Journal of Cancer最新文献

{"title":"Research progress on molecular mechanism of liver metastasis of gastric cancer and treatment with traditional Chinese medicine.","authors":"Caiyue Liu, Zheng Li, Fane Cheng, Weiqiang Li, Tingting Li","doi":"10.7150/jca.105223","DOIUrl":"https://doi.org/10.7150/jca.105223","url":null,"abstract":"<p><p>Gastric cancer liver metastasis (GCLM) refers to the process of cancer cells from the stomach spreading to the liver, which is an important sign of the deterioration of gastric cancer (GC) and has a profound influence on the treatment and prognosis of patients. Once GC has liver metastasis, the treatment becomes more complex and challenging, which seriously affects the survival rate of patients with GC. Therefore, studying the mechanism and treatment of GCLM is extremely necessary. At present, the continuous research on GCLM has revealed that the mechanism of its occurrence and development involves the comprehensive effect of multiple targets and links. Traditional Chinese medicine (TCM) has the advantages of wide sources, excellent efficacy, and small toxicity and side effects, which have become the focus of current antitumor research. TCM, Chinese medicine monomers, or TCM compounds can inhibit the growth and metastasis of GC. In recent years, Chinese medicine has made substantial achievements in experimental research on the intervention of GCLM. This article reviews the progress of its intervention mechanism.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 6","pages":"1944-1957"},"PeriodicalIF":3.3,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11905405/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143648210","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":"Clinical significance and immune landscape analyses of the coagulation-related gene signatures in gastric cancer.","authors":"Yueming Yu, Dingwei Liu, Jun Xie, Zhou Feng, Xiaoping Huang, Hui Li, Yong Xie, Xiaojiang Zhou","doi":"10.7150/jca.104221","DOIUrl":"https://doi.org/10.7150/jca.104221","url":null,"abstract":"<p><p>Gastric cancer (GC) is one of the most common types of clinically malignant tumors and a global health challenge due to its high mortality and poor prognosis. The coagulation cascade is closely related to GC and plays a key role in the tumor immune microenvironment. However, the specific mechanisms by which coagulation-related genes involved in the occurrence and development of GC remains unclear. The data of GC patients and coagulation-related genes were obtained from the TCGA and the GSEA databases, respectively. After univariate Cox regression analysis, the non-negative matrix factorization method was used to identify coagulation-related molecular subtypes. GC patients were categorized into high-risk and low-risk score groups based on median risk scores, which included six genes (PCDHAC1, HABP2, GPC3, GFRA1, F5, and DKK1). There was a significant difference in survival between the two groups, and the predictive abilities for 1-, 3-, and 5-year survival were valid. Here, we demonstrated that coagulation-related gene signatures are valuable in predicting the survival of GC patients. Besides, the high- and low-risk grouping also better reflects the status of tumor mutation burden and the characteristics of tumor immune infiltration in GC, which provides a theoretical basis for individualized chemotherapy and immunotherapy for GC patients.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 6","pages":"1971-1986"},"PeriodicalIF":3.3,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11905418/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143648638","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":"Sleep health: an unappreciated key player in colorectal cancer.","authors":"Jiahua Liu, Qihang Yuan, Yao Zhang, Xinyu Wang, Lijun Zhai, Ruiqi Wang, Chunyu Zheng, Zhijun Hong","doi":"10.7150/jca.107117","DOIUrl":"https://doi.org/10.7150/jca.107117","url":null,"abstract":"<p><p>Colorectal cancer (CRC) poses a significant threat to human life and health. Global cancer prevalence data in 2022 indicated that the number of new cases of CRC was about 1.92 million and the deaths were around 900,000. A variety of risk factors, including genes and environment, can induce the occurrence of CRC. Previous studies have focused on the impact of dietary patterns on the development of CRC and have ignored sleep factors. Sleep deprivation is a common problem as people's work pressure increases. Sleep disorders can lead to metabolic and immune system dysregulation in people, contributing to the development and progression of many tumors. At present, there are few reports on the relationship between sleep disorders and tumors. Therefore, the purpose of this paper is to summarize and interpret the relationship between various sleep disorders and the onset and progression of CRC. This review is the first to investigate the possible mechanisms of sleep leading to CRC from the perspectives of metabolic reprogramming, intestinal microbiota disorders, and the release of inflammatory factors. In conclusion, this study highlights the rational sleep pattern and duration, which can help inhibit the occurrence of CRC.