Cancer Biology & Therapy最新文献

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Association between the IL1B-511 C>T polymorphism and the risk of hematologic malignancies: data from a meta-analysis. IL1B-511 C>T 多态性与血液系统恶性肿瘤风险之间的关系:一项荟萃分析的数据。
IF 4.4 4区 医学
Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-07-22 DOI: 10.1080/15384047.2024.2382503
Fabíola Silva Alves-Hanna, Felipe Rodolfo Pereira Silva, Daniele Sá Pereira, Alessandro Luiz Araújo Bentes Leal, Fábio Magalhães-Gama, Allyson Guimarães Costa
{"title":"Association between the <i>IL1B-511 C>T</i> polymorphism and the risk of hematologic malignancies: data from a meta-analysis.","authors":"Fabíola Silva Alves-Hanna, Felipe Rodolfo Pereira Silva, Daniele Sá Pereira, Alessandro Luiz Araújo Bentes Leal, Fábio Magalhães-Gama, Allyson Guimarães Costa","doi":"10.1080/15384047.2024.2382503","DOIUrl":"10.1080/15384047.2024.2382503","url":null,"abstract":"<p><p>The relationship between the <i>IL1B-511C>T</i> (rs16944) polymorphism and the risk of developing hematologic malignancies remains controversial. Thus, we performed a meta-analysis to evaluate the association between <i>IL1B-511C>T</i> polymorphism and the risk of developing hematologic malignancies. A comprehensive search was conducted to identify all eligible studies on <i>IL1B-511C>T</i> polymorphism and hematologic malignancies. Twelve case-control studies, with 2,896 cases and 3,716 controls, were selected for the analysis. The overall data failed to indicate a significant association between <i>IL1B-511C>T</i> polymorphism and the risk of hematologic malignancies (OR:1.06, 95% Confidence Interval [CI]: 0.93-1.22). Moreover, non-significant associations were observed in a stratified analysis according to neoplasm type (multiple myeloma, Hodgkin's lymphoma, and non-Hodgkin's lymphoma), ethnicity (European and Asian), and Hardy-Weinberg equilibrium. In summary, our results suggest that there is no association between the <i>IL1B-511C>T</i> polymorphism and the risk of hematologic malignancies. As such, further large-scale studies are needed to confirm our findings.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2382503"},"PeriodicalIF":4.4,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11268255/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141747530","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}
引用次数: 0
Mechanism investigation of Forsythoside A against esophageal squamous cell carcinoma in vitro and in vivo. 连翘苷 A 对食管鳞状细胞癌的体内外作用机制研究
IF 4.4 4区 医学
Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-07-24 DOI: 10.1080/15384047.2024.2380023
Yingying Yang, Junru Shen, Peiyuan Deng, Ping Chen
{"title":"Mechanism investigation of Forsythoside A against esophageal squamous cell carcinoma <i>in vitro</i> and <i>in vivo</i>.","authors":"Yingying Yang, Junru Shen, Peiyuan Deng, Ping Chen","doi":"10.1080/15384047.2024.2380023","DOIUrl":"10.1080/15384047.2024.2380023","url":null,"abstract":"<p><strong>Context: </strong>Forsythoside A (FSA) was extracted from Forsythia suspensa, a traditional Chinese medicine, which has been demonstrated to exert anti-inflammatory, antibacterial, and other pharmacological effects. However, the anticancer effect of FSA in esophageal squamous cell carcinoma (ESCC) has not been documented.</p><p><strong>Objective: </strong>The present study aimed to elucidate the mechanism of FSA against ESCC.</p><p><strong>Materials and methods: </strong>Network pharmacology and molecular docking were employed to predict the mechanism. FSA was utilized to treat ESCC cell lines KYSE450 and KYSE30, followed by CCK-8 assay, cell cloning formation assay, flow cytometry, Western blot, RNA-seq analysis, and subsequent in vivo experiments.</p><p><strong>Results: </strong>Network pharmacology and molecular docking predicted that the therapeutic effect of FSA in ESCC is mediated through proteins such as BCL2 and BAX, influencing KEGG pathways associated with apoptosis. In vitro experiments showed that FSA inhibited cell proliferation and plate clone formation, promoted cell apoptosis and impacted the cell cycle distribution of G2/M phase by regulating BCL2, BAX, and p21. Further RNA-seq in KYSE450 cells showed that FSA regulated the expression of 223 genes, specifically affecting the biological process of epidermal development. In vivo experiments showed that gastric administration of FSA resulted in notable reductions in both tumor volume and weight by regulating BCL2, BAX, and p21. 