Cancer Control最新文献

{"title":"The Role of Tumor Stem Cells in Colorectal Cancer Drug Resistance.","authors":"Chen Zhong, Guojuan Wang, Min Guo, Naicheng Zhu, Xiudan Chen, Yuwei Yan, Nanxin Li, Wenyan Yu","doi":"10.1177/10732748241274196","DOIUrl":"10.1177/10732748241274196","url":null,"abstract":"<p><p><b>Background:</b> Colorectal cancer is a major cause of mortality among the prevalent malignant tumors of the gastrointestinal tract. Although chemotherapy is a standard treatment for colorectal cancer, its efficacy is limited by chemoresistance. Recent studies have investigated targeting tumor stem cells as a potential new therapeutic approach for addressing chemoresistance in colorectal cancer. Colorectal cancer frequently relapses, with tumor stem cells often representing one of the leading causes of treatment failure. <b>Purpose:</b> Understanding drug resistance in colorectal cancer stem cells is crucial for improving treatment outcomes. By focusing on developing targeted therapies that specifically address drug resistance in colorectal cancer stem cells, there is potential to make significant advancements in the treatment of colorectal cancer.This approach may lead to more effective and lasting outcomes in patients battling colorectal cancer. <b>Research Design:</b> In this review, a comprehensive overview of recent research on colorectal cancer stem cell treatment resistance is presented.Results: Elucidating the key underlying mechanisms. This review also highlights the potential benefits of targeted therapies in overcoming colorectal cancer resistance to treatment. <b>Conclusions:</b> CCSCs are key players in drug resistance of CRC, indicating their potential as targets for effective therapy. Elucidating their role in this process could aid in discovering tailored treatment strategies.The significance of signaling pathways, TME, and miRNA in regulating drug resistance in CCSCs is been highlighted.</p>","PeriodicalId":49093,"journal":{"name":"Cancer Control","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11367616/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142113873","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Impact of Health Inequities on Population-Based Breast Cancer Survival in a Colombian Population, 2008-2015.","authors":"Nelson Arias-Ortiz, Juan David Rodríguez-Betancourt, Jhon Eder Toro-Toro, Édgar Navarro-Lechuga, Daniel Marcelo Jurado-Fajardo, Karen Cárdenas-Garzón, Gloria Inés Sánchez-Vásquez","doi":"10.1177/10732748241244928","DOIUrl":"10.1177/10732748241244928","url":null,"abstract":"<p><strong>Objective: </strong>To obtain breast cancer survival estimates in Manizales, Colombia, considering socioeconomic level, health insurance regime and residential area, while adjusting for age, histology and stage at diagnosis.</p><p><strong>Methods: </strong>Analytical cohort study based on breast cancer incident cases recorded by the Population-based Manizales Cancer Registry between 2008-2015. Patients were followed-up for 60 months. Cause-specific survival was calculated using the Kaplan-Meier method for variables of interest, with the Wilcoxon-Breslow-Gehan test for differences. Cox multivariate regression models were fitted.</p><p><strong>Results: </strong>856 breast cancer cases were included. The 5-year cause-specific survival for the entire cohort was 78.2%. It was higher in women with special/exception health insurance, high socioeconomic level, <50 years old, ductal carcinoma, and stages I and II. Residential area did not impact survival. In Cox models, the subsidized health insurance regime (HR: 4.87 vs contributory) and low socioeconomic level (HR: 2.45 vs high) were predictors of the hazard of death in women with breast cancer, adjusted for age, histology, stage and interactions age-stage and insurance-stage. A positive interaction (synergistic effect modification) between health insurance regime and stage regarding to survival was observed.</p><p><strong>Conclusion: </strong>Socioeconomic factors significantly contribute to the inequities in breast cancer survival, independent of the stage at diagnosis. This suggests the need for comprehensive interventions to remove barriers to accessing the health system. This research provides evidence of survival gaps mediated by certain social determinants of health and generates data on the overall performance of the Colombian health system.