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 6","pages":"1934-1943"},"PeriodicalIF":3.3,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11905398/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143648528","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":"CCL4 and MIF: Prognostic Biomarkers for Evaluating the Chemoradiotherapy Response and Prognosis in Patients with ESCC.","authors":"Yuwen Wang, Chunxue Ding, Xiaoying Wei, Yuting Li, Xuyao Yu, Xi Chen, Jifeng Sun, Junhong Zhuang, Shuai Cao, Peng Zhen, Fang Fang, Jiarui Zhang, Jun Wang, Dong Qian, Qingsong Pang","doi":"10.7150/jca.104088","DOIUrl":"https://doi.org/10.7150/jca.104088","url":null,"abstract":"<p><p><b>Background</b>: Radiotherapy plays a central role in therapeutic strategy of local-advanced oesophageal squamous cell carcinoma. The aim of this study was to investigate cytokine profiles in serum of patients with ESCC and evaluate the potential utility of cytokine markers in predicting CRT response and prognostic prediction. <b>Methods:</b> CCL4, MIF and CXCL8 in the serum samples who were participating in a phase II clinical trial (NCT02959385) were determined. The association between these cytokines and CRT response as well as prognostic prediction were subsequently assessed in ESCC. Subsequently, the results were verified in ESCC tissue and in the Cancer Genome Atals (TCGA) database. <b>Results:</b> The expression of 120 cytokines were evaluated in serum of 4 ESCC patients with excellent CRT-response and 4 patients with CRT-resistance by cytokine microarrays. CCL3, CCL4, MIF, PLAUR and CXCL8 were screened. CCL4, MIF and CXCL8 were further detected by ELISA in other 60 patients enrolled in this study. Upregulation of CCL4, CXCL8 and MIF were observed in patients with excellent CRT-response. Elevated expression of CCL4 and MIF were closely associated with improved PFS and OS outcomes. Similar results were obtained in other 46 ESCC tumor tissues. 82 ESCC patients in TCGA database with increased CCL4 and MIF expression exhibited the favorable immunocyte infiltration and enriched immune response-related pathways, which indicates the preferable tumor immunogenicity. <b>Conclusions:</b> CCL4 and MIF are identified as dependable and prognostic biomarkers for evaluating the response to CRT and prognosis in patients with ESCC.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 6","pages":"2015-2025"},"PeriodicalIF":3.3,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11905412/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143648700","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":"Anti-proliferative and anti-invasive effects of exogenous thermostable MnSOD in gastric cancer associated with p53 and ZEB1 expression.","authors":"Hailong Li, Hao Wang, Zong Li, Natalia Kelley, Matt Ouyang, Jia-Wei Wu, Fanguo Meng, Wen-Bin Ou","doi":"10.7150/jca.102600","DOIUrl":"https://doi.org/10.7150/jca.102600","url":null,"abstract":"<p><p>The incidence of gastric cancer accounts for the first malignant tumor of the digestive tract. Although some progress in gastric cancer treatments has been made, uncontrollable drug resistance makes the development of new targeted drugs and treatment options increasingly urgent. The biological function of endogenous manganese superoxide dismutase (MnSOD) has been widely studied, whereas the anti-tumor growth effects of exogenous thermostable MnSOD in gastric cancer, an oral recombinant protein drug, are still unclear. Here, compared to normal gastric epithelial cell line and enzymatic dead mutant MnSOD H29A, we show that exogenous MnSOD treatment resulted in reduction of cell viability, colony formation, migration, and invasiveness; inhibition of SGC7901 xenograft growth; induction of apoptosis and arrest of G₂-phase population in gastric cancer by an enzymatic activity-dependent manner; upregulation of p53, p21, and E-cadherin; and downregulation of cyclin D1 and N-cadherin. Unexpectedly, MnSOD treatment induced zinc finger E-box homeobox 1 (ZEB1) expression in SGC7901 gastric cancer cells, which was associated with a poor five-year survival rate and poor prognosis in gastric cancer patients. However, anti-proliferative effects of exogenous MnSOD were enhanced in SGC7901 after ZEB1 knockdown, whereas attenuated in BGC823 after ZEB1 restoration. These findings indicate that the exogenous thermostable MnSOD inhibited gastric cancer growth associated with p53 and ZEB1 expression levels and highlight that the exogenous thermostable MnSOD as an oral drug warrants evaluation as a novel therapeutic strategy in gastric cancer.