16S rRNA sequencing showed that FSA led to significant changes of beta diversity. Abundance of 11 specific bacterial taxa were considerably changed following administration of FSA.</p><p><strong>Conclusions: </strong>This study presents a novel candidate drug against ESCC and establishes a foundation for future clinical application.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2380023"},"PeriodicalIF":4.4,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11271126/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141751184","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}
引用次数: 0
Exploring the molecular mechanisms and therapeutic potential of SMAD4 in colorectal cancer. 探索 SMAD4 在结直肠癌中的分子机制和治疗潜力。
IF 4.4 4区 医学
Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-08-20 DOI: 10.1080/15384047.2024.2392341
Hui Shan, Guangyu Tian, Yeqing Zhang, Zhiyuan Qiu
{"title":"Exploring the molecular mechanisms and therapeutic potential of SMAD4 in colorectal cancer.","authors":"Hui Shan, Guangyu Tian, Yeqing Zhang, Zhiyuan Qiu","doi":"10.1080/15384047.2024.2392341","DOIUrl":"10.1080/15384047.2024.2392341","url":null,"abstract":"<p><p>Colorectal Cancer (CRC) is the third most common cancer worldwide, and the occurrence and development of CRC are influenced by the molecular biology characteristics of CRC, especially alterations in key signaling pathways. The transforming growth factor-β (TGF-β) plays a crucial role in cellular growth, differentiation, migration, and apoptosis, with SMAD4 protein serving as a key transcription factor in the TGF-β signaling pathway, thus playing a significant role in the onset and progression of CRC. CRC is one of the malignancies with a high mortality rate worldwide. Despite significant research progress in recent years, especially regarding the role of SMAD4, its dual role in the early and late stages of tumor progression has promoted further discussion on its complexity as a therapeutic target, highlighting the urgent need for a deeper analysis of its role in CRC. This review aims to explore the function of SMAD4 protein in CRC and its potential as a therapeutic target.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2392341"},"PeriodicalIF":4.4,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11340766/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142008296","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}
引用次数: 0
PDLIM1, a novel miR-3940-5p target, regulates the malignant progression of diffuse large B-cell lymphoma. 新型 miR-3940-5p 靶点 PDLIM1 可调控弥漫大 B 细胞淋巴瘤的恶性进展。
IF 4.4 4区 医学
Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-11-20 DOI: 10.1080/15384047.2024.2429175
Jinfeng Zhu, Huifang Xiao, Chuntuan Li, Xiaofeng Li, Jinyang Zheng, Xihu Yao, Shaoxiong Wang, Xiongpeng Zhu
{"title":"PDLIM1, a novel miR-3940-5p target, regulates the malignant progression of diffuse large B-cell lymphoma.","authors":"Jinfeng Zhu, Huifang Xiao, Chuntuan Li, Xiaofeng Li, Jinyang Zheng, Xihu Yao, Shaoxiong Wang, Xiongpeng Zhu","doi":"10.1080/15384047.2024.2429175","DOIUrl":"10.1080/15384047.2024.2429175","url":null,"abstract":"<p><strong>Background: </strong>PDZ And LIM domain protein 1 (PDLIM1), a protein-coding gene, has been widely reported to exhibit differential expression patterns across various human cancers, including hematological malignancies. This study aimed to investigate PDLIM1 expression pattern and its functional role in diffuse large B-cell lymphoma (DLBCL) both <i>in vitro</i> and <i>in vivo</i>.</p><p><strong>Methods: </strong>PDLIM1 expression patterns were reanalyzed using data from the Gene Expression Omnibus, and the results were subsequently validated in patient tissue samples and a panel of four DLBCL cell lines. MicroRNA-3940-5p (miR-3940-5p) was identified as an upstream regulator of PDLIM1. The interaction between PDLIM1 and miR-3940-5p and its effects on DLBCL cellular activities and cancer development were further explored using a DLBCL mouse model.