; at 6 months: ß=5.40; CI:3.01, 1.80; at 1 year: ß=8.40; CI:5.31, 11.49) and mental wellbeing (at 6 months: ß=6.03; CI:33.25, 8.81; at 1 year: ß=7.71; CI:4.85, 10.58) until 1 year after primary surgery. However, its significant effect was no more apparent at 5 years after primary surgery. At that stage, income was mostly associated with physical (ß=0.002; CI:0.0002, 0.003) and mental wellbeing (ß=0.002; CI:0.0005, 0.003) with higher summary scores for higher income especially in women aged ≤ 61 years. In addition, living with a partner appeared to be an important positively associated factor with better mental wellbeing in women with breast cancer (at 6 months: ß=3.68; CI: 0.72, 6.63; at 5 years: ß=2.85; CI:0.39, 5.32) and the first splitting node that defined vulnerability at 5 years.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusions: &lt;/strong&gt;HRQL in breast cancer appears to be a multidimensional phenomenon associated with disease, treatment and social factors. A special focus should be drawn to women with lower income and those not living with a partner when planning rehabilitation programs and strategies that aim to improve the long term HRQL in breast cancer. As RTW appeared to be positively associated with HRQL, future research should examine potential causal relationships between RTW and HRQL in breast cancer in order to provide evidence needed to plan prevention strategies that aim to improve HRQL af","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"25 1","pages":"98"},"PeriodicalIF":3.4,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000020","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High-throughput methylation sequencing reveals novel biomarkers for the early detection of renal cell carcinoma.","authors":"Wenhao Guo, Weiwu Chen, Jie Zhang, Mingzhe Li, Hongyuan Huang, Qian Wang, Xiaoyi Fei, Jian Huang, Tongning Zheng, Haobo Fan, Yunfei Wang, Hongcang Gu, Guoqing Ding, Yicheng Chen","doi":"10.1186/s12885-024-13380-6","DOIUrl":"https://doi.org/10.1186/s12885-024-13380-6","url":null,"abstract":"<p><strong>Purpose: </strong>Renal cell carcinoma (RCC) is a common malignancy, with patients frequently diagnosed at an advanced stage due to the absence of sufficiently sensitive detection technologies, significantly compromising patient survival and quality of life. Advances in cell-free DNA (cfDNA) methylation profiling using liquid biopsies offer a promising non-invasive diagnostic option, but robust biomarkers for early detection are current not available. This study aimed to identify methylation biomarkers for RCC and establish a DNA methylation signature-based prognostic model for this disease.</p><p><strong>Methods: </strong>High-throughput methylation sequencing was performed on peripheral blood samples obtained from 49 primarily Stage I RCC patients and 44 healthy controls. Comparative analysis and Least Absolute Shrinkage and Selection Operator (LASSO) regression methods were employed to identify RCC methylation signatures.Subsequently, methylation markers-based diagnostic and prognostic models for RCC were independently trained and validated using random forest and Cox regression methodologies, respectively.</p><p><strong>Results: </strong>Comparative analysis revealed 864 differentially methylated CpG islands (DMCGIs), 96.3% of which were hypermethylated. Using a training set from The Cancer Genome Atlas (TCGA) dataset of 443 early-stage RCC tumors and matched normal tissues, we applied LASSO regression and identified 23 methylation signatures. We then constructed a random forest-based diagnostic model for early-stage RCC and validated the model using two independent datasets: a TCGA set of 460 RCC tumors and controls, and a blood sample set from our study of 15 RCC cases and 29 healthy controls. For Stage I RCC tissue, the model showed excellent discrimination (AUC-ROC: 0.999, sensitivity: 98.5%, specificity: 100%). Blood sample validation also yielded commendable results (AUC-ROC: 0.852, sensitivity: 73.9%, specificity: 89.7%). Further analysis using Cox regression identified 7 of the 23 DMCGIs as prognostic markers for RCC, allowing the development of a prognostic model with strong predictive power for 1-, 3-, and 5-year survival (AUC-ROC > 0.7).