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Immunotherapy resistance in solid tumors: mechanisms and potential solutions. 实体瘤的免疫疗法抗药性:机制与潜在解决方案。
IF 3.6 4区 医学 Q1 Pharmacology, Toxicology and Pharmaceutics Pub Date : 2024-12-31 Epub Date: 2024-02-22 DOI: 10.1080/15384047.2024.2315655
Daniel S Lefler, Steven A Manobianco, Babar Bashir

While the emergence of immunotherapies has fundamentally altered the management of solid tumors, cancers exploit many complex biological mechanisms that result in resistance to these agents. These encompass a broad range of cellular activities - from modification of traditional paradigms of immunity via antigen presentation and immunoregulation to metabolic modifications and manipulation of the tumor microenvironment. Intervening on these intricate processes may provide clinical benefit in patients with solid tumors by overcoming resistance to immunotherapies, which is why it has become an area of tremendous research interest with practice-changing implications. This review details the major ways cancers avoid both natural immunity and immunotherapies through primary (innate) and secondary (acquired) mechanisms of resistance, and it considers available and emerging therapeutic approaches to overcoming immunotherapy resistance.

虽然免疫疗法的出现从根本上改变了实体瘤的治疗方法,但癌症利用许多复杂的生物机制,导致对这些药物产生抗药性。这些机制包括广泛的细胞活动--从通过抗原呈递和免疫调节改变传统的免疫模式,到新陈代谢的改变和肿瘤微环境的操控。对这些错综复杂的过程进行干预可克服免疫疗法的抗药性,从而为实体瘤患者带来临床益处,这也是为什么它已成为一个具有改变实践影响的巨大研究兴趣领域。本综述详细介绍了癌症通过原发性(先天性)和继发性(获得性)抗药性机制躲避天然免疫和免疫疗法的主要方式,并探讨了克服免疫疗法抗药性的现有和新兴治疗方法。
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引用次数: 0
Diagnostic value of 18F-PSMA-1007 PET/CT for predicting the pathological grade of prostate cancer. 18F-PSMA-1007 PET/CT 对预测前列腺癌病理分级的诊断价值。
IF 3.6 4区 医学 Q1 Pharmacology, Toxicology and Pharmaceutics Pub Date : 2024-12-31 Epub Date: 2023-12-20 DOI: 10.1080/15384047.2023.2287120
Xiao-Bo Niu, Yan-Peng Li, Jun Wang, Xiao-Li Mei, Xue-Yan Zhao, Ting-Ting Liu, Sha-Sha Xu, Xing-Min Han, Jing-Liang Cheng

This study was designed to evaluate the diagnostic efficacy of relevant parameters of 18F-prostate-specific membrane antigen (PSMA)-1007 PET/CT in predicting the pathological grade of primary prostate cancer. Briefly, a prospective analysis was performed on 53 patients diagnosed with prostate cancer by systematic puncture biopsy, followed by 18F-PSMA-1007 PET/CT examination prior to treatment within 10 d. The patients were grouped in accordance with the Gleason grading system revised by the International Association of Urology Pathology (ISUP). They were divided into high-grade group (ISUP 4-5 group) and low-grade group (ISUP 1-3 group). The differences in maximum standardized uptake value (SUVmax), tumor-to-background ratio (TBR), intraprostatic PSMA-derived tumor volume (iPSMA-TV), and intraprostatic total lesion PSMA (iTL-PSMA) between the high- and low-grade group were statistically significant (p < .001). No significant difference was found for mean standardized uptake value (SUVmean) between the high- and low-grade groups (Z =  -1.131, p = .258). Besides, binary multivariate logistic regression analysis showed that only iPSMA-TV and iTL-PSMA were independent predictors of the pathological grading, for which the odds ratios were 18.821 [95% confidence interval (CI): 2.040-173.614, p = .010] and 0.758 (95% CI: 0.613-0.938, p = .011), respectively. The area under the ROC of this regression model was 0.983 (95% CI: 0.958-1.00, p < .001). Only iTL-PSMA was a significant parameter for distinguishing ISUP-4 and ISUP-5 groups (Z =  -2.043, p = .041). In a nutshell, 18F-PSMA-1007 PET/CT has good application value in predicting the histopathological grade of primary prostate cancer. Three-dimensional volume metabolism parameters iPSMA-TV and iTL-PSMA were found to be independent predictors for pathological grade.