</p><p><strong>Results: </strong>Elevated PDLIM1 expression was observed in DLBCL cells and tissues. Reduced cell proliferation and increased DLBCL cell apoptosis were observed following the knockdown of this gene. Furthermore, short hairpin RNA (shRNA)-mediated PDLIM1 knockdown diminished tumorigenesis of DLBCL cells in nude mice. miR-3940-5p was identified as an upstream regulator of PDLIM1. PDLIM1 expression and function were negatively modulated by the upregulation of miR-3940-5p, consequently affecting the malignant phenotype of DLBCL cells.</p><p><strong>Conclusion: </strong>These findings suggest that the miR-3940-5p/PDLIM1 axis may play a crucial role in DLBCL pathogenesis and could potentially be exploited for therapeutic interventions.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2429175"},"PeriodicalIF":4.4,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11581179/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142675164","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}
引用次数: 0
The predictors of lymphopenia and its effects on survival in locally advanced esophageal squamous cell carcinoma. 局部晚期食管鳞状细胞癌淋巴细胞减少的预测因素及其对生存期的影响。
IF 4.4 4区 医学
Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-07-01 DOI: 10.1080/15384047.2024.2371632
Danjing Luo, Qiulu Zhong, Haiying Yue, Jue Wang, Qianfu Liang, Wenqi Liu, Xiaodong Zhu
{"title":"The predictors of lymphopenia and its effects on survival in locally advanced esophageal squamous cell carcinoma.","authors":"Danjing Luo, Qiulu Zhong, Haiying Yue, Jue Wang, Qianfu Liang, Wenqi Liu, Xiaodong Zhu","doi":"10.1080/15384047.2024.2371632","DOIUrl":"10.1080/15384047.2024.2371632","url":null,"abstract":"<p><p>To investigate the impact of the effective radiation dose to immune cells (EDIC) and gross tumor volume (GTV) on lymphopenia and survival in patients with locally advanced esophageal squamous cell carcinoma (LAESCC). Between January 2013 and December 2020, 272 LAESCC patients were treated with definitive radiotherapy in two institutions. Based on radiation doses to the lungs, heart, and body region scanned, EDIC was calculated as an equal uniform dose to the total blood considering blood flow and fraction effect. The radiotherapy plan was used to calculate the GTVs. Lymphopenia was graded based on the lowest lymphocyte count during RT. The overall survival (OS), progress-free survival (PFS), and local recurrence-free survival (LRFS) were analyzed statistically. The lowest lymphocyte count was significantly correlated with EDIC (<i>r</i>= -0.389, <i>p</i> < .001) and GTV (<i>r</i>= -0.211, <i>p</i> < .001). Lymphopenia, EDIC, and GTV are risk factors for patients with ESCC. In a Kaplan-Meier analysis with EDIC and GTV as stratification factors, lymphopenia was not associated with OS in the EDIC>12.9 Gy group (<i>p</i> = .294)and EDIC ≤ 12.9 Gy group, and it was also not associated with OS in GTV>68.8 cm<sup>3</sup> group (<i>p</i> = .242) and GTV ≤ 68.8 cm<sup>3</sup> group(<i>p</i> = .165). GTV and EDIC had an impact on the relationship between lymphopenia and OS in patients with LAESCC undergoing definitive RT. Poorer OS, PFS, and LRFS are correlated with lymphopenia, higher EDIC, and larger GTV.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2371632"},"PeriodicalIF":4.4,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11218796/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141466345","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}
引用次数: 0
Evaluating massage therapy for radiation-induced fibrosis in rats: preliminary findings and palpation results. 评估按摩疗法对大鼠放射性纤维化的影响:初步发现和触诊结果。
IF 4.4 4区 医学
Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-12-02 DOI: 10.1080/15384047.2024.2436694
Geoffrey M Bove, Holly McMillan, Mary F Barbe
