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Different Role of TRF1 and TRF2 Expression in Non-Small Cell Lung Cancers TRF1 和 TRF2 在非小细胞肺癌中的不同作用
IF 4 4区 医学 Q3 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Pub Date : 2024-06-04 DOI: 10.2147/ott.s461430
Mincheol Chae, Jae-Ho Lee, Jong Ho Park, Dong Yoon Keum, Hanna Jung, Youngok Lee, Deok Heon Lee
Background: TRF1, TRF2, and TERT (Telomerase reverse transcriptase) are telomere-associated factors that regulate telomere length. Genetic changes in these genes may be associated with cancer pathogenesis; however, this relationship has not yet been comprehensively elucidated in lung cancer.
Aim: : Exploring the clinicopathologic and prognostic values of TRF1, TRF2, and TERT mRNA expression in non-small cell lung cancers (NSCLC).
Methods: : The clinical significance of TRF1, TRF2, and TERT expression in 141 patients with NSCLC was investigated. Additionally, these findings were supported by the open big data from The Cancer Genome Atlas (TCGA).
Results: : TRF1 and TRF2 expression levels tended to be associated with smoking, and TERT expression was positively correlated with age. The survival analysis showed that TRF1 expression predicted a better prognosis for squamous cell carcinoma (SCC), whereas TRF2 expression was associated with a shorter survival in adenocarcinoma. TCGA data also showed a better prognosis for SCC with TRF1 expression. However, the TRF2 results were not in agreement with our data.
Conclusions: : We present the clinical and prognostic values of TRF1, TRF2, and TERT expression in NSCLC tissues and TCGA. Our findings suggest that TRF1 expression is a possible prognostic marker for NSCLC, particularly SCC.

背景:TRF1、TRF2和TERT(端粒酶逆转录酶)是调节端粒长度的端粒相关因子。这些基因的遗传变化可能与癌症发病机制有关;然而,这种关系在肺癌中尚未得到全面阐明:探索 TRF1、TRF2 和 TERT mRNA 表达在非小细胞肺癌(NSCLC)中的临床病理和预后价值:方法:研究了141例NSCLC患者中TRF1、TRF2和TERT表达的临床意义。此外,这些发现还得到了癌症基因组图谱(TCGA)开放大数据的支持:结果:TRF1和TRF2的表达水平往往与吸烟有关,TERT的表达与年龄呈正相关。生存分析表明,TRF1的表达预示着鳞状细胞癌(SCC)的预后较好,而TRF2的表达则与腺癌的较短生存期有关。TCGA数据也显示,TRF1表达的SCC预后较好。然而,TRF2的结果与我们的数据并不一致:我们介绍了TRF1、TRF2和TERT在NSCLC组织和TCGA中表达的临床和预后价值。我们的研究结果表明,TRF1的表达可能是NSCLC,尤其是SCC的预后标志物。
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引用次数: 0
The Role and Mechanism of the Histone Methyltransferase G9a in Tumors: Update 组蛋白甲基转移酶 G9a 在肿瘤中的作用和机制最新进展
IF 4 4区 医学 Q3 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Pub Date : 2024-05-30 DOI: 10.2147/ott.s451108
Hangsheng Zhou, Jiandong Gui, Lijie Zhu, Yuanyuan Mi
Abstract: Methylation-mediated gene silencing is closely related to the occurrence and development of human tumors. The euchromatic histone lysine methyltransferase 2 (EHMT2, also known as G9a) is highly expressed in many tumors and is generally considered to be an oncogene, which is associated with the poor outcome of many tumors. Combined immunotherapy and immune checkpoint blockade therapy also have good efficacy and certain safety. However, there are still many difficulties in the drugs targeting G9a, and the combined effect and safety of G9a with many drugs is still under study. This article aims to summarize the role and mechanism of G9a and its inhibitors in tumors in the past two years, and to understand the application prospect of G9a from the perspective of diagnosis and treatment.