</p>","PeriodicalId":49093,"journal":{"name":"Cancer Control","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10986169/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140337420","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SMU1 Knockdown Suppresses Gastric Carcinoma Growth, Migration, and Invasion and Modulates the Cell Cycle.","authors":"Meirui Qian, Xue Liang, Qingmei Zeng, Chen Zhang, Nan He, Jing Ma","doi":"10.1177/10732748241281716","DOIUrl":"10.1177/10732748241281716","url":null,"abstract":"<p><strong>Introduction: </strong>The role of SMU1 in DNA replication and RNA splicing is well-established, yet its specific function and dysregulated mechanisms in gastric cancer (GC) remain inadequately elucidated. This study seeks to investigate the potential oncogenic and progression-promoting effects of SMU1 in GC, with the ultimate goal of informing novel approaches for treatment and diagnosis.</p><p><strong>Methods: </strong>The study investigated the expression levels of SMU1 in GC and adjacent normal tissues by analyzing data from the TCGA (27 tissue pairs) and GEO (47 tissue pairs) databases. Immunohistochemistry was used to examine 277 tumor tissue and adjacent non-tumor tissue spots from GC tissue chips, along with relevant follow-up information. The study further assessed the proliferation, invasion, and migration capabilities of cells by manipulating SMU1 expression levels and conducting various assays, including CCK-8, EdU incorporation, colony formation, transwells, flow cytometry, and subcutaneous tumorigenesis assays.</p><p><strong>Results: </strong>Our study revealed a significant upregulation of SMU1 mRNA and protein levels in GC tissues compared to adjacent tissues. Univariate and multivariate Cox analysis demonstrated that elevated levels of SMU1 were independent prognostic factors for GC prognosis (<i>P</i> = 0.036). Additionally, median survival analysis indicated a significant association between high SMU1 expression and poor prognosis in GC patients (<i>P</i> = 0.0002). In experiments conducted both in vivo and in vitro, it was determined that elevated levels of SMU1 can enhance the proliferation, invasion, and migration of GC cells, whereas suppression of SMU1 can impede the progression of GC by modulating the G1/S checkpoint of the cell cycle.</p><p><strong>Conclusions: </strong>Our research introduces the novel idea that SMU1 could serve as a prognostic marker for GC progression, influencing cell proliferation through cell cycle activation. These results offer valuable insights into the understanding, diagnosis, and management of gastric carcinoma.</p>","PeriodicalId":49093,"journal":{"name":"Cancer Control","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11378178/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142141506","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Belief that Progress has Been Made in Curing Cancer Varies by Perception of Social Media Health Mis- and Disinformation, Education, Frequency of Social Media Use, and Healthcare System Trust: A Cross-Sectional Study.","authors":"Jim P Stimpson, Sungchul Park, Aditi Srivastava, Miguel Ángel Cano","doi":"10.1177/10732748241289259","DOIUrl":"10.1177/10732748241289259","url":null,"abstract":"<p><strong>Objective: </strong>This study explored the relationship between perceptions of health mis/disinformation on social media and belief that progress has been made in curing cancer.</p><p><strong>Methods: </strong>We analyzed cross-sectional, retrospective data collected from 4246 adult social media users in the 2022 Health Information National Trends Survey (HINTS 6). The outcome variable was the belief in whether progress has been made in curing cancer. The primary predictor variable was the perception of health mis/disinformation on social media, categorized as 'Substantial' and '< Substantial'. We also examined whether the relationship varied by health care system trust, frequency of social media use, and education. The analysis controlled for demographic, socioeconomic, and health-related factors.</p><p><strong>Results: </strong>Perception of substantial social media health mis- and disinformation was associated with a lower likelihood of believing progress has been made in curing cancer (odds ratios = 0.74, 95% CI = 0.59-0.94). Persons who perceived substantial social media health mis-and disinformation and had low trust in the health care system were less likely to believe progress has been made in curing cancer: 36% (95% CI: 28-45%). Persons who perceived substantial social media health mis-and disinformation and used social media less than daily were less likely to believe progress has been made in curing cancer: 44% (95% CI: 36-52%). Persons without a college degree who perceived substantial social media health mis-and disinformation were less likely to agree that progress has been made in curing cancer: 44% (95% CI: 39-50%).</p><p><strong>Conclusion: </strong>Exposure to misinformation on social media may be associated with negative attitudes about advances in curing cancer, particularly among social media users with low trust in the health care system trust, less frequent social media users, or those without a college degree.