{"title":"Evaluating massage therapy for radiation-induced fibrosis in rats: preliminary findings and palpation results.","authors":"Geoffrey M Bove, Holly McMillan, Mary F Barbe","doi":"10.1080/15384047.2024.2436694","DOIUrl":"10.1080/15384047.2024.2436694","url":null,"abstract":"<p><p>Radiation-induced fibrosis (RIF) is a common side effect of cancer treatment, but can manifest into a devastating syndrome for which there is no preventive measure or cure. In rats who perform a repetitive work task, who left untreated develop signs and symptoms that resemble repetitive motion disorders in humans, we have shown that manual therapy prevents the development of fibrosis and other key biomarkers. The fibrosis of RIF and repetitive motion disorders has similar biomarkers. In rats, we sought to determine if manual therapy would alter key biomarkers of post-irradiation fibrosis following X-ray irradiation given to the rat forelimb. One limb of rats was given a damaging dose of X-ray irradiation. Some limbs were massaged using a protocol previously described and characterized. Serum inflammatory markers, histological assays of tissue fibrosis and nerve pathology, and electrophysiology for neuropathic discharge were assayed after 8 weeks. We also tested if an experienced therapist could identify the irradiated limb using blinded palpation at the 8 week end-point. While preliminary assays showed robust changes compared to control limbs, the other assays did not show similar pathology. Our therapist could detect each irradiated limb. Serum inflammatory markers were reduced by massage to the irradiated limb. We conclude that blinded palpation is sensitive to detect subtle changes in tissue following irradiation. In contrast to the preliminary studies, the dose of irradiation used was insufficient to induce long-lasting deep fibrosis or nerve degeneration. We suspect that a difference in housing, and thus physical activity, was the plausible reason for this difference.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2436694"},"PeriodicalIF":4.4,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11622610/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142766511","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}
引用次数: 0
Role and mechanism of COL3A1 in regulating the growth, metastasis, and drug sensitivity in cisplatin-resistant non-small cell lung cancer cells. COL3A1在调节顺铂耐药非小细胞肺癌细胞的生长、转移和药物敏感性中的作用和机制
IF 3.6 4区 医学
Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-03-26 DOI: 10.1080/15384047.2024.2328382
Jiankun Ren, Songwei Zhao, Junyu Lai
{"title":"Role and mechanism of COL3A1 in regulating the growth, metastasis, and drug sensitivity in cisplatin-resistant non-small cell lung cancer cells.","authors":"Jiankun Ren, Songwei Zhao, Junyu Lai","doi":"10.1080/15384047.2024.2328382","DOIUrl":"10.1080/15384047.2024.2328382","url":null,"abstract":"<p><p>Non-small cell lung cancer (NSCLC) is among the most difficult malignancies to treat. Type III collagen (COL3A1) can affect the progression and chemoresistance development of NSCLC. We herein explored the mechanism that drives COL3A1 dysregulation in NSCLC. Potential RNA-binding proteins (RBPs) and transcription factors (TFs) that could bind to COL3A1 were searched by bioinformatics. mRNA expression was detected by quantitative PCR. Protein expression was evaluated using immunoblotting and immunohistochemistry. The effects of the variables were assessed by gauging cell growth, invasiveness, migratory capacity, apoptosis, and cisplatin (DDP) sensitivity. The direct YY1/COL3A1 relationship was confirmed by ChIP and luciferase reporter experiments. Xenograft experiments were done to examine COL3A1's function in DDP efficacy. COL3A1 showed enhanced expression in DDP-resistant NSCLC. In H460/DDP and A549/DDP cells, downregulation of COL3A1 exerted inhibitory functions in cell growth, invasiveness, and migration, as well as promoting effects on cell DDP sensitivity and apoptosis. Mechanistically, ELAV-like RNA binding protein 1 (ELAVL1) enhanced the mRNA stability and expression of COL3A1, and Yin Yang 1 (YY1) promoted the transcription and expression of COL3A1. Furthermore, upregulation of COL3A1 reversed ELAVL1 inhibition- or YY1 deficiency-mediated functions in DDP-resistant NSCLC cells. Additionally, COL3A1 downregulation enhanced the anti-tumor efficacy of DDP in vivo. Our investigation demonstrates that COL3A1 upregulation, induced by both RBP ELAVL1 and TF YY1, exerts important functions in phenotypes of NSCLC cells with DDP resistance, offering an innovative opportunity in the treatment of drug-resistant NSCLC.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2328382"},"PeriodicalIF":3.6,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10968311/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140287029","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}