Keywords: cancer, G9a, methyltransferase, function, mechanism
摘要:甲基化介导的基因沉默与人类肿瘤的发生和发展密切相关。半色素组蛋白赖氨酸甲基转移酶2(EHMT2,又称G9a)在许多肿瘤中高表达,被普遍认为是一种癌基因,与许多肿瘤的不良预后有关。联合免疫疗法和免疫检查点阻断疗法也具有良好的疗效和一定的安全性。然而,针对G9a的药物仍存在诸多难点,G9a与多种药物的联合作用及安全性仍在研究之中。本文旨在总结近两年来G9a及其抑制剂在肿瘤中的作用和机制,并从诊断和治疗的角度了解G9a的应用前景。关键词:肿瘤;G9a;甲基转移酶;功能;机制
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引用次数: 0
Characterization of Patients with EGFR Mutation-Positive NSCLC Following Emergence of the Osimertinib Resistance Mutations, L718Q or G724S: A Multicenter Retrospective Observational Study in France 奥希替尼耐药突变 L718Q 或 G724S 出现后表皮生长因子受体突变阳性 NSCLC 患者的特征:法国一项多中心回顾性观察研究
IF 4 4区 医学 Q3 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Pub Date : 2024-05-29 DOI: 10.2147/ott.s448909
Mateo Sanchis-Borja, Florian Guisier, Aurélie Swalduz, Hubert Curcio, Victor Basse, Christophe Maritaz, Christos Chouaid, Jean-Bernard Auliac
Purpose: The third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), osimertinib, is an effective first-line therapy for patients with common EGFR mutation-positive non-small cell lung cancer (NSCLC). However, almost all patients become resistant to treatment. In some patients, emergence of tertiary EGFR mutations is implicated as a resistance mechanism. This study describes patients with NSCLC who acquired the rare EGFR mutations, L718Q or G724S, following EGFR TKI treatment.
Patients and Methods: This was a retrospective, observational study undertaken in France from Feb–Nov 2021, in patients with EGFR mutation-positive NSCLC with an acquired L718Q or G724S mutation. Primary objectives were description of tumor characteristics, progression, and progression under treatment.
Results: Nine eligible patients were identified. Acquired resistance to initial EGFR TKI treatment was associated with T790M emergence in six patients, who then received osimertinib monotherapy. Overall, eight patients received osimertinib monotherapy treatment at some point (average treatment duration: 18.3 months). Following the emergence of L718Q or G724S, patients received chemotherapy (n = 4; two of whom subsequently received afatinib), nivolumab (n = 2), afatinib (n = 2), or immunochemotherapy (n = 1). In the four patients who received afatinib after identification of L718Q or G724S, 2 achieved a partial response, one had stable disease and one had progressive disease. Treatment duration was 1.6– 31.7 months. In patients with controlled disease (n = 3), progression-free survival was 6.1– 31.7 months. Two of these patients had previously received osimertinib.
Conclusion: Currently, there is no consensus regarding the treatment of EGFR mutation-positive NSCLC following emergence of the osimertinib resistance mutations, L718Q or G724S. Afatinib appears to be a promising treatment option in this setting.