本研究旨在评估18F-前列腺特异性膜抗原(PSMA)-1007 PET/CT相关参数对预测原发性前列腺癌病理分级的诊断效果。简而言之,该研究对53名通过系统穿刺活检确诊为前列腺癌的患者进行了前瞻性分析,并在治疗前10天内进行了18F-PSMA-1007 PET/CT检查。根据国际泌尿病理学协会(ISUP)修订的格里森分级系统对患者进行分组。他们被分为高级别组(ISUP 4-5 组)和低级别组(ISUP 1-3 组)。高分级组和低分级组的最大标准化摄取值(SUVmax)、肿瘤与背景比(TBR)、泌尿系前列腺内 PSMA 衍生肿瘤体积(iPSMA-TV)和泌尿系前列腺内病变总 PSMA(iTL-PSMA)差异均有统计学意义(P P = .258)。此外,二元多变量逻辑回归分析显示,只有 iPSMA-TV 和 iTL-PSMA 是病理分级的独立预测因子,其几率分别为 18.821 [95% 置信区间 (CI):2.040-173.614,p = .010] 和 0.758 (95% CI:0.613-0.938,p = .011)。该回归模型的 ROC 下面积为 0.983(95% CI:0.958-1.00,p = .041)。总之,18F-PSMA-1007 PET/CT 在预测原发性前列腺癌组织病理学分级方面具有良好的应用价值。研究发现,三维体积代谢参数iPSMA-TV和iTL-PSMA是病理分级的独立预测因子。
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引用次数: 0
Correction. 更正。
IF 3.6 4区 医学 Q1 Pharmacology, Toxicology and Pharmaceutics Pub Date : 2024-12-31 Epub Date: 2024-05-05 DOI: 10.1080/15384047.2024.2350871
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引用次数: 0
Natural killer cell memory: challenges and opportunities for cancer immunotherapy. 自然杀伤细胞记忆:癌症免疫疗法的挑战与机遇。
IF 4.4 4区 医学 Q2 ONCOLOGY Pub Date : 2024-12-31 Epub Date: 2024-07-10 DOI: 10.1080/15384047.2024.2376410
Yuhua Qu, Anhui Zeng, Yulu Cheng, Shengchun Li

Substantial advancements have been made in recent years in comprehending immune memory, which enhances the secondary response through prior infections. The ability of vertebrate T and B lymphocytes to exhibit classic recall responses has long been regarded as a distinguishing characteristic. However, natural killer (NK) cells have been found to acquire immunological memory in a manner akin to T and B cells. The fundamental principles derived from the investigation of NK cell memory offer novel insights into innate immunity and have the potential to pave the way for innovative strategies to enhance therapeutic interventions against multiple diseases including cancer. Here, we reviewed the fundamental characteristics, memory development and regulatory mechanism of NK cell memory. Moreover, we will conduct a comprehensive evaluation of the accomplishments, obstacles, and future direction pertaining to the utilization of NK cell memory in the field of cancer immunotherapy.

