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Reactive oxygen species from non-thermal gas plasma (CAP): implication for targeting cancer stem cells. 来自非热气等离子体(CAP)的活性氧:对靶向癌症干细胞的影响。
IF 5.3 2区 医学 Q1 ONCOLOGY Pub Date : 2024-10-22 DOI: 10.1186/s12935-024-03523-x
Amirhesam Babajani, Afshin Eftekharinasab, Sander Bekeschus, Hassan Mehdian, Faezeh Vakhshiteh, Zahra Madjd

Cancer remains a major global health challenge, with the persistence of cancer stem cells (CSCs) contributing to treatment resistance and relapse. Despite advancements in cancer therapy, targeting CSCs presents a significant hurdle. Non-thermal gas plasma, also known as CAP, represents an innovative cancer treatment. It has recently gained attention for its often found to be selective, immunogenic, and potent anti-cancer properties. CAP is composed of a collection of transient, high-energy, and physically and chemically active entities, such as reactive oxygen species (ROS). It is acknowledged that the latter are responsible for a major portion of biomedical CAP effects. The dynamic interplay of CAP-derived ROS and other components contributes to the unique and versatile properties of CAP, enabling it to interact with biological systems and elicit various therapeutic effects, including its potential in cancer treatment. While CAP has shown promise in various cancer types, its application against CSCs is relatively unexplored. This review assesses the potential of CAP as a therapeutic strategy for targeting CSCs, focusing on its ability to regulate cellular states and achieve redox homeostasis. This is done by providing an overview of CSC characteristics and demonstrating recent findings on CAP's efficacy in targeting these cells. By contributing insights into the unique attributes of CSCs and the potential of CAP, this work contributes to an advanced understanding of innovative oncology strategies.

癌症仍然是全球健康的一大挑战,癌症干细胞(CSCs)的持续存在导致了治疗耐药性和复发。尽管癌症治疗取得了进展,但针对癌干细胞的治疗仍是一个重大障碍。非热气体等离子体(又称CAP)是一种创新的癌症治疗方法。最近,它因其经常被发现具有选择性、免疫原性和强效抗癌特性而备受关注。CAP 由一系列瞬时、高能、物理和化学活性实体组成,如活性氧(ROS)。众所周知,后者是 CAP 生物医学效应的主要原因。CAP 衍生的 ROS 和其他成分之间的动态相互作用造就了 CAP 独特而多变的特性,使其能够与生物系统相互作用并激发各种治疗效果,包括在癌症治疗中的潜力。虽然 CAP 已在多种癌症类型中显示出前景,但其对 CSCs 的应用还相对缺乏探索。本综述评估了 CAP 作为针对 CSCs 的治疗策略的潜力,重点关注其调节细胞状态和实现氧化还原平衡的能力。本文概述了 CSC 的特征,并展示了 CAP 在靶向这些细胞方面的最新研究成果。通过深入了解 CSCs 的独特属性和 CAP 的潜力,这项研究有助于加深对创新肿瘤学策略的理解。
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引用次数: 0
Curcumin attenuates smoking and drinking activated NF-κB/IL-6 inflammatory signaling axis in cervical cancer. 姜黄素可减轻吸烟和饮酒激活的宫颈癌NF-κB/IL-6炎症信号轴。
IF 5.3 2区 医学 Q1 ONCOLOGY Pub Date : 2024-10-20 DOI: 10.1186/s12935-024-03513-z
Vivek K Kashyap, Prashanth K B Nagesh, Ajay K Singh, Andrew Massey, Godwin P Darkwah, Aaron George, Sheema Khan, Bilal B Hafeez, Nadeem Zafar, Santosh Kumar, Namita Sinha, Murali M Yallapu, Meena Jaggi, Subhash C Chauhan

Background: High-risk strains of HPV are known to cause cervical cancer. Multiple clinical studies have emphasized that smoking and drinking are critical risk factors for cervical cancer and its high-grade precursors. In this study, we investigated if smoking and/or drinking augment the molecular mechanisms of cervical carcinogenesis and defined a potential therapeutic approach for their attenuation.