Keywords: osimertinib, afatinib, real-world evidence, tertiary EGFR mutations
目的:第三代表皮生长因子受体(EGFR)酪氨酸激酶抑制剂(TKI)奥西莫替尼是治疗常见EGFR突变阳性非小细胞肺癌(NSCLC)患者的有效一线疗法。然而,几乎所有患者都会对治疗产生耐药性。在一些患者中,表皮生长因子受体三级突变的出现被认为是一种耐药机制。本研究描述了在接受表皮生长因子受体 TKI 治疗后获得罕见表皮生长因子受体突变 L718Q 或 G724S 的 NSCLC 患者:这是一项回顾性观察研究,于2021年2月至11月在法国进行,研究对象为获得L718Q或G724S突变的表皮生长因子受体突变阳性NSCLC患者。研究的主要目的是描述肿瘤特征、病情进展和治疗进展:结果:确定了九名符合条件的患者。6名患者对最初的表皮生长因子受体TKI治疗获得性耐药与T790M的出现有关,这些患者随后接受了奥希替尼单药治疗。总体而言,八名患者在某一阶段接受了奥希替尼单药治疗(平均治疗时间:18.3个月)。出现L718Q或G724S后,患者接受了化疗(4例;其中2例随后接受了阿法替尼治疗)、nivolumab(2例)、阿法替尼(2例)或免疫化疗(1例)。在确定L718Q或G724S后接受阿法替尼治疗的4名患者中,2人获得部分应答,1人病情稳定,1人病情进展。治疗持续时间为 1.6-31.7 个月。在病情得到控制的患者中(n = 3),无进展生存期为 6.1-31.7 个月。其中两名患者曾接受过奥希替尼治疗:目前,对于出现奥希替尼耐药突变(L718Q或G724S)后如何治疗表皮生长因子受体突变阳性的NSCLC尚未达成共识。在这种情况下,阿法替尼似乎是一种很有前景的治疗选择。关键词:奥西美替尼;阿法替尼;真实世界证据;EGFR三级突变
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引用次数: 0
Identification and Validation of Nicotinamide Metabolism-Related Gene Signatures as a Novel Prognostic Model for Hepatocellular Carcinoma 烟酰胺代谢相关基因特征的鉴定和验证作为肝细胞癌的新型预后模型
IF 4 4区 医学 Q3 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Pub Date : 2024-05-28 DOI: 10.2147/ott.s464709
Sijia Yang, Ang Li, Lihong Lv, Jinxin Duan, Zhihua Zheng, Wenfeng Zhuo, Jun Min, Jinxing Wei
Background: Nicotinamide (NAM+) regulates redox and metabolic activities in the mitochondria. The intention of the research was to identify key genes that relate to nicotinamide in hepatocellular carcinoma (HCC).
Methods: Relevant clinical information were collected as well as RNA-seq data using the Cancer Genome Atlas (TCGA) database. Differential analysis was used to discover the genes that were differently expressed. On the key genes associated with NAM, functional enrichment analysis was carried out. Next, receiver operating characteristic (ROC) and prognosis Kaplan-Meier (K-M) curve analyses were used to evaluate the importance of important gene expression, respectively. The immune cell signatures were estimated using the CIBERSORT algorithm. Finally, the anticancer impact of NAM on HCC was experimentally confirmed, and important genes NADSYN1 and NT5C were validated at the protein level in clinical specimens.
Results: Six prognostic key genes (NAXE, NADSYN1, NT5C, NT5C3A, PNP and NT5E) were identified. There is an association between the level of key gene expression and the clinical prognosis. Four key genes (NAXE, NADSYN1, NT5C and NT5C3A) have statistical significance of survival prognosis. Finally, the expression of NAM-related genes and the inhibitory effect of NAM on HCC were verified by experiments.
Conclusion: The study first found some Nicotinamide metabolism-related differentially expressed genes (NMRDEGs) that are related to HCC can contribute to predicting survival and monitoring the treatment.