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 6","pages":"2062-2074"},"PeriodicalIF":3.3,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11905419/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143648683","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":"Identification of hub genes for the diagnosis and prognosis in triple negative breast cancer using transcriptome and differential methylation integration analysis.","authors":"Baoe Liu, Xiaoli Yang, Huxia Wang, Peijun Liu, Qing Feng, Cuixiang Xu, Zhangjun Song","doi":"10.7150/jca.104472","DOIUrl":"https://doi.org/10.7150/jca.104472","url":null,"abstract":"&lt;p&gt;&lt;p&gt;&lt;b&gt;Introduction:&lt;/b&gt; Triple-negative breast cancer (TNBC) is characterized by the absence of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2) expression. It is highly invasive and aggressive, making it the subtype of breast cancer with the poorest prognosis. Currently, systemic chemotherapy is the primary treatment option, but targeted therapies remain unavailable. Therefore, there is an urgent need to identify novel biomarkers for the early diagnosis and treatment of TNBC. &lt;b&gt;Methods:&lt;/b&gt; We conducted an integrated analysis of transcriptome and methylation data to identify methylation-regulated differentially expressed genes (MDEGs). Gene Ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, and protein-protein interaction (PPI) network analysis were performed on MDEGs to investigate the impact of hub genes on the diagnosis and prognosis of TNBC. Subsequently, the expression levels and DNA methylation patterns of key genes were validated in the TNBC cell line MDA-MB-231 and the normal breast epithelial cell line MCF-10A using reverse transcription quantitative PCR (RT-qPCR) and quantitative methylation-specific PCR (qMSP). &lt;b&gt;Results:&lt;/b&gt; A total of 98 upregulated and 87 downregulated genes were identified through transcriptomic profiling integration analysis. By incorporating methylation data, we further identified 22 genes with high expression of hypomethylation (hypo-MDEGs) and 32 genes with low expression of hypermethylation (hyper-MDEGs). The hypo-MDEGs were primarily involved in nuclear division, organelle fission, spindle formation, chromosome and kinetochore development, and protein binding. KEGG pathway analysis revealed that these genes were enriched in progesterone-mediated oocyte maturation, cell cycle regulation, and oocyte meiosis. Hyper-MDEGs were associated with cell proliferation, hormone response, pain, extracellular matrix composition, and binding to sulfur compounds, heparin, and glycosaminoglycans. PPI network analysis identified seven hub genes-&lt;i&gt;EXO1, KIF11&lt;/i&gt;, &lt;i&gt;FOXM1, CENPF, CCNB1&lt;/i&gt;, &lt;i&gt;PLK1&lt;/i&gt;, and &lt;i&gt;KIF23&lt;/i&gt;-which were all significantly overexpressed in TNBC tissues and positively correlated with each other (&lt;i&gt;p&lt;/i&gt; &lt; 0.05). Receiver operating characteristic curve analysis showed that the area under the curve (AUC) for all seven genes exceeded 0.9 (&lt;i&gt;p&lt;/i&gt; &lt; 0.05), suggesting strong diagnostic potential. Kaplan-Meier survival analysis indicated that &lt;i&gt;KIF11&lt;/i&gt;, &lt;i&gt;CCNB1&lt;/i&gt;, and &lt;i&gt;PLK1&lt;/i&gt; were associated with a higher hazard ratio (HR &gt; 1, &lt;i&gt;p&lt;/i&gt; &lt; 0.05) in TNBC. &lt;i&gt;In vitro&lt;/i&gt; validation experiments demonstrated that, compared to MCF-10A cells, MDA-MB-231 cells exhibited higher mRNA expression levels of &lt;i&gt;KIF11&lt;/i&gt;, &lt;i&gt;CCNB1&lt;/i&gt;, and &lt;i&gt;PLK1&lt;/i&gt;, while their DNA methylation levels were lower. Conclusions: This study identified seven hypo-MDEGs, including &lt;i&gt;EXO1, KIF11&lt;/i&gt;, &lt;i&gt;FOXM1, CENPF, CCNB1&lt;/i&gt;, &lt;i&gt;P","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 6","pages":"2026-2040"},"PeriodicalIF":3.3,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11905416/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143648747","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":"Deciphering the Role of CD14 in <i>Helicobacter Pylori</i>-associated Gastritis and Gastric Cancer: Combing Bioinformatics Analysis and Experiments.","authors":"Xuefei Yang, Jiaqi Zhang, Ping Wang, Fengyun Wang, Xudong Tang","doi":"10.7150/jca.106847","DOIUrl":"https://doi.org/10.7150/jca.106847","url":null,"abstract":"<p><p><b>Background:</b> Gastric cancer (GC) is the third leading cause of cancer-related death and is associated with high mortality and morbidity. <i>Helicobacter