引用次数: 0
MDFI promotes the proliferation and tolerance to chemotherapy of colorectal cancer cells by binding ITGB4/LAMB3 to activate the AKT signaling pathway. MDFI 通过结合 ITGB4/LAMB3 激活 AKT 信号通路,促进结直肠癌细胞的增殖和对化疗的耐受性。
IF 3.6 4区 医学
Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-02-20 DOI: 10.1080/15384047.2024.2314324
Ding Ma, Shuwen Liu, Kua Liu, Lingkai Kong, Lingjun Xiao, Qilei Xin, Chunping Jiang, Junhua Wu
{"title":"MDFI promotes the proliferation and tolerance to chemotherapy of colorectal cancer cells by binding ITGB4/LAMB3 to activate the AKT signaling pathway.","authors":"Ding Ma, Shuwen Liu, Kua Liu, Lingkai Kong, Lingjun Xiao, Qilei Xin, Chunping Jiang, Junhua Wu","doi":"10.1080/15384047.2024.2314324","DOIUrl":"10.1080/15384047.2024.2314324","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is one of the most lethal cancers. Single-cell RNA sequencing (scRNA-seq) and protein-protein interactions (PPIs) have enabled the systematic study of CRC. In our research, the activation of the AKT pathway in CRC was analyzed by KEGG using single-cell sequencing data from the GSE144735 dataset. The correlation and PPIs of MDFI and ITGB4/LAMB3 were examined. The results were verified in the TCGA and CCLE and further tested by coimmunoprecipitation experiments. The effect of MDFI on the AKT pathway via ITGB4/LAMB3 was validated by knockdown and lentiviral overexpression experiments. The effect of MDFI on oxaliplatin/fluorouracil sensitivity was probed by colony formation assay and CCK8 assay. We discovered that MDFI was positively associated with ITGB4/LAMB3. In addition, MDFI was negatively associated with oxaliplatin/fluorouracil sensitivity. MDFI upregulated the AKT pathway by directly interacting with LAMB3 and ITGB4 in CRC cells, and enhanced the proliferation of CRC cells via the AKT pathway. Finally, MDFI reduced the sensitivity of CRC cells to oxaliplatin and fluorouracil. In conclusion, MDFI promotes the proliferation and tolerance to chemotherapy of colorectal cancer cells, partially through the activation of the AKT signaling pathway by the binding to ITGB4/LAMB3. Our findings provide a possible molecular target for CRC therapy.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2314324"},"PeriodicalIF":3.6,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10880501/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139905144","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}
引用次数: 0
Establishment of a visualized mouse orthotopic xenograft model of nasopharyngeal carcinoma. 建立鼻咽癌可视化小鼠正位异种移植模型。
IF 4.4 4区 医学
Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-08-29 DOI: 10.1080/15384047.2024.2382531
Wei Chen, Wei-Min Chen, Si-Xia Chen, Li Jiang, Ge-Ge Shu, Yuan-Xiu Yin, Zhi-Peng Quan, Zi-Yan Zhou, Ming-Jun Shen, Ya-Ting Qin, Chao-Lin Yang, Xue-Jin Su, Min Kang
{"title":"Establishment of a visualized mouse orthotopic xenograft model of nasopharyngeal carcinoma.","authors":"Wei Chen, Wei-Min Chen, Si-Xia Chen, Li Jiang, Ge-Ge Shu, Yuan-Xiu Yin, Zhi-Peng Quan, Zi-Yan Zhou, Ming-Jun Shen, Ya-Ting Qin, Chao-Lin Yang, Xue-Jin Su, Min Kang","doi":"10.1080/15384047.2024.2382531","DOIUrl":"10.1080/15384047.2024.2382531","url":null,"abstract":"<p><p>Mouse orthotopic xenograft tumor models are commonly employed in studies investigating the mechanisms underlying the development and progression of tumors and their preclinical treatment. However, the unavailability of mature and visualized orthotopic xenograft models of nasopharyngeal carcinoma limits the development of treatment strategies for this cancer. The aim of this study was to provide a simple and reliable method for building an orthotopic xenograft