背景:烟酰胺(NAM+)调节线粒体中的氧化还原和代谢活动。该研究旨在确定肝细胞癌(HCC)中与烟酰胺相关的关键基因:方法:利用癌症基因组图谱(TCGA)数据库收集相关临床信息和RNA-seq数据。差异分析用于发现表达不同的基因。对与 NAM 相关的关键基因进行了功能富集分析。然后,分别使用接收者操作特征(ROC)和预后卡普兰-梅耶(K-M)曲线分析来评估重要基因表达的重要性。使用 CIBERSORT 算法估算了免疫细胞特征。最后,实验证实了NAM对HCC的抗癌作用,并从蛋白水平验证了临床标本中的重要基因NADSYN1和NT5C:结果:发现了六个预后关键基因(NAXE、NADSYN1、NT5C、NT5C3A、PNP 和 NT5E)。关键基因的表达水平与临床预后有关。4个关键基因(NAXE、NADSYN1、NT5C和NT5C3A)对生存预后有统计学意义。最后,通过实验验证了NAM相关基因的表达以及NAM对HCC的抑制作用:该研究首次发现了一些与HCC相关的烟酰胺代谢相关差异表达基因(NMRDEGs),有助于预测生存率和监测治疗效果。
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引用次数: 0
MCM5 is a Novel Therapeutic Target for Glioblastoma MCM5 是胶质母细胞瘤的新型治疗靶点
IF 4 4区 医学 Q3 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Pub Date : 2024-05-13 DOI: 10.2147/ott.s457600
Jian Zhou, Housheng Zheng, Huiru Zhang, Wenqiang Yu, Baoer Li, Liang Ye, Lu Wang
Objective: MCM5 is a DNA licensing factor involved in cell proliferation and has been previously established as an excellent biomarker in a number of malignancies. Nevertheless, the role of MCM5 in GBM has not been fully clarified. The present study aimed to investigate the potential roles of MCM5 in the treatment of GBM and to elucidate its underlying mechanism, which is beneficial for developing new therapeutic strategies and predicting prognosis.
Methods: Firstly, we obtained transcriptomic and proteomic data from the TCGA and CPTAC databases on glioma patients. Employing the DeSeq2 R package, we then identified genes with joint differential expression in GBM tissues subjected to chemotherapy. To develop a prognostic risk score model, we performed univariate and multivariate Cox regression analyses. In vitro knockdown and overexpression of MCM5 were used to further investigate the biological functions of GBM cells. Additionally, we also delved into the upstream regulation of MCM5, revealing associations with several transcription factors. Finally, we investigated differences in immune cell infiltration and drug sensitivity across diverse risk groups identified in the prognostic risk model.
Results: In this study, the chemotherapy-treated GBM samples exhibited consistent alterations in 46 upregulated and 94 downregulated genes at both the mRNA and protein levels. Notably, MCM5 emerged as a gene with prognostic significance as well as potential therapeutic relevance. In vitro experiments subsequently validated the role of increased MCM5 expression in promoting GBM cell proliferation and resistance to TMZ. Correlations with transcription factors such as CREB1, CTCF, NFYB, NRF1, PBX1, TEAD1, and USF1 were discovered during upstream regulatory analysis, enriching our understanding of MCM5 regulatory mechanisms. The study additionally delves into immune cell infiltration and drug sensitivity, providing valuable insights for personalized treatment approaches.
Conclusion: This study identifies MCM5 as a key player in GBM, demonstrating its prognostic significance and potential therapeutic relevance by elucidating its role in promoting cell proliferation and resistance to chemotherapy.