近年来,人们在理解免疫记忆方面取得了长足进步,免疫记忆可增强对先前感染的次级反应。脊椎动物的 T 淋巴细胞和 B 淋巴细胞能够表现出典型的记忆反应,这一点一直被认为是与众不同的特征。然而,人们发现自然杀伤(NK)细胞获得免疫记忆的方式与 T 和 B 细胞相似。从对 NK 细胞记忆的研究中得出的基本原理提供了对先天性免疫的新见解,并有可能为创新战略铺平道路,以加强对包括癌症在内的多种疾病的治疗干预。在此,我们回顾了 NK 细胞记忆的基本特征、记忆发展和调控机制。此外,我们还将对癌症免疫疗法领域利用 NK 细胞记忆的成就、障碍和未来方向进行全面评估。
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引用次数: 0
Understanding the molecular mechanism responsible for developing therapeutic radiation-induced radioresistance of rectal cancer and improving the clinical outcomes of radiotherapy - A review. 了解直肠癌放射治疗耐药性的分子机制,改善放射治疗的临床疗效--综述。
IF 3.6 4区 医学 Q1 Pharmacology, Toxicology and Pharmaceutics Pub Date : 2024-12-31 Epub Date: 2024-03-06 DOI: 10.1080/15384047.2024.2317999
Samatha M Jain, Shruthi Nagainallur Ravichandran, Makalakshmi Murali Kumar, Antara Banerjee, Alexander Sun-Zhang, Hong Zhang, Rupak Pathak, Xiao-Feng Sun, Surajit Pathak

Rectal cancer accounts for the second highest cancer-related mortality, which is predominant in Western civilizations. The treatment for rectal cancers includes surgery, radiotherapy, chemotherapy, and immunotherapy. Radiotherapy, specifically external beam radiation therapy, is the most common way to treat rectal cancer because radiation not only limits cancer progression but also significantly reduces the risk of local recurrence. However, therapeutic radiation-induced radioresistance to rectal cancer cells and toxicity to normal tissues are major drawbacks. Therefore, understanding the mechanistic basis of developing radioresistance during and after radiation therapy would provide crucial insight to improve clinical outcomes of radiation therapy for rectal cancer patients. Studies by various groups have shown that radiotherapy-mediated changes in the tumor microenvironment play a crucial role in developing radioresistance. Therapeutic radiation-induced hypoxia and functional alterations in the stromal cells, specifically tumor-associated macrophage (TAM) and cancer-associated fibroblasts (CAF), play a crucial role in developing radioresistance. In addition, signaling pathways, such as - the PI3K/AKT pathway, Wnt/β-catenin signaling, and the hippo pathway, modulate the radiation responsiveness of cancer cells. Different radiosensitizers, such as small molecules, microRNA, nanomaterials, and natural and chemical sensitizers, are being used to increase the effectiveness of radiotherapy. This review highlights the mechanism responsible for developing radioresistance of rectal cancer following radiotherapy and potential strategies to enhance the effectiveness of radiotherapy for better management of rectal cancer.

直肠癌占癌症相关死亡率的第二位,在西方文明中占主导地位。直肠癌的治疗方法包括手术、放疗、化疗和免疫疗法。放疗,特别是体外放射治疗,是治疗直肠癌最常用的方法,因为放射治疗不仅能限制癌症的进展,还能显著降低局部复发的风险。然而,治疗性放射引起的直肠癌细胞放射抗性和对正常组织的毒性是其主要缺点。因此,了解放疗过程中和放疗后产生放射抗性的机理基础,对于改善直肠癌患者放疗的临床疗效至关重要。不同研究小组的研究表明,放疗介导的肿瘤微环境变化在产生放射抗性方面起着至关重要的作用。治疗性放疗引起的缺氧和基质细胞(特别是肿瘤相关巨噬细胞(TAM)和癌相关成纤维细胞(CAF))的功能改变在产生放射抗性方面起着至关重要的作用。此外,PI3K/AKT 通路、Wnt/β-catenin 信号转导和 hippo 通路等信号通路也会调节癌细胞对辐射的反应性。不同的放射增敏剂,如小分子、微RNA、纳米材料、天然和化学增敏剂,正被用于提高放疗的有效性。这篇综述重点介绍了直肠癌放疗后产生放射抗性的机制,以及提高放疗有效性以更好地治疗直肠癌的潜在策略。
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引用次数: 0
The effects of Aurora Kinase inhibition on thyroid cancer growth and sensitivity to MAPK-directed therapies. 极光激酶抑制对甲状腺癌生长的影响以及对 MAPK 导向疗法的敏感性。
IF 3.6 4区 医学 Q1 Pharmacology, Toxicology and Pharmaceutics Pub Date : 2024-12-31 Epub Date: 2024-03-23 DOI: 10.1080/15384047.2024.2332000
Hannah M Hicks, Veronica L Nassar, Jane Lund, Madison M Rose, Rebecca E Schweppe

