Journal of Cancer最新文献

{"title":"Malignant Transformation of Meningiomas.","authors":"Jinxiu Yu, Jiaojiao Deng, Leihao Ren, Lingyang Hua, Ye Gong","doi":"10.7150/jca.105024","DOIUrl":"10.7150/jca.105024","url":null,"abstract":"<p><p>Meningioma is the most common intracranial tumor. Sometimes, meningiomas can develop malignant transformation (MT). In this review, we review the incidence of MT of meningiomas. The incidence of MT of grade 2 meningiomas is likely to be higher than benign meningiomas. Approximately 1% to 4% of WHO Grade 1 meningiomas may undergo MT, while about 26% to 33% of Grade 2 meningiomas experience MT. Time to MT of grade 2 meningiomas seemed to be shorter than MT of grade 1 meningiomas. The time for Grade I meningiomas to undergo MT is approximately 5 years, while Grade II meningiomas typically experience MT in about 3 years. Several risk factors may be associated with MT, including non-skull base location, high mitotic Index, a larger primary tumor size, shorter recurrence time interval and male. Potential molecular mechanisms of MT include chromosomal abnormalities (Chromosome 22q deletion, NF2 gene mutation, loss of chromosome 1p), genomic alterations (FOXM1, CDKN2A/B and TERTp), and meningioma cancer stem cells. Secondary meningiomas may have poor tumor control rates and overall survival rates than primary meningiomas. Besides, the role of radiotherapy in MT of meningiomas is unclear. Major concerns are whether radiotherapy can induce MT of meningiomas, and whether radiotherapy can prolong time to MT through long term control of meningiomas. This review summarizes the MT of meningiomas, and may provide the direction for further study of meningiomas.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 5","pages":"1684-1693"},"PeriodicalIF":3.3,"publicationDate":"2025-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11843249/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143483193","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":"LINC00899 suppresses the progression of triple-negative breast cancer via the miRNA-425/PTEN axis and is a biomarker for neoadjuvant chemotherapy efficacy.","authors":"Lianjie Niu, Yongtao Bai, Meng Yu, Xianfu Sun","doi":"10.7150/jca.100619","DOIUrl":"10.7150/jca.100619","url":null,"abstract":"<p><p><b>Background:</b> Close clinical attention has been paid to triple-negative breast cancer (TNBC) due to its poor prognosis, high recurrence and mortality rates and rapid invasion and metastasis. The present study aimed to explore the potential mechanism of LINC00899 in the progression of TNBC and its effect on the proliferation and migration of TNBC cells via the microRNA (miR)-425/phosphatase and tensin homolog (PTEN) axis. <b>Methods:</b> For this purpose, plasma exosomes and related clinical data from 119 patients with breast cancer receiving neoadjuvant chemotherapy (59 patients with TNBC, 32 with HER2⁺ and with 28 luminal-type) and 20 healthy women were collected. Functional assays were then used to verify the role of the LINC00899/miR-425/PTEN axis in the proliferation and migration of TNBC cells. <b>Results:</b> The results showed that the expression of LINC00899 was reduced in plasma exosomes and breast cancer cell lines, which was associated with the Ki-67 index, tumor size and the presence or absence of lymph node metastasis but was not associated with patient age, androgen receptor expression or cholangiocarcinoma thrombus. The receiver operating characteristic curve results showed that LINC00899 had a high predictive value for the pathological outcome of patients with TNBC receiving neoadjuvant treatment. The results of the functional experiments also showed that LINC00899 targeted and regulated miR-425 in TNBC, and miR-425 negatively regulated the expression of PTEN. <b>Conclusions:</b> In conclusion, the results of the present indicated that LINC00899 may predict neoadjuvant chemotherapy efficacy in patients with TNBC and that LINC00899 inhibited the proliferation and migration of MDA-MB-231 cells via the miR-425/PTEN axis.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 5","pages":"1647-1655"},"PeriodicalIF":3.3,"publicationDate":"2025-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11843232/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143483173","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":"Incidence and survival patterns of clear cell renal cell carcinoma from 2000 to 2017: A SEER Database Analysis.","authors":"Sijue Zou, Liwen Cui, Pearl Pai, Yiping Lu, XiangYang Li, Gang Wang, Wen Huang, Dan Wang, Nikhat Shaikh, Zhangzhe Peng, Zhuoming Peng, Haiyan He, Zhouning Liao","doi":"10.7150/jca.105713","DOIUrl":"10.7150/jca.105713","url":null,"abstract":"<p><p><b>Background</b>: Clear cell renal cell carcinoma (ccRCC) incidence and death have considerably changed in recent years. Our study aimed to investigate the incidence, survival, and tumor characteristics