Methods: The impact of benzo[a]pyrene (B[a]P) and/or ethanol (EtOH) exposure on cervical cancer cells was assessed by measuring changes in their cell migration and invasion characteristics. Expression of HPV16 E6/E7, NF-κB, cytokines, and inflammation mediators was determined using qRT-PCR, immunoblotting, ELISA, luciferase reporter assay, and confocal microscopy. Herein, we used curcumin (Cur), and PLGA nanoparticle formulation of curcumin (PLGA-Cur) and determined effectiveness of free Cur and PLGA-Cur formulation on smoking and drinking activated NF-κB/IL-6 mediated inflammatory signaling pathways using in vitro cervical cancer models.

Results: Treatments with B[a]P and/or EtOH altered the expression of HPV16 E6/E7 oncogenes and EMT markers in cervical cancer cells; it also enhanced migration and invasion. In addition, B[a]P and/or EtOH exposure promoted inflammation pathways through TNF-α and NF-κB signaling, leading to IL-6 upregulation and activation of VEGF. The molecular effects caused by B[a]P and/or EtOH exposure were effectively attenuated by curcumin (Cur)/PLGA-Cur treatment.

Conclusions: These data suggest a molecular link between smoking, drinking, and HPV infectivity in cervical carcinogenesis. In addition, attenuation of these effects by treatment with Cur/PLGA-Cur treatment, implies the role of curcumin in cervical cancer prevention and treatment.

背景:众所周知,高危型人乳头瘤病毒可导致宫颈癌。多项临床研究强调,吸烟和饮酒是宫颈癌及其高级别前体的关键风险因素。在本研究中,我们调查了吸烟和/或饮酒是否会增强宫颈癌发生的分子机制,并确定了一种潜在的治疗方法来减轻其影响:方法:通过测量细胞迁移和侵袭特性的变化,评估了苯并[a]芘(B[a]P)和/或乙醇(EtOH)暴露对宫颈癌细胞的影响。使用 qRT-PCR、免疫印迹、ELISA、荧光素酶报告分析和共聚焦显微镜测定了 HPV16 E6/E7、NF-κB、细胞因子和炎症介质的表达。在此,我们使用姜黄素(Cur)和姜黄素的PLGA纳米颗粒制剂(PLGA-Cur),并利用体外宫颈癌模型确定游离姜黄素和PLGA-Cur制剂对吸烟和饮酒激活的NF-κB/IL-6介导的炎症信号通路的有效性:结果:B[a]P和/或EtOH能改变宫颈癌细胞中HPV16 E6/E7癌基因和EMT标记物的表达,还能增强迁移和侵袭。此外,B[a]P和/或EtOH暴露通过TNF-α和NF-κB信号促进炎症通路,导致IL-6上调和VEGF活化。姜黄素(Cur)/PLGA-Cur处理可有效减轻B[a]P和/或EtOH暴露引起的分子效应:这些数据表明,吸烟、饮酒和人乳头瘤病毒感染在宫颈癌发生过程中存在分子联系。此外,姜黄素/PLGA-Cur治疗可减轻这些影响,这意味着姜黄素在宫颈癌预防和治疗中的作用。
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引用次数: 0
Retraction Note: Circular RNA MYLK promotes hepatocellular carcinoma progression by increasing Rab23 expression by sponging miR-362-3p. 撤稿说明:环状 RNA MYLK 通过海绵状 miR-362-3p 增加 Rab23 的表达,从而促进肝细胞癌的进展。
IF 5.3 2区 医学 Q1 ONCOLOGY Pub Date : 2024-10-19 DOI: 10.1186/s12935-024-03530-y
Zhiqin Li, Yushu Hu, Qinglei Zeng, Hongyan Wang, Jingya Yan, Hua Li, Zujiang Yu
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引用次数: 0
CD74 is a potential biomarker predicting the response to immune checkpoint blockade. CD74 是预测免疫检查点阻断反应的潜在生物标志物。
IF 5.3 2区 医学 Q1 ONCOLOGY Pub Date : 2024-10-14 DOI: 10.1186/s12935-024-03524-w
Wen-Qi Shi, Dan-Xun Chen, Ze-Sen Du, Chun-Peng Liu, Tian-Tian Zhai, Feng Pan, Hai-Lu Chen, Wei-Nan Liao, Shao-Hong Wang, Jun-Hui Fu, Si-Qi Qiu, Zhi-Yong Wu

Background: Immune checkpoint blockade (ICB) has been improving the patient outcome in multiple cancer types. However, not all patients respond to ICB. Biomarkers are needed for selecting appropriate patients to receive ICB. CD74 is an important chaperone that regulates antigen presentation for immune response. However, the relationship between CD74 expression and ICB response remains elusive.