Thyroid cancer is one of the deadliest endocrine cancers, and its incidence has been increasing. While mutations in BRAF are common in thyroid cancer, advanced PTC patients currently lack therapeutic options targeting the MAPK pathway, and despite the approved combination of BRAF and MEK1/2 inhibition for BRAF-mutant ATC, resistance often occurs. Here, we assess growth and signaling responses to combined BRAF and MEK1/2 inhibition in a panel of BRAF-mutant thyroid cancer cell lines. We first showed that combined BRAF and MEK1/2 inhibition synergistically inhibits cell growth in four out of six of the -BRAF-mutant thyroid cancer cell lines tested. Western blotting showed that the MAPK pathway was robustly inhibited in all cell lines. Therefore, to identify potential mechanisms of resistance, we performed RNA-sequencing in cells sensitive or resistant to MEK1/2 inhibition. In response to MEK1/2 inhibition, we identified a downregulation of Aurora Kinase B (AURKB) in sensitive but not resistant cells. We further demonstrated that combined MEK1/2 and AURKB inhibition slowed cell growth, which was phenocopied by inhibiting AURKB and ERK1/2. Finally, we show that combined AURKB and ERK1/2 inhibition induces apoptosis in BRAF-mutant thyroid cancer cell lines, together suggesting a potential combination therapy for BRAF-mutant thyroid cancer patients.

甲状腺癌是最致命的内分泌癌症之一,其发病率呈上升趋势。虽然 BRAF 突变在甲状腺癌中很常见,但晚期 PTC 患者目前缺乏针对 MAPK 通路的治疗选择,尽管 BRAF 和 MEK1/2 联合抑制 BRAF 突变的 ATC 已获批准,但仍经常出现耐药性。在这里,我们评估了一组 BRAF 突变甲状腺癌细胞系对 BRAF 和 MEK1/2 联合抑制的生长和信号反应。我们首先发现,联合抑制 BRAF 和 MEK1/2 能协同抑制所测试的六种 -BRAF 突变甲状腺癌细胞系中四种的细胞生长。Western 印迹显示,MAPK 通路在所有细胞系中都受到了强有力的抑制。因此,为了确定潜在的耐药性机制,我们对对 MEK1/2 抑制敏感或耐受的细胞进行了 RNA 测序。针对 MEK1/2 抑制,我们在敏感细胞中发现了极光激酶 B(AURKB)的下调,而在耐药细胞中没有发现。我们进一步证明,联合抑制 MEK1/2 和 AURKB 会减慢细胞生长,而抑制 AURKB 和 ERK1/2 则会抑制细胞生长。最后,我们发现联合抑制 AURKB 和 ERK1/2 可诱导 BRAF 突变甲状腺癌细胞系凋亡,这表明 BRAF 突变甲状腺癌患者有可能采用联合疗法。
{"title":"The effects of Aurora Kinase inhibition on thyroid cancer growth and sensitivity to MAPK-directed therapies.","authors":"Hannah M Hicks, Veronica L Nassar, Jane Lund, Madison M Rose, Rebecca E Schweppe","doi":"10.1080/15384047.2024.2332000","DOIUrl":"10.1080/15384047.2024.2332000","url":null,"abstract":"<p><p>Thyroid cancer is one of the deadliest endocrine cancers, and its incidence has been increasing. While mutations in <i>BRAF</i> are common in thyroid cancer, advanced PTC patients currently lack therapeutic options targeting the MAPK pathway, and despite the approved combination of BRAF and MEK1/2 inhibition for <i>BRAF-</i>mutant ATC, resistance often occurs. Here, we assess growth and signaling responses to combined BRAF and MEK1/2 inhibition in a panel of <i>BRAF-</i>mutant thyroid cancer cell lines. We first showed that combined BRAF and MEK1/2 inhibition synergistically inhibits cell growth in four out of six of the -<i>BRAF</i>-mutant thyroid cancer cell lines tested. Western blotting showed that the MAPK pathway was robustly inhibited in all cell lines. Therefore, to identify potential mechanisms of resistance, we performed RNA-sequencing in cells sensitive or resistant to MEK1/2 inhibition. In response to MEK1/2 inhibition, we identified a downregulation of Aurora Kinase B (AURKB) in sensitive but not resistant cells. We further demonstrated that combined MEK1/2 and AURKB inhibition slowed cell growth, which was phenocopied by inhibiting AURKB and ERK1/2. Finally, we show that combined AURKB and ERK1/2 inhibition induces apoptosis in <i>BRAF-</i>mutant thyroid cancer cell lines, together suggesting a potential combination therapy for <i>BRAF</i>-mutant thyroid cancer patients.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10962586/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140193439","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 facilitating effects of KRT80 on chemoresistance, lipogenesis, and invasion of esophageal cancer. KRT80 对食管癌化疗抗性、脂肪生成和侵袭的促进作用
IF 3.6 4区 医学 Q1 Pharmacology, Toxicology and Pharmaceutics Pub Date : 2024-12-31 Epub Date: 2024-01-19 DOI: 10.1080/15384047.2024.2302162
Wen-Jing Yun, Jun Li, Nan-Chang Yin, Cong-Yu Zhang, Zheng-Guo Cui, Li Zhang, Hua-Chuan Zheng