</p>","PeriodicalId":49093,"journal":{"name":"Cancer Control","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11450579/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142330739","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advances in Predictive Biomarkers for Anti-Angiogenic Therapy in Non-Small Cell Lung Cancer.","authors":"Weixing Zhao, Jun Jiang","doi":"10.1177/10732748241270589","DOIUrl":"10.1177/10732748241270589","url":null,"abstract":"<p><p>This study aimed to explore advances in biomarkers related to anti-angiogenic therapy in patients with non-small cell lung cancer (NSCLC), thereby enhancing treatment selection, advancing personalized and precision medicine to improve treatment outcomes and patient survival rates. This article reviews key discoveries in predictive biomarkers for anti-angiogenic therapy in NSCLC in recent years, such as (1) liquid biopsy predictive biomarkers: studies have identified activated circulating endothelial cells (aCECs) via liquid biopsy as potential predictive biomarkers for the efficacy of anti-angiogenic therapy; (2) imaging biomarkers: advanced imaging technologies, such as dynamic contrast-enhanced integrated magnetic resonance positron emission tomography (MR-PET), are used to assess tumor angiogenesis in patients with NSCLC and evaluate the clinical efficacy of anti-angiogenic drugs; (3) genetic predictive biomarkers: research has explored polymorphisms of Vascular Endothelial Growth Factor Receptor-1 (VEGFR-1) and vascular endothelial growth factor-A (VEGF-A), as well as how plasma levels of VEGF-A can predict the outcomes and prognosis of patients with non-squamous NSCLC undergoing chemotherapy combined with bevacizumab. Despite progress in identifying biomarkers related to anti-angiogenic therapy, several challenges remain, including limitations in clinical trials, heterogeneity in NSCLC, and technical hurdles. Future research will require extensive clinical validation and in-depth mechanistic studies to fully exploit the potential of these biomarkers for personalized treatment.</p>","PeriodicalId":49093,"journal":{"name":"Cancer Control","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11363049/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142082372","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"How do Cancer Patients in Economically Marginalized Neighborhoods Decide Where to Seek Care: Perspectives From Cancer Patients and Healthcare Professionals.","authors":"Rebecca Brown, Brian Petersen, Bryan O Buckley, Michael A Kyle, Jeffrey Glenn","doi":"10.1177/10732748241275404","DOIUrl":"https://doi.org/10.1177/10732748241275404","url":null,"abstract":"<p><strong>Background: </strong>The quality of cancer care affects patient outcomes. It is therefore important to understand what factors and/or barriers shape a cancer patient's decision about where to seek care. We sought to understand factors influencing decision-making for historically marginalized communities in a large metropolitan area with multiple options for cancer care, including a National Cancer Institute (NCI)-designated comprehensive cancer center.</p><p><strong>Methods: </strong>We conducted semi-structured interviews with cancer patients from economically marginalized neighborhoods in Washington D.C., and with healthcare professionals who work with patients from these areas. Participants were recruited through flyers, social media posts, and word of mouth. Two researchers analyzed the data using a combination of inductive and deductive approaches supported by the ATLAS. ti software.</p><p><strong>Results: </strong>A total of 15 interviews were conducted. Analysis revealed 3 major factors influencing where patients decide to seek care: health insurance, transportation, and prioritization of needs. Participants repeatedly identified navigating the bureaucracy of insurance enrollment and high medical costs as prohibitive to seeking care. Transportation was often mentioned in terms of convenience of use and proximity to the care center. Prioritization of needs refers to circumstances such as unstable housing, poverty, and mental illness, that some patients prioritize over seeking quality cancer care. Across these themes 2 findings arose: a discrepancy between stated and actual factors in choosing an oncologist, and the extent to which a cancer patient is able to choose their oncologist.</p><p><strong>Conclusion: </strong>This study helps explain some of the factors that influence how cancer patients in urban settings choose an oncology center, and the barriers which prohibit access.