Methods: The unified normalized pan-cancer dataset was downloaded from the UCSC database. Wilcoxon Rank Sum Rank Tests were used to analyze the expression differences between normal and tumor samples in each tumor type. Then, the prognostic value of CD74 was determined using univariable Cox proportional hazards regression analysis. The STRING database was utilized to construct the protein-protein interaction (PPI) network of CD74 and the signal pathways were analyzed as well. The correlation of CD74 expression with immune cells and immune regulating genes was investigated in the TIMER database. The TIDE framework was utilized to evaluate the relationship between CD74 expression and the response to immunotherapy. Moreover, the localization of CD74 in the tumor immune microenvironment was verified using multiplex immunohistochemistry. Clinically annotated samples from 38 patients with esophageal cancer treated with neoadjuvant chemotherapy combined with ICB were analyzed for CD74 expression using immunohistochemistry.

Results: In this study, we investigated the prognostic and predictive value of CD74 in different types of cancer. Compared with normal tissue, the expression of CD74 was higher in tumor tissue in various cancers. High expression of CD74 was associated with improved patient prognosis in the majority of cancers. CD74 and its interacting proteins were mainly enriched in the immune-related pathways. The expression of CD74 was significantly positively correlated with B cells, CD4 T-cells, CD8 T-cells, neutrophils, macrophages and dendritic cells. TIDE analysis showed that tumors with high CD74 expression may have better responses to immunotherapy and improved patient survival. In patients with esophageal cancer who had received ICB, higher intratumoral CD74 expression was associated with improved response to ICB.

Conclusions: The findings of this study suggest that the high expression of CD74 may be a potential predictive biomarker of response to ICB.

背景:免疫检查点阻断疗法(ICB)可改善多种癌症患者的预后。然而,并非所有患者都对 ICB 有反应。需要生物标志物来选择合适的患者接受 ICB。CD74 是一种重要的伴侣蛋白,可调节免疫反应中的抗原递呈。然而,CD74的表达与ICB反应之间的关系仍然难以捉摸:方法:从 UCSC 数据库下载统一归一化的泛癌症数据集。方法:从 UCSC 数据库下载统一归一化泛癌数据集,采用 Wilcoxon 秩和检验分析各肿瘤类型中正常样本和肿瘤样本的表达差异。然后,利用单变量 Cox 比例危险回归分析确定 CD74 的预后价值。利用STRING数据库构建了CD74的蛋白-蛋白相互作用(PPI)网络,并对信号通路进行了分析。TIMER 数据库研究了 CD74 表达与免疫细胞和免疫调节基因的相关性。利用 TIDE 框架评估了 CD74 表达与免疫疗法反应之间的关系。此外,还利用多重免疫组化技术验证了 CD74 在肿瘤免疫微环境中的定位。利用免疫组化技术分析了38例接受新辅助化疗联合ICB治疗的食管癌患者的临床标本中CD74的表达情况:本研究探讨了CD74在不同类型癌症中的预后和预测价值。与正常组织相比,CD74在各种癌症的肿瘤组织中表达量更高。在大多数癌症中,CD74的高表达与患者预后的改善有关。CD74及其相互作用蛋白主要富集在免疫相关通路中。CD74的表达与B细胞、CD4 T细胞、CD8 T细胞、中性粒细胞、巨噬细胞和树突状细胞呈明显正相关。TIDE分析表明,CD74高表达的肿瘤可能对免疫疗法有更好的反应,并能提高患者的生存率。在接受过 ICB 的食管癌患者中,瘤内 CD74 表达较高的患者对 ICB 的反应较好:本研究结果表明,CD74的高表达可能是预测对ICB反应的潜在生物标志物。
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引用次数: 0
Pan-cancer analysis of Sp1 with a focus on immunomodulatory roles in gastric cancer. 对 Sp1 的泛癌症分析,重点关注其在胃癌中的免疫调节作用。
IF 5.3 2区 医学 Q1 ONCOLOGY Pub Date : 2024-10-14 DOI: 10.1186/s12935-024-03521-z
Yang Zhou, Zhenzhen Luo, Jinfeng Guo, Lixia Wu, Xiaoli Zhou, Jun Jie Huang, Daijia Huang, Li Xiao, Qiuhua Duan, Jianhua Chang, Libao Gong, Junjie Hang

Background: Sp1, a transcription factor, regulates essential cellular processes and plays important tumorigenic roles across diverse cancers. However, comprehensive pan-cancer analyses of its expression and potential immunomodulatory roles remain unexplored.