model of nasopharyngeal carcinoma. Human nasopharyngeal carcinoma (C666-1-luc) cells, stably expressing the firefly luciferase gene, were injected subcutaneously into the right axilla of BALB/C nude mice. Four weeks later, the resulting subcutaneous tumors were cut into small blocks and grafted into the nasopharynx of immunodeficient BALB/C nude mice to induce tumor formation. Tumor growth was monitored by bioluminescence imaging and small animal magnetic resonance imaging (MRI). The expression of histological and immunological antigens associated with orthotopic xenograft nasopharyngeal carcinoma was analyzed by tissue section analysis and immunohistochemistry (IHC). A visualized orthotopic xenograft nasopharyngeal carcinoma model was successfully developed in this study. Luminescence signal detection, micro-MRI, and hematoxylin and eosin staining revealed the successful growth of tumors in the nasopharynx of the nude mice. Moreover, IHC analysis detected cytokeratin (CK), CK5/6, P40, and P63 expression in the orthotopic tumors, consistent with the reported expression of these antigens in human nasopharyngeal tumors. This study established a reproducible, visual, and less lethal orthotopic xenograft model of nasopharyngeal carcinoma, providing a platform for preclinical research.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2382531"},"PeriodicalIF":4.4,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11364074/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142104699","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}
引用次数: 0
HSPB8-BAG3 chaperone complex modulates cell invasion in intrahepatic cholangiocarcinoma by regulating CASA-mediated Filamin A degradation. HSPB8-BAG3伴侣复合物通过调节CASA介导的Filamin A降解来调节肝内胆管癌的细胞侵袭。
IF 4.4 4区 医学
Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-08-31 DOI: 10.1080/15384047.2024.2396694
Bo Shu, Yu Wen, Ronghua Lin, Chao He, Cailan Luo, Fazhao Li
{"title":"HSPB8-BAG3 chaperone complex modulates cell invasion in intrahepatic cholangiocarcinoma by regulating CASA-mediated Filamin A degradation.","authors":"Bo Shu, Yu Wen, Ronghua Lin, Chao He, Cailan Luo, Fazhao Li","doi":"10.1080/15384047.2024.2396694","DOIUrl":"10.1080/15384047.2024.2396694","url":null,"abstract":"<p><p>The incidence of intrahepatic cholangiocarcinoma (ICC) is steadily rising, and it is associated with a high mortality rate. Clinical samples were collected to detect the expression of HSPB8 and BAG3 in ICC tissues. ICC cells were cultured and transfected with plasmids that overexpressed or silenced specific genes to investigate the impact of gene expression alterations on cell function. qPCR and Western blot techniques were utilized to measure gene and protein expression levels. A wound healing assay was conducted to assess cell migration ability. The Transwell assay was used to assess cell invasion ability. Co-IP was used to verify the binding relationship between HSPB8 and BAG3. The effects of HSPB8 and BAG3 on lung metastasis of tumors in vivo were verified by constructing a metastatic tumor model. Through the above experiments, we discovered that the expressions of HSPB8 and BAG3 were up-regulated in ICC tissues and cells, and their expressions were positively correlated. The metastatic ability of ICC cells could be promoted or inhibited by upregulating or downregulating the expression of BAG3. Furthermore, the HSPB8-BAG3 chaperone complex resulted in the abnormal degradation of Filamin A by activating autophagy. Increased expression of Filamin A inhibits the migration and invasion of ICC cells. Overexpression of HSPB8 and BAG3 in vivo promoted the lung metastasis ability of ICC cells. The HSPB8-BAG3 chaperone complex promotes ICC cell migration and invasion by regulating CASA-mediated degradation of Filamin A, offering insights for enhancing ICC therapeutic strategies.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2396694"},"PeriodicalIF":4.4,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11370900/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142104700","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}
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