</p><p><strong>Aims of the study: </strong>This study aimed to understand how cancer patients decide where to seek treatment.</p>","PeriodicalId":49093,"journal":{"name":"Cancer Control","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11437576/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142330755","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"APOBEC-1 Complementation Factor: From RNA Binding to Cancer.","authors":"Longfei Wang, Qiong Cheng","doi":"10.1177/10732748241284952","DOIUrl":"10.1177/10732748241284952","url":null,"abstract":"<p><strong>Background: </strong>APOBEC-1 complementation factor (A1CF) and Apolipoprotein B mRNA editing enzyme, catalytic polypeptide-1 (APOBEC-1) constitute the minimal proteins necessary for the editing of apolipoprotein B (apoB) mRNA in vitro. Unlike APOBEC-1 and apoB mRNA, the ubiquitous expression of A1CF in human tissues suggests its unique biological significance, with various factors such as protein kinase C, thyroid hormones, and insulin regulating the activity and expression of A1CF. Nevertheless, few studies have provided an overview of this topic.</p><p><strong>Objective: </strong>We conducted a literature review to describe the molecular mechanisms of A1CF and its relevance to human diseases.</p><p><strong>Method: </strong>In the PubMed database, we used the keywords 'A1CF' and 'APOBEC-1 complementation factor' to collect peer-reviewed articles published in English from 2000 to 2023. Two authors independently reviewed the articles and reached the consensus.</p><p><strong>Result: </strong>After reviewing 127 articles, a total of 61 articles that met the inclusion criteria were included in the present review. Studies revealed that A1CF is involved in epigenetic regulation of reproductive cells affecting embryonic development, and that it is closely associated with the occurrence of gout due to its editing properties on apoB. A1CF can also affect the process of epithelial-mesenchymal transition in renal tubular epithelial cells and promote liver regeneration by controlling the stability of IL-6 mRNA, but no influence on cardiac function was found. Furthermore, increasing evidence suggests that A1CF may promote the occurrence and development of breast cancer, lung cancer, renal cell carcinoma, hepatocellular carcinoma, endometrial cancer, and glioma.</p><p><strong>Conclusion: </strong>This review clarifies the association between A1CF and other complementary factors and their impact on the development of human diseases, aiming to provide guidance for further research on A1CF, which can help treat human diseases and promote health.</p>","PeriodicalId":49093,"journal":{"name":"Cancer Control","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11439182/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142330738","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prediction Model of Cervical Lymph Node Metastasis in Papillary Thyroid Carcinoma.","authors":"Huiting Chen, Li Zhu, Yong Zhuang, Xiaojian Ye, Fang Chen, Jinshu Zeng","doi":"10.1177/10732748241295347","DOIUrl":"10.1177/10732748241295347","url":null,"abstract":"<p><strong>Background: </strong>The objective of this study is to develop a predictive model for the assessment of cervical lymph node metastasis risk in papillary thyroid carcinoma (PTC).</p><p><strong>Methods: </strong>A retrospective study was conducted on 212 patients with PTC who underwent initial surgical treatment from August 2022 to April 2023 in 2 hospitals. Data were randomly split into 7:3 training-validation sets. Logistic regression was used for feature selection and predictive model creation. Model performance was assessed using receiver operating characteristic (ROC) and calibration curves. Clinical utility was determined using decision curves.</p><p><strong>Results: </strong>Among the 212 patients with PTC, 104 cases (49.1%) exhibited cervical lymph node metastasis, while 108 cases (50.9%) did not. Multivariate logistic regression analysis revealed that age (OR = 0.95), FT3 (OR = 0.41), tumor maximum diameter ≥0.9 cm (OR = 1.85), intratumoral microcalcifications (OR = 1.84), and suspicious lymph node on ultrasound (OR = 2.96) were independent risk factors for lymph node metastasis in PTC patients (<i>P</i> < 0.05). The constructed model for predicting the risk of cervical lymph node metastasis demonstrated a training set ROC curve area under the curve (AUC) of 0.742 (95% CI: 0.664 - 0.821), with a cut-off value of 0.615, specificity of 87.8%, and sensitivity of 51.4%. The validation set exhibited an AUC of 0.648 (95% CI: 0.501 - 0.788), with a cut-off value of 0.644, specificity of 91.2%, and sensitivity of 43.3%. Including the BRAF V600 E mutation did not improve the model's diagnostic performance significantly. Decision curve analysis indicated clinical feasibility of the model.