Methods: Utilizing bioinformatics tools and public datasets, we examined the expression of Sp1 across normal tissues, tumors, and immune cells, and screened for pre- and post-transcriptional modifications, including genetic alterations, DNA methylation, and protein phosphorylation, affecting its expression or function. The association of Sp1 expression with immune cell infiltration, tumor mutational burden, and immune checkpoint signaling was also investigated. Single-cell transcriptome data was used to assess Sp1 expression in immune cells in gastric cancer (GC), and findings were corroborated using immunohistochemistry and multiplex immunofluorescence in an immunotherapy-treated patient cohort. The prognostic value of Sp1 in GC patients receiving immunotherapy was evaluated with Cox regression models.

Results: Elevated Sp1 levels were observed in various cancers compared to normal tissues, with notable prominence in GC. High Sp1 expression correlated with advanced stage, poor prognosis, elevated tumor mutational burden (TMB), and microsatellite instability (MSI) status, particularly in GC. Significant correlations between Sp1 levels and CD8+ T cell and the M1 phenotype of tumor-associated macrophages were further detected upon multiplex immunofluorescence in GC samples. Interestingly, we verified that GC patients with higher Sp1 levels exhibited improved response to immunotherapy. Moreover, Sp1 emerged as a prognostic and predictive biomarker for GC patients undergoing immunotherapy.

Conclusions: Our pan-cancer analysis sheds light on the multifaceted role of Sp1 in tumorigenesis and underscores its potential as a prognostic and predictive biomarker for patients with GC undergoing immunotherapy.