</p><p><strong>Conclusions: </strong>Our findings highlight the critical role of hypermethylation in RCC etiology and progression, and present these identified biomarkers as promising candidates for diagnostic and prognostic applications.</p>","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"25 1","pages":"96"},"PeriodicalIF":3.4,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11737265/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000043","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The efficacy and safety of induction chemotherapy combined with sintilimab followed by concurrent chemoradiotherapy plus sintilimab sequencing maintaining with sintilimab for patients with unresectable locally advanced esophageal squamous cell carcinoma.","authors":"Ruifeng Wang, Tianhui Guo, Qi Wang, Wen Gao, Yimiao Yu, Jun Zhang, Wenqian Fu, Haiji Wang, Biyuan Zhang","doi":"10.1186/s12885-025-13457-w","DOIUrl":"https://doi.org/10.1186/s12885-025-13457-w","url":null,"abstract":"<p><strong>Purpose: </strong>To evaluate the efficacy and safety of induction chemotherapy combined with programmed death protein 1 (PD-1) inhibitor (sintilimab) followed by concurrent chemoradiotherapy (CCRT) plus sintilimab, and subsequent maintenance with sintilimab (IC-ICCRT-IO) for patients with unresectable locally advanced esophageal squamous cell carcinoma (ESCC) in a retrospective study.</p><p><strong>Methods: </strong>Data from patients with histologically confirmed, locally advanced, inoperable ESCC who received IC-ICCRT-IO were retrospectively analyzed. Treatment effects were evaluated after 2 cycles of induction therapy and after CCRT by contrast-enhanced CT scans and esophagograms, followed by subsequent evaluations every 3 months post-treatment. The primary endpoints included progression-free survival (PFS) and PFS rates at 6, 12, and 18 months. Secondary endpoints involved overall response rate (ORR), disease control rate (DCR), overall survival (OS), and safety. The influence of the expression level of programmed death ligand-1 (PD-L1) as well as neutrophil-to-lymphocyte ratio (NLR) on efficacy of the IC-ICCRT-IO was analyzed.</p><p><strong>Results: </strong>In total, 29 eligible patients were enrolled and analyzed. The median follow-up time was 20.5 months. The median PFS was not reached; the 6-, 12-, and 18-month PFS rates were 100.0%, 93.1%, and 82.8%, respectively. The median OS was not reached, and the 6-, 12-, and 18-month OS rates were all 100.0%. The ORR and DCR were 89.7% and 100.0%. Adverse events (AEs) were manageable, with grade 3 or higher AEs observed in 48.2% of patients, primarily nonimmune-related and clinically manageable. Hematologic toxicity was predominant. Two patients developed grade 3 immune-related rash, and two patients developed grade 3 radiation pneumonitis, all of whom were managed with appropriate symptomatic treatment. No significant differences in survival outcomes were observed with respect to PD-L1 and NLR.</p><p><strong>Conclusion: </strong>Our results indicated that the IC-ICCRT-IO regimen for unresectable locally advanced ESCC provided a survival benefit with manageable safety profile. More prospective clinical studies should be warranted.</p><p><strong>Trial registration: </strong>2024-04-22, No. QYFY WZLL 28,684, retrospectively registered.</p>","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"25 1","pages":"97"},"PeriodicalIF":3.4,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11736957/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000062","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transcriptomic landscape of Hras12V oncogene-induced hepatocarcinogenesis with gender disparity.","authors":"Huaiyuan Di, Zhuona Rong, Nan Mao, Huiling Li, Jun Chen, Renwu Liu, Aiguo Wang","doi":"10.1186/s12885-025-13476-7","DOIUrl":"https://doi.org/10.1186/s12885-025-13476-7","url":null,"abstract":"<p><p>The genesis of hepatocellular carcinoma (HCC) is closely related to male factors and hyper-activated Ras signals. A transcriptomic database was established via RNA-Seq of HCC (T) and the adjacent precancerous liver tissue (P) of Hras12V transgenic mice (Ras-Tg, HCC model) and the normal liver tissue of wild-type mice (W) of both sexes. Comparative analysis within W, P, and T and correlation expression pattern analysis revealed common/unique cluster-enriched items towards HCC between the sexes. Specifically, the numbers of differentially expressed genes (DEGs) were much higher in females than in males, and tumor suppressor genes, such as p21^Waf1/Cip1 and C6, were significantly higher in the female P. This finding denotes the higher sensitivity of female hepatocytes to the Ras oncogene and, therefore, the difficulty in developing HCC. Moreover, convergence in HCC between the sexes suggests the underlying mechanisms for the ineffectiveness of sex hormone therapies. Additionally, expression pattern analysis revealed that the DEGs and their relevant pathways were either positively or negatively associated with the HCC/Ras oncogene. Among them, the vital role of glutathione metabolism in HCC was established. This work provides a basis for future research on elucidating the underlying mechanisms, selecting the diagnostic biomarker, and planning the clinical therapy in HCC.</p>","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"25 1","pages":"94"},"PeriodicalIF":3.4,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11737189/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000048","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prostate cancer cells elevate glycolysis and G6PD in response to caffeic acid phenethyl ester-induced growth inhibition.","authors":"Tzu-Ping Lin, Pei-Chun Chen, Ching-Yu Lin, Bi-Juan Wang, Ying-Yu Kuo, Chien-Chih Yeh, Jen-Chih Tseng, Chieh Huo, Cheng-Li Kao, Li-Jane Shih, Jen-Kun Chen, Chia-Yang Li, Tzyh-Chyuan Hour, Chih-Pin Chuu","doi":"10.1186/s12885-025-13477-6","DOIUrl":"https://doi.org/10.1186/s12885-025-13477-6","url":null,"abstract":"<p><strong>Background: </strong>Caffeic acid phenethyl ester (CAPE) is the main bioactive component of poplar type propolis. We previously reported that treatment with caffeic acid phenethyl ester (CAPE) suppressed the cell proliferation, tumor growth, as well as migration and invasion of prostate cancer (PCa) cells via inhibition of signaling pathways of AKT, c-Myc, Wnt and EGFR. We also demonstrated that combined treatment of CAPE and docetaxel altered the genes involved in glycolysis and tricarboxylic acid (TCA) cycle. We therefore suspect that CAPE treatment may interfere glucose metabolism in PCa cells.</p><p><strong>Methods: </strong>Seahorse Bioenergetics platform was applied to analyzed the extra cellular acidification rate (ECAR) and oxygen consumption rate (OCR) of PCa cells under CAPE treatment. UPLC-MSMS with Multiple Reaction Monitoring (MRM), PCR, and western blot were used to analyze the effects of CAPE on metabolites, genes, and proteins involved in glycolysis, TCA cycle and pentose phosphate pathway in PCa cells. Flow cytometry and ELISA were used to determine the level of reactive oxygen species in PCa cells being treated with CAPE.</p><p><strong>Results: </strong>Seahorse Bioenergetics analysis revealed that ECAR, glycolysis, OCR, and ATP production were elevated in C4-2B cells under CAPE treatment. Protein levels of glucose-6-phosphate dehydrogenase (G6PD), phosphogluconate dehydrogenase (PGD), glutaminase (GLS), phospho-AMPK Thr172 as well as abundance of pyruvate, lactate, ribulose-5-phosphate, and sedoheptulose-7-phosphate were increased in CAPE-treated C4-2B cells. ROS level decreased 48 h after treatment with CAPE. Co-treatment of AMPK inhibitor with CAPE exhibited additive growth inhibition on PCa cells.</p><p><strong>Conclusions: </strong>Our study indicated that PCa cells attempted to overcome the CAPE-induced stress by upregulation of glycolysis and G6PD but failed to impede the growth inhibition caused by CAPE. Concurrent treatment of CAPE and inhibitors targeting glycolysis may be effective therapy for advanced PCa.</p>","PeriodicalId":9131,"journal":{"name":"BMC Cancer","volume":"25 1","pages":"95"},"PeriodicalIF":3.4,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11737093/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000014","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}