pylori</i> (HP) infection is the most important cause of GC. We aimed to identify the core genes of HP caused GC and further elucidate the underlying mechanisms. <b>Methods:</b> GC and HP associated gastritis (HPAG) gene expression data were sourced from Gene Expression Omnibus. Key genes affecting GC prognosis were identified using Cytoscape software. Patient groups were formed based on key gene expression, and the immune analyses were performed with R. MNU, derived from nitrite by HP, was given to GC mice (240ppm) for histology and fluorescence assays. For in vitro experiments, cells received MNU (20 μM) stimulation for 24 hours. <b>Results:</b> CD14 was the only key gene identified. A total of 412 GC patients were divided into CD14-high and CD14-low groups. The two groups showed significant differences in immune cell populations and immune checkpoints. In particular, there was a notable increase in M2 macrophages in GC patients with high CD14 expression (<i>P</i> <0.001). GC Patients with high CD14 expression exhibited a more pronounced immune response than those with low CD14 expression, and elevated CD14 expression positively correlated with the efficacy of CTLA4 therapy (<i>P</i> <0.05). These results indicated that CD14 expression was strongly correlated with the GC immune response. A noticeable increase in CD14 levels was observed in MNU-induced GC animals, cell models, and GC patients. In addition, the number of M2 macrophages was increased in MNU-induced GC mice. <b>Conclusion:</b> Reducing CD14 expression may increase the survival rate of GC patients through the modulation of immune responses. The complex mechanism of CD14's influence on prognosis deserves further investigation.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 6","pages":"1918-1933"},"PeriodicalIF":3.3,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11905408/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143648642","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":"A machine learning model utilizing CT radiomics features and peripheral blood inflammatory markers predicts the prognosis of patients with unresectable esophageal squamous cell carcinoma undergoing PD-1 inhibitor combined with concurrent chemoradiotherapy.","authors":"Xudong Liu, Fei Gao, Shusheng Wu, Haoyu Wang, Wenxi Dang, Mingjie Sun, Zhihua Zhang, Mengge Li, Zhirun Cai, Wen Li, Yifu He","doi":"10.7150/jca.105171","DOIUrl":"https://doi.org/10.7150/jca.105171","url":null,"abstract":"<p><p><b>Objective:</b> To investigate the value of a machine learning model that integrates radiomics features and peripheral blood inflammatory markers in predicting the prognosis of patients with unresectable esophageal squamous cell carcinoma (ESCC) receiving PD-1 inhibitor combined with concurrent chemoradiotherapy. <b>Methods:</b> A retrospective collection was conducted involving 105 patients with unresectable ESSC who received PD-1 inhibitors combined with concurrent chemoradiotherapy at the First Affiliated Hospital of the University of Science and Technology of China from January 2020 to August 2023. These patients were randomly divided into a training set (n=74) and a validation set (n=31). Radiomics features were extracted from arterial phase CT images obtained before initial treatment, with feature selection performed using Pearson Correlation and LASSO-COX methods. Baseline clinical characteristics were analyzed, and hematological parameters were collected before the start of immunotherapy and within 4-6 weeks post-treatment to calculate inflammatory markers. Subsequently, independent radiomics features influencing patient prognosis were identified using a multivariate Cox proportional hazards model, and these features were incorporated into a clinical feature-based multivariate Cox model to derive independent prognostic factors combining radiomics and clinical characteristics. Nomograms were constructed to predict the 2-year progression-free survival (PFS) of patients based on the results of COX analysis involving clinical characteristics, radiomic features, and combined indicators. The models were evaluated and assessed using ROC curves and calibration curves. <b>Results:</b> In the training cohort, the AUC was 0.705 for the clinical model, 0.573 for the radiomics model, and 0.834 for the combined model. In the validation cohort, the AUC was 0.784 for the clinical model, 0.775 for the radiomics model, and 0.872 for the combined model. <b>Conclusion:</b> The combined model integrating the radiomic feature NGTDM-busyness, the inflammatory marker ΔNLR, and the clinical characteristic M stage offers the optimal predictive value for the 2-year PFS in patients.