Keratin 80 (KRT80) is a filament protein that makes up one of the major structural fibers of epithelial cells, and involved in cell differentiation and epithelial barrier integrity. Here, KRT80 mRNA expression was found to be higher in esophageal cancer than normal epithelium by RT-PCR and bioinformatics analysis (p < .05), opposite to KRT80 methylation (p < .05). There was a negative relationship between promoter methylation and expression level of KRT80 gene in esophageal cancer (p < .05). KRT80 mRNA expression was positively correlated with the differentiation, infiltration of immune cells, and poor prognosis of esophageal cancer (p < .05). KRT80 mRNA expression was positively linked to no infiltration of immune cells, the short survival time of esophageal cancers (p < .05). The differential genes of KRT80 mRNA were involved in fat digestion and metabolism, peptidase inhibitor, and intermediate filament, desosome, keratinocyte differentiation, epidermis development, keratinization, ECM regulator, complement cascade, metabolism of vitamins and co-factor (p < .05). KRT-80-related genes were classified into endocytosis, cell adhesion molecule binding, cadherin binding, cell-cell junction, cell leading edge, epidermal cell differentiation and development, T cell differentiation and receptor complex, plasma membrane receptor complex, external side of plasma membrane, metabolism of amino acids and catabolism of small molecules, and so forth (p < .05). KRT80 knockdown suppressed anti-apoptosis, anti-pyroptosis, migration, invasion, chemoresistance, and lipogenesis in esophageal cancer cells (p < .05), while ACC1 and ACLY overexpression reversed the inhibitory effects of KRT80 on lipogenesis and chemoresistance. These findings indicated that up-regulated expression of KRT80 might be involved in esophageal carcinogenesis and subsequent progression, aggravate aggressive phenotypes, and induced chemoresistance by lipid droplet assembly and ACC1- and ACLY-mediated lipogenesis.