of ccRCC in the year of diagnosis. <b>Methods</b>: Our study participants were selected from the SEER database (2000-2017). Age-standardized incidence rates were calculated to compare incidence rates across time. In addition, we used Kaplan-Meier curves to calculate overall survival (OS) and Cox proportional hazards models to explore risk factors associated with mortality outcomes in patients with ccRCC. <b>Results</b>: In the SEER analysis from 2000 to 2017, the increasing trend in age-adjusted incidence of ccRCC has remained relatively stable over the years, increasing from 2.63 per 100,000 in 2000 to 8.79 per 100,000 in 2017. The increase in the incidence of patients at a localized stage plays a decisive role in the overall increase in the incidence of ccRCC. <b>Conclusions</b>: In the general population, patients diagnosed between 2009-2017 had a higher survival rate than those diagnosed between 2000-2008, which is consistent with all stages of the tumor. The incidence of ccRCC increases steadily with the year of diagnosis, while overall survival has significantly improved.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 5","pages":"1591-1597"},"PeriodicalIF":3.3,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11843228/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143483186","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":"Stigmasterol Attenuates Triple-negative Breast Cancer Stem Cell Properties by Inhibiting JAK3.","authors":"Ruijuan Zhou, Yuzhu Zhang, Leqin Xu, Yang Sun","doi":"10.7150/jca.94822","DOIUrl":"10.7150/jca.94822","url":null,"abstract":"<p><p><b>Background:</b> Breast cancer stem-like cells (BCSCs) are considered a source of tumor origins, metastasis and drug resistance, thereby limiting current treatment regimens. Stigmasterol has been reported to inhibit various cancer processes, but its effects and mechanisms in BCSCs have not been investigated. <b>Methods:</b> To generate spheroids, we enriched parental and SUM159 cells with BCSCs in a serum-free medium. The effects on the stemness, metastasis and drug resistance of CSC-enriched SUM159 cells were detected for the first time by <i>in vivo</i> and <i>in vitro</i> experiments. <b>Results:</b> CSC-enriched SUM159 and 4T1 cells demonstrated higher potential for tumorigenesis and metastasis. Stigmasterol suppresses BCSCs' spheroid formation, cell viability, and migration ability and promotes cell apoptosis. Stigmasterol also inhibited BCSCs-originated cancer formation in rat models. Stigmasterol also attenuated the growth of TNBC organoids from human breast cancer tissues. These data revealed the inhibitory effects of stigmasterol on BCSC traits. In the meantime, we found that JAK3 was upregulated in BCSCs, and Stigmasterol could effectively inhibit its expression. In addition, JAK3 was evidenced to negatively regulate BCSC activity and stemness both <i>in vitro</i> and <i>in vivo</i>. More importantly, the results indicated that Stigmasterol suppresses BCSC activity by inhibiting JAK3 expression. <b>Conclusion:</b> This study is the first to demonstrate that Stigmasterol inhibited metastasis and stemness of BCSCs by downregulating JAK3, which might provide a new method for the clinical application of Stigmasterol in breast cancer.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 5","pages":"1618-1630"},"PeriodicalIF":3.3,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11843247/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143483306","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 mutualistic relationship between M2c macrophages of TGFβ1 induction and gastric cancer cells: the correlation between protective mechanisms in the tumor microenvironment and polarization of subtypes of cells.","authors":"Kaiqiang Meng, Jian Song, Fan Qi, Jiamin Li, Zhichao Fang, Liang Song, Shaonan Shi","doi":"10.7150/jca.97784","DOIUrl":"10.7150/jca.97784","url":null,"abstract":"<p><p><b>Background:</b> Gastric cancer (GC) is one of the most common malignant tumors worldwide, with fast metastasis and high mortality rate. GC cells and tumor immune microenvironment exhibit high heterogeneity. Multiple pieces of evidence suggest that TGFβ1 intervenes in the tumor microenvironment, immune cells and GC prognosis. The aim of this study is to comprehensively investigate the functional intervention of macrophage polarization subtypes on gastric cancer cell lines in the GC tumor microenvironment, providing valuable insights into tumor microenvironment research and potential targets for treatment strategies. <b>Methods:</b> TCGA database and multiple GEO datasets were used to validate the role of TGFβ1 in cancer prognosis, immune infiltration and subtype macrophage polarization. Construct different subtypes of macrophages and establish cell co culture systems using Transwell chambers. Enzyme linked immunosorbent assay (ELISA), western blotting (WB) and reverse transcription