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 6","pages":"2001-2014"},"PeriodicalIF":3.3,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11905411/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143648681","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":"CKS2 Silencing Affects Proliferation and Apoptosis in Multiple Myeloma through the PTEN/ AKT/mTOR Pathway.","authors":"Jing Zi-Zi, Yu Wei, Tang Jia-Lin, Zhou Xiao-Bin, Chen Jian-Bin","doi":"10.7150/jca.106190","DOIUrl":"https://doi.org/10.7150/jca.106190","url":null,"abstract":"<p><p>Multiple myeloma (MM), a prevalent plasma cell malignancy, represents a life-threatening hematological disorder with significant clinical morbidity. Despite its recognized impact on global health burdens, the precise molecular pathogenesis underlying disease progression remains incompletely elucidated. Transcriptomic profiling via RNA sequencing revealed significant upregulation of cyclin-dependent kinase regulatory subunit 2 (CKS2) in multiple myeloma. Clinical validation was performed through quantitative analysis of CKS2 expression in patient-derived specimens. Two established MM cell models (MM.1S and RPMI-8226) were selected for functional characterization. Cellular proliferation dynamics were quantified using CCK-8 metabolic assays and EdU DNA incorporation analysis, with flow cytometric evaluation employed to assess apoptotic indices. A xenograft mouse model was established to investigate CKS2-mediated tumorigenesis <i>in vivo</i>, complemented by western blot analysis of pathway-associated protein expression. Bioinformatic interrogation of the HumanBase database identified putative CKS2 interactomes, subsequently validated through co-immunoprecipitation assays and confocal immunofluorescence microscopy. Structural modeling via AlphaFold2 predicted molecular interaction interfaces, with three-dimensional visualization achieved through PyMOL rendering. In this study, we demonstrated that CKS2 knockdown in MM.1S and RPMI-8226 cell lines significantly inhibited cellular proliferation and induced apoptosis. Conversely, CKS2 overexpression enhanced malignant proliferation while suppressing apoptotic processes, establishing its functional role in myeloma pathogenesis. Mechanistic investigations revealed that CKS2 depletion modulates cell proliferation and apoptosis via PTEN/AKT/mTOR signaling axis. Notably, co-immunoprecipitation assays demonstrated direct protein-protein interaction between CKS2 and thioredoxin (TXN), with subsequent functional validation suggesting TXN appears to function as a key upstream regulatory factor governing CKS2 stability. These findings establish CKS2 as a critical regulator of myeloma cell homeostasis and identify it as a promising therapeutic target warranting further preclinical validation.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 6","pages":"1987-2000"},"PeriodicalIF":3.3,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11905417/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143648721","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":"EIF4A3 Promotes Cell Proliferation via CDC5L Upregulation in Human Breast Cancer Cells.","authors":"Miao Zhang, Yuchen Xie, Shaoran Song, Ruiqi Wang, He Chen, Yazhao Li, Jie Liu, Juan Li, Yina Jiang, Peijun Liu, Bo Wang","doi":"10.7150/jca.108895","DOIUrl":"https://doi.org/10.7150/jca.108895","url":null,"abstract":"<p><p>Breast cancer is one of the most common diseases affecting women's health. While research on breast cancer has made progress in recent years, it remains a major health concern. Studies have shown that the translation initiation factor EIF4A3 is closely related to the occurrence and development of tumors, but the specific mechanism is still unclear. In this study, we aimed to explore the specific molecular mechanism of EIF4A3 in promoting the malignant process of breast cancer <i>in vivo</i> and <i>in vitro</i>. Our results showed that the expression of EIF4A3 was significantly upregulated in breast cancer, and overexpression of EIF4A3 could accelerate the growth of breast cancer cells. RIP-seq and RIP-RT-qPCR analyses indicated that EIF4A3 can bind to the mRNA of CDC5L and influence its expression. From the catRAPID we predicted that EIF4A3-protein could bind to CDC5L by the 5705-5954 region of CDC5L-mRNA. CDC5L was the downstream effector of EIF4A3. These results suggested that the EIF4A3-CDC5L axis promotes the proliferation of breast cancer cells. This study provides a theoretical basis for understanding the role of EIF4A3 in the malignant process of breast cancer.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 6","pages":"1958-1970"},"PeriodicalIF":3.3,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11905404/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143648742","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}