背景:Sp1是一种转录因子,它调控着细胞的基本过程,并在各种癌症中发挥着重要的致癌作用。然而,对其表达和潜在免疫调节作用的泛癌症综合分析仍有待探索:利用生物信息学工具和公共数据集,我们检测了Sp1在正常组织、肿瘤和免疫细胞中的表达,并筛选了影响其表达或功能的转录前和转录后修饰,包括基因改变、DNA甲基化和蛋白质磷酸化。此外,还研究了 Sp1 表达与免疫细胞浸润、肿瘤突变负荷和免疫检查点信号转导的关系。研究人员利用单细胞转录组数据评估了胃癌(GC)免疫细胞中Sp1的表达情况,并利用免疫组化和多重免疫荧光技术在接受免疫治疗的患者队列中证实了研究结果。利用Cox回归模型评估了Sp1在接受免疫治疗的胃癌患者中的预后价值:结果:与正常组织相比,Sp1在各种癌症中的水平都有所升高,在GC中尤为突出。Sp1的高表达与晚期、预后不良、肿瘤突变负荷(TMB)升高和微卫星不稳定性(MSI)状态相关,尤其是在GC中。多重免疫荧光进一步检测了 GC 样本中 Sp1 水平与 CD8+ T 细胞和肿瘤相关巨噬细胞 M1 表型之间的显著相关性。有趣的是,我们证实 Sp1 水平较高的 GC 患者对免疫疗法的反应更好。此外,Sp1还是接受免疫治疗的GC患者的预后和预测生物标志物:我们的泛癌症分析揭示了Sp1在肿瘤发生中的多方面作用,并强调了其作为接受免疫治疗的GC患者的预后和预测生物标志物的潜力。
{"title":"Pan-cancer analysis of Sp1 with a focus on immunomodulatory roles in gastric cancer.","authors":"Yang Zhou, Zhenzhen Luo, Jinfeng Guo, Lixia Wu, Xiaoli Zhou, Jun Jie Huang, Daijia Huang, Li Xiao, Qiuhua Duan, Jianhua Chang, Libao Gong, Junjie Hang","doi":"10.1186/s12935-024-03521-z","DOIUrl":"https://doi.org/10.1186/s12935-024-03521-z","url":null,"abstract":"<p><strong>Background: </strong>Sp1, a transcription factor, regulates essential cellular processes and plays important tumorigenic roles across diverse cancers. However, comprehensive pan-cancer analyses of its expression and potential immunomodulatory roles remain unexplored.</p><p><strong>Methods: </strong>Utilizing bioinformatics tools and public datasets, we examined the expression of Sp1 across normal tissues, tumors, and immune cells, and screened for pre- and post-transcriptional modifications, including genetic alterations, DNA methylation, and protein phosphorylation, affecting its expression or function. The association of Sp1 expression with immune cell infiltration, tumor mutational burden, and immune checkpoint signaling was also investigated. Single-cell transcriptome data was used to assess Sp1 expression in immune cells in gastric cancer (GC), and findings were corroborated using immunohistochemistry and multiplex immunofluorescence in an immunotherapy-treated patient cohort. The prognostic value of Sp1 in GC patients receiving immunotherapy was evaluated with Cox regression models.</p><p><strong>Results: </strong>Elevated Sp1 levels were observed in various cancers compared to normal tissues, with notable prominence in GC. High Sp1 expression correlated with advanced stage, poor prognosis, elevated tumor mutational burden (TMB), and microsatellite instability (MSI) status, particularly in GC. Significant correlations between Sp1 levels and CD8+ T cell and the M1 phenotype of tumor-associated macrophages were further detected upon multiplex immunofluorescence in GC samples. Interestingly, we verified that GC patients with higher Sp1 levels exhibited improved response to immunotherapy. Moreover, Sp1 emerged as a prognostic and predictive biomarker for GC patients undergoing immunotherapy.</p><p><strong>Conclusions: </strong>Our pan-cancer analysis sheds light on the multifaceted role of Sp1 in tumorigenesis and underscores its potential as a prognostic and predictive biomarker for patients with GC undergoing immunotherapy.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2024-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11476248/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142458558","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
RhoA-ROCK2 signaling possesses complex pathophysiological functions in cancer progression and shows promising therapeutic potential. RhoA-ROCK2 信号在癌症进展过程中具有复杂的病理生理功能,并显示出巨大的治疗潜力。
IF 5.3 2区 医学 Q1 ONCOLOGY Pub Date : 2024-10-14 DOI: 10.1186/s12935-024-03519-7
Yidi Ning, Minying Zheng, Yue Zhang, Yuqi Jiao, Jiangping Wang, Shiwu Zhang

The Rho GTPase signaling pathway is responsible for cell-specific processes, including actin cytoskeleton organization, cell motility, cell division, and the transcription of specific genes. The implications of RhoA and the downstream effector ROCK2 in cancer epithelial-mesenchymal transition, migration, invasion, and therapy resistance associated with stem cells highlight the potential of targeting RhoA/ROCK2 signaling in therapy. Tumor relapse can occur due to cancer cells that do not fully respond to adjuvant chemoradiotherapy, targeted therapy, or immunotherapy. Rho signaling-mediated mitotic defects and cytokinesis failure lead to asymmetric cell division, allowing cells to form polyploids to escape cytotoxicity and promote tumor recurrence and metastasis. In this review, we elucidate the significance of RhoA/ROCK2 in the mechanisms of cancer progression and summarize their inhibitors that may improve treatment strategies.