角蛋白 80 (KRT80) 是一种丝状蛋白,是上皮细胞的主要结构纤维之一,参与细胞分化和上皮屏障完整性。通过 RT-PCR 和生物信息学分析发现,食管癌患者的 KRT80 mRNA 表达量高于正常上皮细胞(p p p p p p p p p
{"title":"The facilitating effects of KRT80 on chemoresistance, lipogenesis, and invasion of esophageal cancer.","authors":"Wen-Jing Yun, Jun Li, Nan-Chang Yin, Cong-Yu Zhang, Zheng-Guo Cui, Li Zhang, Hua-Chuan Zheng","doi":"10.1080/15384047.2024.2302162","DOIUrl":"10.1080/15384047.2024.2302162","url":null,"abstract":"<p><p>Keratin 80 (KRT80) is a filament protein that makes up one of the major structural fibers of epithelial cells, and involved in cell differentiation and epithelial barrier integrity. Here, KRT80 mRNA expression was found to be higher in esophageal cancer than normal epithelium by RT-PCR and bioinformatics analysis (<i>p</i> < .05), opposite to KRT80 methylation (<i>p</i> < .05). There was a negative relationship between promoter methylation and expression level of KRT80 gene in esophageal cancer (<i>p</i> < .05). KRT80 mRNA expression was positively correlated with the differentiation, infiltration of immune cells, and poor prognosis of esophageal cancer (<i>p</i> < .05). KRT80 mRNA expression was positively linked to no infiltration of immune cells, the short survival time of esophageal cancers (<i>p</i> < .05). The differential genes of KRT80 mRNA were involved in fat digestion and metabolism, peptidase inhibitor, and intermediate filament, desosome, keratinocyte differentiation, epidermis development, keratinization, ECM regulator, complement cascade, metabolism of vitamins and co-factor (<i>p</i> < .05). KRT-80-related genes were classified into endocytosis, cell adhesion molecule binding, cadherin binding, cell-cell junction, cell leading edge, epidermal cell differentiation and development, T cell differentiation and receptor complex, plasma membrane receptor complex, external side of plasma membrane, metabolism of amino acids and catabolism of small molecules, and so forth (<i>p</i> < .05). KRT80 knockdown suppressed anti-apoptosis, anti-pyroptosis, migration, invasion, chemoresistance, and lipogenesis in esophageal cancer cells (<i>p</i> < .05), while ACC1 and ACLY overexpression reversed the inhibitory effects of KRT80 on lipogenesis and chemoresistance. These findings indicated that up-regulated expression of KRT80 might be involved in esophageal carcinogenesis and subsequent progression, aggravate aggressive phenotypes, and induced chemoresistance by lipid droplet assembly and ACC1- and ACLY-mediated lipogenesis.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10802210/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139501973","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
Exosome-transmitted circular RNA circ-LMO7 facilitates the progression of osteosarcoma by regulating miR-21-5p/ARHGAP24 axis. 外泌体传递的环状 RNA circ-LMO7 通过调控 miR-21-5p/ARHGAP24 轴促进骨肉瘤的进展。
IF 4.4 4区 医学 Q2 ONCOLOGY Pub Date : 2024-12-31 Epub Date: 2024-05-14 DOI: 10.1080/15384047.2024.2343450
Anyu Luo, Hanlin Liu, Chen Huang, Sheng Wei

The potential function and mechanism of circRNAs in regulating malignant performances of Osteosarcoma (OS) cells have not been well investigated. The expression level of CircLMO7, miR-21-5p and ARHGAP24 were detected by RT-qPCR. The relationship between miR-21-5p and circ-LMO7, as well as between miR-21-5p and ARHGAP24, was predicted and examined through bioinformatics analysis and luciferase reporter gene experiments. Moreover, OS cell growth, invasion, migration, and apoptosis were detected using the cell counting kit-8 (CCK-8), transwell and flow cytometry assays, respectively. ARHGAP24 protein level was measured using western blotting. In present study, we choose to investigate the role and mechanism of circ-LOM7 on OS cell proliferation, migration and invasion. circ-LOM7 was found to be down-regulated in OS tissues and cell lines. Enforced expression of circ-LOM7 suppressed the growth, invasion, and migration of OS cells. In contrast, decreasing circ-LMO7 expression had opposite effects. Furthermore, miR-21-5p was predicted to be sponged by circ-LMO7, and had an opposite role of circ-LMO7 in OS. Moreover, ARHGAP24 served as miR-21-5p's downstream target. Mechanistically, circ-LMO7 was packed in exosomes and acted as a cancer-suppresser on OS by sponging miR-21-5p and upregulating the expression of ARHGAP24. The exosomal circ-LMO7 expression was significantly decreased in OS cell exosomes, and co-culture experiments showed that exosomal circ-LMO7 suppressed the proliferation ability of OS cells. Circ-LMO7 exerts as a tumor suppressor in OS, and the circ-LMO7/miR-21-5P/ARHGAP24 axis is involved in OS progression.