quantitative polymerase chain reaction (RT-qPCR) were used to verify the changes in the metastatic function and defense mechanism of gastric cancer cells (Hgc27 and MKN45) in different co culture systems. Further analyze the effect of gastric cancer cell metabolites on macrophage subtype polarization. <b>Results:</b> TGFβ1 was highly expressed in GC tissues, highly expressed TGFβ1 could reduce the survival time of GC patients. The GC immune infiltration results confirmed the correlation between TGFβ1 and M2 macrophages. The GEO dataset results of gastric cancer at different stages showed that some M2 macrophage markers showed consistent changes with TGFβ1. The WB, ELISA and RT-qPCR have identified TGFβ1-induced polarization of M2c macrophages, most biomarkers are associated with M2c. M2c macrophages can enhance cell migration and function, can inhibit ferroptosis in gastric cancer cells, endowing them with stronger special environmental resistance. Gastric cancer cells tend to polarize towards M2 macrophages, with M2c being the main M2 subtype of macrophages. <b>Conclusion:</b> In conclusion, our study reveals a mutually beneficial symbiotic relationship between M2c macrophages and cancer cells in the microenvironment of gastric cancer tumors. TGFβ1 promotes the production of M2c macrophages, which enhance the function and ferroptosis resistance of gastric cancer cells. Gastric cancer cells provide the material basis for M2c macrophage polarization. This new evidence may provide new insights into developing more effective targeted therapies for gastric cancer to combat the formation of immune escape and metastasis in gastric cancer.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 5","pages":"1598-1617"},"PeriodicalIF":3.3,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11843238/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143483310","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":"CRABP2 (Cellular Retinoic Acid Binding Protein 2D): A novel biomarker for the diagnosis and prognosis involved in immune infiltration of lung adenocarcinoma.","authors":"DaXia Cai, Feng Tian, DengKe Zhang, JianFei Tu, YongHui Wang","doi":"10.7150/jca.96518","DOIUrl":"10.7150/jca.96518","url":null,"abstract":"<p><p><b>Objective:</b> Overexpressed CRABP2 (Cellula Retinoi Aci Bindin Protei 2D) can promote progression of various tumors. However, there are few comprehensive analysis studies on CRABP2 in lung adenocarcinoma (LUAD). <b>Methods:</b> Several large public databases and online analysis tools such as TCGA, GEO, GEPIA2, UALCAN, Kaplan Meier plotter, LinkedOmics, TIMER, CCLE and Metascape were used for big data mining analysis. RNA interference technology, CCK8 assay, flow cytometry and apoptosis detection, and western blot were used for <i>in vitro</i> experiments. <b>Results:</b> The study revealed that the expression level of CRABP2 in plasma were higher (mean level 31.6587 ±13.8541 ng/mL vs. 13.9328 ± 5.5805 ng/mL, <i>p</i><0.0001) in patients with early stage (stage IA) LUAD compared to the control group based on analysis of 640 LUAD patients and 640 matched healthy control plasma samples from Lishui Central Hospital. Receiver Operating Characteristic curve showed that CRABP2 had certain accuracy in predicting early LUAD, with a sensitivity of 70.98%, a specificity of 94.53%, a cut-off value of 0.6551 ng/mL, and an Area Under the Curve of 0.839 (95%CI: 0.817 - 0.859, <i>p</i><0.0001). Compared with normal lung tissue, CRABP2 was significantly overexpressed in LUAD (<i>p</i><0.05). High CRABP2 expression in LUAD predicts poor prognosis both in Overall Survival (95%CI: 1.04-1.46, HR:1.23, <i>p</i>=0.018) and FP (First Progression, 95%CI: 1.10-1.65, HR = 1.35, <i>p</i>=0.0032) in LUAD patients. CRABP2 can promote the progression of LUAD by promoting the G2/M phase transition, inhibiting the apoptosis and participating in the regulation of immune microenvironment. The high expression of CRABP2 will inhibit the recruitment of immune effector cells and promote the proportion of immuno-suppressive cells, thus promoting the progression of LUAD. The low expression of CRABP2 may enhance the expression of CD274(PD-L1), HAVCR2 and PDCD1LG2(PD-L2) in LUAD. While, the high expression of CRABP2 may enhance the expression of CTLA4, LAG3, PDCD1(PD-1), TIGIT and IGSF8 in LUAD. <b>Conclusions:</b> CRABP2 may be a valuable biomarker for diagnosis, treatment and prognosis of LUAD. Patients with high expression of CRABP2 in LUAD may have suboptimal efficacy when treated with inhibitors targeting CD274, HAVCR2, and PDCD1LG2, whereas they may experience better efficacy with inhibitors targeting CTLA4, LAG3, PDCD1, TIGIT, and IGSF8. Most of cancer patients with high CRABP2 expression may benefit from immune checkpoint inhibitor therapy. Our study results have laid a positive foundation for LUAD diagnosis and therapy.