Rho GTPase信号通路负责细胞特异性过程,包括肌动蛋白细胞骨架组织、细胞运动、细胞分裂和特定基因的转录。RhoA和下游效应物ROCK2在癌症上皮-间充质转化、迁移、侵袭以及与干细胞相关的耐药性中的作用,凸显了靶向RhoA/ROCK2信号在治疗中的潜力。肿瘤复发可能是由于癌细胞对辅助化放疗、靶向治疗或免疫治疗没有完全反应。Rho 信号介导的有丝分裂缺陷和细胞分裂失败会导致细胞不对称分裂,使细胞形成多倍体以逃避细胞毒性并促进肿瘤复发和转移。在这篇综述中,我们阐明了 RhoA/ROCK2 在癌症进展机制中的重要作用,并总结了可改善治疗策略的抑制剂。
{"title":"RhoA-ROCK2 signaling possesses complex pathophysiological functions in cancer progression and shows promising therapeutic potential.","authors":"Yidi Ning, Minying Zheng, Yue Zhang, Yuqi Jiao, Jiangping Wang, Shiwu Zhang","doi":"10.1186/s12935-024-03519-7","DOIUrl":"https://doi.org/10.1186/s12935-024-03519-7","url":null,"abstract":"<p><p>The Rho GTPase signaling pathway is responsible for cell-specific processes, including actin cytoskeleton organization, cell motility, cell division, and the transcription of specific genes. The implications of RhoA and the downstream effector ROCK2 in cancer epithelial-mesenchymal transition, migration, invasion, and therapy resistance associated with stem cells highlight the potential of targeting RhoA/ROCK2 signaling in therapy. Tumor relapse can occur due to cancer cells that do not fully respond to adjuvant chemoradiotherapy, targeted therapy, or immunotherapy. Rho signaling-mediated mitotic defects and cytokinesis failure lead to asymmetric cell division, allowing cells to form polyploids to escape cytotoxicity and promote tumor recurrence and metastasis. In this review, we elucidate the significance of RhoA/ROCK2 in the mechanisms of cancer progression and summarize their inhibitors that may improve treatment strategies.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2024-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11475559/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142458560","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Dysregulation of pseudouridylation in small RNAs contributes to papillary thyroid carcinoma metastasis. 小核糖核酸假苷酸化失调导致甲状腺乳头状癌转移
IF 5.3 2区 医学 Q1 ONCOLOGY Pub Date : 2024-10-14 DOI: 10.1186/s12935-024-03482-3
Xi Wang, Hengyuan Gao, Wenjun Pu, Zhipeng Zeng, Nan Xu, Xunpeng Luo, Donge Tang, Yong Dai

Background: Previous studies have indicated that ψ-modified small RNAs play crucial roles in tumor metastasis. However, the ψ-modified small RNAs during metastasis of PTC are still unclear.

Methods: We compared the pseudouridine synthase 7 (PUS7) alteration between metastatic and non-metastatic PTCs, and investigated its correlation with clinicopathological features. Additionally, we employed a small RNA ψ modification microarray to examine the small RNA ψ modification profile in both metastatic and non-metastatic PTCs, as well as paired paracancerous tissues. The key molecule involved in ψ modification, pre-miR-8082, was identified and found to regulate the expression of CD47. Experiments in vitro were conducted to further investigate the function of PUS7 and CD47 in PTC.

Results: Our results demonstrated that PUS7 was down-regulated in PTC and was closely associated with metastasis. Moreover, the ψ modification of pre-miR-8082 was found to be decreased, resulting in down-expression of pre-miR-8082 and miR-8082, leading to the loss of the inhibitory effect on CD47, thereby promoting tumor migration.

Conclusions: Our study demonstrates that PUS7 promotes the inhibition of CD47 and inhibits metastasis of PTC cells by regulating the ψ modification of pre-miR-8082. These results suggest that PUS7 and ψ pre-miR-8082 may serve as potential targets and diagnostic markers for PTC metastasis.

背景:以往的研究表明,ψ修饰的小RNA在肿瘤转移中起着至关重要的作用。然而,PTC 转移过程中的ψ修饰小 RNA 仍不清楚:方法:我们比较了转移性和非转移性PTC的假尿苷合成酶7(PUS7)改变,并研究了其与临床病理特征的相关性。此外,我们还利用小 RNA ψ修饰芯片研究了转移性和非转移性 PTC 以及配对癌旁组织的小 RNA ψ修饰概况。研究发现了参与ψ修饰的关键分子pre-miR-8082,并发现它能调控CD47的表达。为了进一步研究 PUS7 和 CD47 在 PTC 中的功能,我们进行了体外实验:结果:我们的研究结果表明,PUS7在PTC中下调,并与转移密切相关。此外,研究还发现pre-miR-8082的ψ修饰减少,导致pre-miR-8082和miR-8082下调,从而失去对CD47的抑制作用,进而促进肿瘤迁移:我们的研究表明,PUS7通过调节pre-miR-8082的ψ修饰,促进对CD47的抑制并抑制PTC细胞的转移。这些结果表明,PUS7 和 ψ pre-miR-8082 可作为 PTC 转移的潜在靶点和诊断标志物。
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引用次数: 0
Serum exosomal small nucleolar RNA (snoRNA) signatures as a predictive biomarker for benign and malignant pulmonary nodules. 血清外泌体小核RNA(snoRNA)特征作为良性和恶性肺结节的预测性生物标记物。
IF 5.3 2区 医学 Q1 ONCOLOGY Pub Date : 2024-10-14 DOI: 10.1186/s12935-024-03522-y
Fei Cao, Qian You, Feng Zhu, Yu Zhang