circRNAs在调控骨肉瘤(OS)细胞恶性表现方面的潜在功能和机制尚未得到很好的研究。本研究采用 RT-qPCR 方法检测了 CircLMO7、miR-21-5p 和 ARHGAP24 的表达水平。通过生物信息学分析和荧光素酶报告基因实验,预测并研究了 miR-21-5p 与 circ-LMO7 以及 miR-21-5p 与 ARHGAP24 之间的关系。此外,还分别使用细胞计数试剂盒-8(CCK-8)、透孔法和流式细胞术检测了 OS 细胞的生长、侵袭、迁移和凋亡。Western印迹法检测了ARHGAP24蛋白水平。本研究选择探究circ-LOM7在OS细胞增殖、迁移和侵袭中的作用和机制。强制表达 circ-LOM7 可抑制 OS 细胞的生长、侵袭和迁移。相反,降低 circ-LMO7 的表达则会产生相反的效果。此外,预计miR-21-5p会被circ-LMO7疏导,并在OS中发挥与circ-LMO7相反的作用。此外,ARHGAP24是miR-21-5p的下游靶标。从机理上讲,circ-LMO7被包裹在外泌体中,通过海绵化miR-21-5p和上调ARHGAP24的表达对OS起到抑癌作用。外泌体circ-LMO7在OS细胞外泌体中的表达明显下降,共培养实验表明外泌体circ-LMO7抑制了OS细胞的增殖能力。Circ-LMO7是OS的肿瘤抑制因子,而circ-LMO7/miR-21-5P/ARHGAP24轴参与了OS的进展。
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引用次数: 0
Effects of combined radiotherapy with immune checkpoint blockade on immunological memory in luminal-like subtype murine bladder cancer model. 免疫检查点阻断联合放疗对腔隙样亚型鼠膀胱癌模型免疫记忆的影响
IF 3.6 4区 医学 Q1 Pharmacology, Toxicology and Pharmaceutics Pub Date : 2024-12-31 Epub Date: 2024-06-11 DOI: 10.1080/15384047.2024.2365452
JiaMin Huang, Eva Michaud, Surashri Shinde-Jadhav, Sabina Fehric, Gautier Marcq, Jose Joao Mansure, Fabio Cury, Fadi Brimo, Ciriaco A Piccirillo, Wassim Kassouf

MIBC is a highly lethal disease, and the patient survival rate has not improved significantly over the last decades. UPPL is a cell line that can be used to recapitulate the luminal-like molecular subtype of bladder cancer and to discover effective treatments to be translated in patients. Here, we investigate the effects of combinational treatments of radiotherapy and immunotherapy in this recently characterized UPPL tumor-bearing mice. We first characterized the baseline tumor microenvironment and the effect of radiation, anti-PD-L1, and combinatorial treatments. Then, the mice were re-challenged with a second tumor (rechallenged tumor) in the contralateral flank of the first tumor to assess the immunological memory. Radiation slowed down the tumor growth. All treatments also decreased the neutrophil population and increased the T cell population. Anti-PD-L1 therapy was not able to synergize with radiation to further delay tumor growth. Furthermore, none of the treatments were able to generate immune memory. The treatments were not sufficient to induce a significant and lasting pool of memory cells. We show here that anti-PD-L1 treatment added to radiotherapy was not enough to achieve T cell-mediated memory in UPPL tumors. Stronger T cell activation signals may be required to enhance radiation efficacy in luminal-like bladder cancer.