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 5","pages":"1631-1646"},"PeriodicalIF":3.3,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11843236/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143483158","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":"Overexpression of MCM3 as a prognostic biomarker correlated with cell proliferation, cell cycle and immune regulation in hepatocellular carcinoma.","authors":"Linling Ju, Huixuan Wang, Yunfeng Luo, Yichen Wang, Lin Chen, Xudong Han, Rujian Lu","doi":"10.7150/jca.104325","DOIUrl":"10.7150/jca.104325","url":null,"abstract":"<p><p><b>Background:</b> Hepatocellular carcinoma (HCC) is a common malignant tumor and has a poor prognosis. Minichromosome maintenance 3 (MCM3) protein is upregulated in several cancers, but the biological function, molecular mechanisms and the relationship with tumor immunity of MCM3 in HCC remain poorly understood. <b>Methods:</b> The expression levels and prognosis role of MCM3 in HCC were analyzed based on TCGA, GEO and LIHC databases, and 40 paired tissue samples. We conducted Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) analyses on these DEGs to explore the potential impact of MCM3 on the biological behavior of HCC. In addition, flow cytometry, CCK-8, EdU, colony formation and nude mice xenograft models were employed to investigate the biological functions of MCM3. Furthermore, immune cell infiltration, markers and checkpoint-associated genes were analyzed by TIMER 2.0, ACLBI and TCGA database. <b>Results:</b> In this study, we investigated the expression and function of MCM3 in HCC. MCM3 was highly expressed in a variety of tumors including HCC, and high MCM3 expression was positively associated with various clinicopathological parameters and acted as an independent factor of the poor prognosis for overall survival in HCC. Meanwhile, immune characteristics analysis indicated that high MCM3 expression was related to the level of immune cell infiltration and immune checkpoints in HCC. Our functional enrichment analysis indicated that MCM3 is mainly involved in the cell cycle and cell metabolic related pathways. Moreover, <i>in vitro</i> and <i>in vivo</i> experiments further confirmed that MCM3 could promote the proliferation of HCC by regulating cell cycle progression. <b>Conclusions:</b> Our results indicated that MCM3 was up-regulated in HCC and might become a biomarker in the diagnosis and treatment of patients with HCC.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 5","pages":"1538-1554"},"PeriodicalIF":3.3,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11843239/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143483301","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":"Integrative multi-omics and machine learning identify a robust signature for discriminating prognosis and therapeutic targets in bladder cancer.","authors":"Zhiyong Tan, Xiaorong Chen, Yinglong Huang, Shi Fu, Haihao Li, Chen Gong, Dihao Lv, Chadanfeng Yang, Jiansong Wang, Mingxia Ding, Haifeng Wang","doi":"10.7150/jca.105066","DOIUrl":"10.7150/jca.105066","url":null,"abstract":"<p><p><b>Background:</b> Bladder cancer (BLCA) is a common malignant tumor whose pathogenesis has not yet been fully elucidated. This study analyzed prognostic genes in BLCA by integrating transcriptomics and proteomics data, and established prognostic models, aiming to offer novel insights for BLCA therapy. <b>Methods:</b> Transcriptomic, proteomic, and protein acetylation sequencing were conducted on six BLCA tumor tissues and six paraneoplastic tissue samples. Furthermore, data from TCGA-BLCA, GSE13507, and single-cell RNA sequencing (scRNA-seq) datasets were integrated. Initially, differential expression analysis identified candidate genes regulated by acetylation. These genes were further refined by intersecting with scRNA-DEG obtained from the scRNA-seq dataset, resulting in the identification of key genes. Subsequently, consistency clustering analysis was performed based on these key genes. Prognostic models were then developed utilizing Cox regression analysis and least absolute shrinkage and selection operator (LASSO) Cox regression. Independent prognostic factors were determined through independent prognostic analysis, followed by the establishment of a nomogram model. Additionally, gene set enrichment analysis (GSEA), immune cell infiltration analysis, mutation analysis, and drug sensitivity analysis were conducted between the two risk groups to elucidate underlying mechanisms. <b>Results:</b> A total of 15 key genes were obtained by crossing 284 candidate genes with 510 scRNA-DEGs. Patients in the TCGA-BLCA dataset were categorized into two subtypes based on the 15 key genes. Next, a risk model was developed using five prognostic genes (CTSE, XAGE2, MAP1A, CASQ2, and FXYD6), and a nomogram model was developed using age, pathologic T, pathologic N, and risk score. A total of 1089 GO entries and 49 KEGG pathways, including cytokine-cytokine receptor interactions, ECM receptor interactions, etc., were involved in all genes in both risk groups. The immunization score, matrix score, and ESTIMATE score were significantly higher in the low-risk group than in the high-risk group. <b>Conclusion:</b> CTSE, XAGE2, MAP1A, CASQ2 and FXYD6 were selected as prognostic genes in BLCA, risk model and nomogram model predicting the prognosis of BLCA patients were constructed. These were helpful for prognostic assessment of BLCA.