Low-dose CT (LDCT) is increasingly recognized as the preferred method for detecting pulmonary nodules. However, distinguishing whether a nodule is benign or malignant often necessitates repeated scans or invasive tissue sampling procedures. Therefore, there is a pressing need for non-invasive techniques to minimize unnecessary interventions. This study aim to investigate the expression profile of exosomal snoRNA in the serum of patients with benign and malignant pulmonary nodules. We identified a total of 278 snoRNAs in serum exosomes, revealing significant differences in snoRNA levels between patients with malignant and benign nodules. Specifically, the upregulated snoRNAs U78 and U37 were validated through qRT-PCR and were found significantly elevated in the serum of patients with malignant pulmonary nodules, positioning them as promising biomarkers for the early detection of lung cancer. This study underscores the potential of serum exosomal U78 and U37 as critical tools for assessing the risk of pulmonary nodules identified through CT screening.

低剂量 CT(LDCT)越来越被认为是检测肺结节的首选方法。然而,要区分结节是良性还是恶性,往往需要反复扫描或进行侵入性组织取样手术。因此,迫切需要无创技术来减少不必要的干预。本研究旨在调查良性和恶性肺结节患者血清中外泌体 snoRNA 的表达谱。我们在血清外泌体中共鉴定出 278 个 snoRNA,发现恶性和良性结节患者的 snoRNA 水平存在显著差异。特别是,通过 qRT-PCR 验证,发现恶性肺结节患者血清中上调的 snoRNA U78 和 U37 显著升高,这两个 snoRNA 有希望成为早期检测肺癌的生物标志物。这项研究强调了血清外泌体 U78 和 U37 作为评估 CT 筛查发现的肺结节风险的重要工具的潜力。
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引用次数: 0
Hypoxia-related lncRNA correlates with prognosis and immune microenvironment in uveal melanoma. 缺氧相关lncRNA与葡萄膜黑色素瘤的预后和免疫微环境有关
IF 5.3 2区 医学 Q1 ONCOLOGY Pub Date : 2024-10-09 DOI: 10.1186/s12935-024-03509-9
Yu Chen, Shen Chen, Zhenkai Wu, Quan Cheng, Dan Ji

Background: Hypoxia-related genes are linked to the prognosis of various solid malignant tumors. However, the role of hypoxia-related long non-coding RNAs (HRLs) in uveal melanoma (UVM) remains unclear. This study aimed to identify HRLs associated with UVM prognosis and develop a novel risk signature to predict patient outcomes.

Methods: Data from 80 UVM samples were obtained from The Cancer Genome Atlas. Prognostic HRLs were screened using Cox univariate and Pearson correlation analyses. HRL signature were constructed using Lasso analysis, and gene enrichment analysis was performed to explore the association between HRLs and immune features. Cell Counting Kit-8 assay was used to measure the propagation of human uveal melanoma (MuM2B) cells, while tumor invasion and migration were evaluated using Transwell and wound-healing experiments. Inflammatory factors and macrophage polarization were evaluated using quantitative PCR.

Results: In total, 621 prognostic HRLs were screened and constructed in 12 HRLs. The risk score showed a significant correlation with the survival time of patients with UVM. Additionally, HRL correlated with diverse key immune checkpoints, revealing possible targets for immunotherapy. Immune-related pathways were highly enriched in the high-risk group. LINC02367, a protective HRL, was associated with the tumor microenvironment and survival time of patients with UVM. In vitro, LINC02367 significantly influenced MuM2B proliferation and migration. It also modulated macrophage polarization by regulating inflammatory factor levels, thereby affecting the immune microenvironment.

Conclusions: We developed a novel HRL signature to predict prognosis in patients with UVM. HRLs are potential biomarkers and therapeutic targets for the treatment of UVM.