膀胱癌(MIBC)是一种致死率很高的疾病,在过去几十年中,患者的生存率一直没有显著提高。UPPL 是一种细胞系,可用来再现膀胱癌的腔镜样分子亚型,并发现可用于患者的有效治疗方法。在这里,我们研究了放疗和免疫疗法联合治疗对这种新近表征的 UPPL 肿瘤小鼠的影响。我们首先描述了基线肿瘤微环境以及放射、抗 PD-L1 和组合治疗的效果。然后,小鼠在第一个肿瘤的对侧再次受到第二个肿瘤(再挑战肿瘤)的挑战,以评估免疫记忆。辐射减缓了肿瘤的生长。所有治疗也都减少了中性粒细胞数量,增加了T细胞数量。抗PD-L1疗法无法与放射治疗协同进一步延缓肿瘤生长。此外,所有疗法都无法产生免疫记忆。这些疗法不足以诱导大量持久的记忆细胞。我们在此表明,在放疗中加入抗PD-L1治疗不足以在UPPL肿瘤中实现T细胞介导的记忆。要提高腔隙样膀胱癌的放射疗效,可能需要更强的T细胞激活信号。
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引用次数: 0
P4HA2 promotes tumor progression and is transcriptionally regulated by SP1 in colorectal cancer. P4HA2 在结直肠癌中促进肿瘤进展并受 SP1 的转录调控。
IF 3.6 4区 医学 Q1 Pharmacology, Toxicology and Pharmaceutics Pub Date : 2024-12-31 Epub Date: 2024-06-10 DOI: 10.1080/15384047.2024.2361594
Xuening Dang, Xiaojian Chen, Zhonglin Liang, Zhujiang Dai, Wenjun Ding, Jinglue Song, Jihong Fu

P4HA2 has been implicated in various malignant tumors; however, its expression and functional role in colorectal cancer (CRC) remain poorly elucidated. This study aims to investigate the involvement of P4HA2 in CRC metastasis and progression, uncovering the underlying mechanisms. In colorectal cancer (CRC), P4HA2 exhibited overexpression, and elevated levels of P4HA2 expression were associated with an unfavorable prognosis. Functional assays demonstrated P4HA2's regulation of cell proliferation, and epithelial-mesenchymal transition (EMT) both in vitro and in vivo. Additionally, the AGO1 expression was correlated with P4HA2, and depletion of AGO1 reversed the proliferation and EMT function induced by P4HA2. Chromatin immunoprecipitation (ChIP) and luciferase assays suggested that the transcription factor SP1 binds to the promoter sequence of P4HA2, activating its expression in CRC. This study unveiled SP1 as a transcriptional regulator of P4HA2 in CRC and AGO1 is a probable target of P4HA2. In conclusion, P4HA2 emerges as a potential prognostic biomarker and promising therapeutic target in colorectal cancer.

P4HA2与多种恶性肿瘤有关,但其在结直肠癌(CRC)中的表达和功能作用仍未得到充分阐明。本研究旨在探讨 P4HA2 参与 CRC 转移和进展的机制。在结直肠癌(CRC)中,P4HA2表现出过表达,P4HA2表达水平的升高与预后不良有关。功能测试表明,P4HA2 在体外和体内都能调节细胞增殖和上皮-间质转化(EMT)。此外,AGO1的表达与P4HA2相关,而AGO1的缺失会逆转P4HA2诱导的细胞增殖和EMT功能。染色质免疫沉淀(ChIP)和荧光素酶检测表明,转录因子SP1与P4HA2的启动子序列结合,激活了P4HA2在CRC中的表达。这项研究揭示了 SP1 是 P4HA2 在 CRC 中的转录调节因子,而 AGO1 可能是 P4HA2 的靶点。总之,P4HA2是结直肠癌潜在的预后生物标志物和有希望的治疗靶点。
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引用次数: 0
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Cancer Biology & Therapy
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