</p><p><strong>Conclusion: </strong>The predictive model developed in this study effectively predicts lymph node metastasis risk in PTC patients by incorporating ultrasound features, demographic characteristics, and serum parameters. However, including the BRAF V600 E mutation does not significantly improve the model's diagnostic performance.</p>","PeriodicalId":49093,"journal":{"name":"Cancer Control","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11497514/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142478683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Update on Combination Strategies of PARP Inhibitors.","authors":"Zhuoqun Lin, Lingfang Wang, Ziyu Xing, Fenfen Wang, Xiaodong Cheng","doi":"10.1177/10732748241298329","DOIUrl":"10.1177/10732748241298329","url":null,"abstract":"<p><p>The application of PARP inhibitors has revolutionized cancer treatment and has achieved significant advancements, particularly with regard to tumors with defects in genes involved in homologous recombination repair (HRR) processes, such as BRCA1 and BRCA2. Despite the promising outcomes of PARP inhibitors, certain limitations and challenges still exist, including acquired drug resistance, severe side effects, and limited therapeutic benefits for patients without homologous recombination deficiency (HRD). Various combinations involving PARP inhibitors have been developed to overcome these limitations. Among these, combinations with immune checkpoint inhibitors, antiangiogenic agents, and various small-molecule inhibitors are well-studied strategies that show great potential for optimizing the efficacy of PARP inhibitors, overcoming resistance mechanisms, and expanding target populations. However, the efficiency and overlapping toxicity of these combination strategies for cancers vary among studies, thereby limiting their use. In this review, we describe the mechanisms and limitations of PARP inhibitors to better understand the mechanisms of combination treatments. Furthermore, we have summarized recent studies on the combination of PARP inhibitors with a range of medications and discussed their clinical efficacy. The objective of this review is to enhance the comprehensiveness of information pertaining to this topic.</p>","PeriodicalId":49093,"journal":{"name":"Cancer Control","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11539152/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142584840","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CCL21 and CLDN11 Are Key Driving Factors of Lymph Node Metastasis in Gastric Cancer.","authors":"Shaofei Yang, Dandan Dong, Xunxia Bao, Rongting Lu, Pufei Cheng, Sibo Zhu, Guanghua Yang","doi":"10.1177/10732748241238616","DOIUrl":"10.1177/10732748241238616","url":null,"abstract":"<p><strong>Background: </strong>Gastric cancer (GC) is a leading cause of cancer-related deaths worldwide. Understanding the molecular mechanisms of GC metastasis is crucial for improving patient survival outcomes.</p><p><strong>Methods: </strong>RNA sequencing and analysis were performed on tissue samples from primary and lymph node metastatic lesions of gastric cancer. Differential gene analysis and functional pathway analysis were conducted. Immune infiltrating environment and protein expression levels were evaluated using immunohistochemistry. Cell experiments were conducted to investigate the role of CCL21 in GC metastasis.</p><p><strong>Results: </strong>ACTG2, CNN1, DES, MUC6, and PGC were significantly upregulated in primary tumor cells, while CCL21, MS4A1, CR2, CLDN11, and FDCSP were significantly upregulated in metastatic tumor cells. Functional pathway analysis revealed enrichment in pathways related to immune response. CLDN11 and CCL21 were found to play important roles in promoting gastric cancer metastasis. Cell experiments confirmed the role of CCL21 in promoting GC cell growth and metastasis. CCL21 is highly expressed in GC tissues and binds to CCR7, leading to upregulation of CLDN11. This results in GC-lymph node metastasis and abnormal activation of immune cells (B cells and CD4⁺ T cells).</p><p><strong>Conclusion: </strong>Inhibition of CCL21 and CLDN11 proteins may be a promising strategy for treating GC and preventing lymph node metastasis. These findings provide specific molecular markers for early lymph node metastases of GC, which can aid in developing treatment strategies and predicting patient prognosis.</p>","PeriodicalId":49093,"journal":{"name":"Cancer Control","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10981215/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140327280","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}