背景:缺氧相关基因与各种实体恶性肿瘤的预后有关。然而,缺氧相关长非编码 RNA(HRLs)在葡萄膜黑色素瘤(UVM)中的作用仍不清楚。本研究旨在鉴定与葡萄膜黑色素瘤预后相关的HRLs,并开发一种新的风险特征来预测患者的预后:方法:从癌症基因组图谱(The Cancer Genome Atlas)中获得了80个UVM样本的数据。利用Cox单变量分析和Pearson相关分析筛选出预后相关的HRL。利用Lasso分析构建了HRL特征,并进行了基因富集分析,以探索HRL与免疫特征之间的关联。细胞计数试剂盒-8测定了人葡萄膜黑色素瘤(MuM2B)细胞的繁殖,Transwell和伤口愈合实验评估了肿瘤的侵袭和迁移。利用定量 PCR 评估了炎症因子和巨噬细胞极化:结果:共筛选出621个预后HRL,并在12个HRL中构建了预后HRL。风险评分与 UVM 患者的生存时间有明显相关性。此外,HRL与多种关键免疫检查点相关,揭示了免疫疗法的可能靶点。免疫相关通路在高风险组中高度富集。LINC02367是一种保护性HRL,它与UVM患者的肿瘤微环境和生存时间有关。在体外,LINC02367能显著影响MuM2B的增殖和迁移。它还通过调节炎症因子水平来调节巨噬细胞的极化,从而影响免疫微环境:我们发现了一种新的HRL特征,可用于预测紫癜患者的预后。HRL是治疗紫癜的潜在生物标志物和治疗靶点。
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引用次数: 0
The axis of tumor-associated macrophages, extracellular matrix proteins, and cancer-associated fibroblasts in oncogenesis. 肿瘤相关巨噬细胞、细胞外基质蛋白和癌症相关成纤维细胞在肿瘤发生中的轴心作用。
IF 5.3 2区 医学 Q1 ONCOLOGY Pub Date : 2024-10-07 DOI: 10.1186/s12935-024-03518-8
Shuhong Yu, Siyu Wang, Xuanyu Wang, Ximing Xu

The extracellular matrix (ECM) is a complex, dynamic network of multiple macromolecules that serve as a crucial structural and physical scaffold for neighboring cells. In the tumor microenvironment (TME), ECM proteins play a significant role in mediating cellular communication between cancer-associated fibroblasts (CAFs) and tumor-associated macrophages (TAMs). Revealing the ECM modification of the TME necessitates the intricate signaling cascades that transpire among diverse cell populations and ECM proteins. The advent of single-cell sequencing has enabled the identification and refinement of specific cellular subpopulations, which has substantially enhanced our comprehension of the intricate milieu and given us a high-resolution perspective on the diversity of ECM proteins. However, it is essential to integrate single-cell data and establish a coherent framework. In this regard, we present a comprehensive review of the relationships among ECM, TAMs, and CAFs. This encompasses insights into the ECM proteins released by TAMs and CAFs, signaling integration in the TAM-ECM-CAF axis, and the potential applications and limitations of targeted therapies for CAFs. This review serves as a reliable resource for focused therapeutic strategies while highlighting the crucial role of ECM proteins as intermediates in the TME.

细胞外基质(ECM)是由多种大分子组成的复杂动态网络,是邻近细胞的重要结构和物理支架。在肿瘤微环境(TME)中,ECM 蛋白在介导癌症相关成纤维细胞(CAFs)和肿瘤相关巨噬细胞(TAMs)之间的细胞通讯方面发挥着重要作用。要揭示 TME 的 ECM 修饰,就必须了解不同细胞群和 ECM 蛋白之间错综复杂的信号级联。单细胞测序技术的出现使特定细胞亚群的鉴定和细化成为可能,这大大提高了我们对错综复杂的环境的理解,并为我们提供了有关 ECM 蛋白多样性的高分辨率视角。然而,整合单细胞数据并建立一个连贯的框架至关重要。为此,我们对 ECM、TAMs 和 CAFs 之间的关系进行了全面综述。这包括对 TAMs 和 CAFs 释放的 ECM 蛋白、TAM-ECM-CAF 轴的信号整合以及 CAFs 靶向疗法的潜在应用和局限性的深入了解。本综述是重点治疗策略的可靠资源,同时强调了 ECM 蛋白作为 TME 中间体的关键作用。
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Cancer Cell International
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