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 5","pages":"1479-1503"},"PeriodicalIF":3.3,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11843231/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143483201","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":"Molecular insight into histone methylation as a novel target for oral squamous cell carcinoma: future hope in personalised medicine.","authors":"Peramaiyan Rajendran, Monisha Prasad, Enas M Ali, Ramya Sekar, Abdullah M AlZahrani, Mohmed Isaqali Karobari, Marwa Azmy M Genena, Basem M Abdallah","doi":"10.7150/jca.103243","DOIUrl":"10.7150/jca.103243","url":null,"abstract":"<p><p>Oral squamous cell carcinoma (OSCC) is the most prevalent type of malignant epithelial neoplasm that affects the oral cavity. It has been a significant health concern in many countries for a long time since it was usually treated with surgery, radiation, and/or chemotherapy. Drug resistance is the primary issue in patient populations and scientific research, which promotes OSCC tumour cell invasion and migration. Thus, identifying highly specific therapeutic targets could be the potential approach for more successful treatment of OSCC. It is still challenging to understand the genetic causes of oral carcinogenesis due to its highly varied clinic-pathological parameters. It is important to remember that signaling channels and complexes that affect chromatin accessibility control gene expression, which in turn affects cell development and differentiation. Histones undergo post-translational alteration to give this platform. Understanding the processes of gene regulation through histone methylation and its modifications could enhance the early detection, prognostic prediction, and therapy of OSCC. To be properly used as a therapeutic target, histone methylation in OSCC requires more investigation. This review details the dysregulated histone methylation and the modifying enzymes linked to the development and aetiology of OSCC. Furthermore, the part that lysine methylation plays in cell migration, chemo-resistance, and OSCC invasion is also investigated.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 5","pages":"1575-1590"},"PeriodicalIF":3.3,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11843246/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143483287","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":"Tumor cell-derived hyaluronan fragments induce endocytosis of S1PR1 to promote lymphangiogenesis through LYVE-1-Src pathway.","authors":"Mengying Jiang, Dandan Chen, Zhangrun Xu, Yiwen Liu, Cuixia Yang, Guoliang Zhang, Qian Guo, Feng Gao, Yiqing He, Yan Du","doi":"10.7150/jca.104309","DOIUrl":"10.7150/jca.104309","url":null,"abstract":"<p><p>Sphingosine-1-phosphate receptor-1 (S1PR1), a G protein-coupled receptor, has been reported to be involved in lymphangiogenesis. Degradations of extracellular matrix (ECM) are recognized as dynamic modulators in regulating the formation of new lymphatic vessels. However, little research has studied the ECM on S1PR1 in the regulation of lymphatic endothelial cells (LECs) in tumor lymphangiogenesis. Here we attempt to investigate hyaluronan fragments abundant in tumor microenvironment (TME) on S1PR1 in new lymphatic vessel formation. First, we verified that low molecular weight hyaluronan (LMW-HA) derived from tumor cells could promote LECs migration and capillary-like tube formation. Then, we demonstrated that S1PR1 on LECs underwent internalization into the endoplasmic reticulum in response to LMW-HA treatments. Notably, the S1PR1 endocytosis could upregulate lymphangiogenesis. Next, we found that the ablation of lymphatic vessel endothelial hyaluronan receptor 1 (LYVE-1) could attenuate the S1PR1 endocytosis, implying a novel role of LMW-HA/LYVE-1 in the S1PR1 cycling pathway. Furthermore, we identified that LMW-HA/LYVE-1 interaction could activate Src kinase which in turn upregulates S1PR1 tyrosine phosphorylation, resulting in S1PR1 endocytosis. Collectively, our findings suggested that hyaluronan fragments in TME could induce S1PR1 internalization in LECs, leading to lymphangiogenesis promotion.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 5","pages":"1466-1478"},"PeriodicalIF":3.3,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11843240/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143482041","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}