Keywords: glioblastoma, minichromosome maintenance protein 5, chemotherapeutic drug resistance
目的:MCM5 是一种参与细胞增殖的 DNA 许可因子:MCM5 是一种参与细胞增殖的 DNA 许可因子,以前曾被确定为多种恶性肿瘤的优良生物标志物。然而,MCM5 在 GBM 中的作用尚未完全明确。本研究旨在探究 MCM5 在 GBM 治疗中的潜在作用,并阐明其潜在机制,这有利于开发新的治疗策略和预测预后:首先,我们从 TCGA 和 CPTAC 数据库中获得了胶质瘤患者的转录组和蛋白质组数据。方法:首先,我们从 TCGA 和 CPTAC 数据库中获取了胶质瘤患者的转录组和蛋白质组数据,然后利用 DeSeq2 R 软件包确定了化疗后 GBM 组织中具有联合差异表达的基因。为了建立预后风险评分模型,我们进行了单变量和多变量 Cox 回归分析。我们利用体外敲除和过表达 MCM5 来进一步研究 GBM 细胞的生物学功能。此外,我们还深入研究了 MCM5 的上游调控,发现其与多个转录因子存在关联。最后,我们还研究了预后风险模型中确定的不同风险群体在免疫细胞浸润和药物敏感性方面的差异:在这项研究中,化疗后的 GBM 样本在 mRNA 和蛋白质水平上表现出 46 个上调基因和 94 个下调基因的一致改变。值得注意的是,MCM5 是一个具有预后意义和潜在治疗相关性的基因。体外实验随后验证了 MCM5 表达的增加在促进 GBM 细胞增殖和对 TMZ 产生抗药性方面的作用。在上游调控分析中发现了与 CREB1、CTCF、NFYB、NRF1、PBX1、TEAD1 和 USF1 等转录因子的相关性,丰富了我们对 MCM5 调控机制的理解。该研究还深入研究了免疫细胞浸润和药物敏感性,为个性化治疗方法提供了有价值的见解:本研究确定了 MCM5 在 GBM 中的关键作用,通过阐明其在促进细胞增殖和化疗耐药性方面的作用,证明了其预后意义和潜在的治疗相关性。 关键词:胶质母细胞瘤;迷你染色体维护蛋白 5;化疗耐药性
{"title":"MCM5 is a Novel Therapeutic Target for Glioblastoma","authors":"Jian Zhou, Housheng Zheng, Huiru Zhang, Wenqiang Yu, Baoer Li, Liang Ye, Lu Wang","doi":"10.2147/ott.s457600","DOIUrl":"https://doi.org/10.2147/ott.s457600","url":null,"abstract":"<strong>Objective:</strong> MCM5 is a DNA licensing factor involved in cell proliferation and has been previously established as an excellent biomarker in a number of malignancies. Nevertheless, the role of MCM5 in GBM has not been fully clarified. The present study aimed to investigate the potential roles of MCM5 in the treatment of GBM and to elucidate its underlying mechanism, which is beneficial for developing new therapeutic strategies and predicting prognosis.<br/><strong>Methods:</strong> Firstly, we obtained transcriptomic and proteomic data from the TCGA and CPTAC databases on glioma patients. Employing the DeSeq2 R package, we then identified genes with joint differential expression in GBM tissues subjected to chemotherapy. To develop a prognostic risk score model, we performed univariate and multivariate Cox regression analyses. In vitro knockdown and overexpression of MCM5 were used to further investigate the biological functions of GBM cells. Additionally, we also delved into the upstream regulation of MCM5, revealing associations with several transcription factors. Finally, we investigated differences in immune cell infiltration and drug sensitivity across diverse risk groups identified in the prognostic risk model.<br/><strong>Results:</strong> In this study, the chemotherapy-treated GBM samples exhibited consistent alterations in 46 upregulated and 94 downregulated genes at both the mRNA and protein levels. Notably, MCM5 emerged as a gene with prognostic significance as well as potential therapeutic relevance. In vitro experiments subsequently validated the role of increased MCM5 expression in promoting GBM cell proliferation and resistance to TMZ. Correlations with transcription factors such as CREB1, CTCF, NFYB, NRF1, PBX1, TEAD1, and USF1 were discovered during upstream regulatory analysis, enriching our understanding of MCM5 regulatory mechanisms. The study additionally delves into immune cell infiltration and drug sensitivity, providing valuable insights for personalized treatment approaches.<br/><strong>Conclusion:</strong> This study identifies MCM5 as a key player in GBM, demonstrating its prognostic significance and potential therapeutic relevance by elucidating its role in promoting cell proliferation and resistance to chemotherapy.<br/><br/><strong>Keywords:</strong> glioblastoma, minichromosome maintenance protein 5, chemotherapeutic drug resistance<br/>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"60 1","pages":""},"PeriodicalIF":4.0,"publicationDate":"2024-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140927974","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Long Noncoding RNA NEAT1 Promotes Cell Proliferation and Invasion and Suppresses Apoptosis in Hepatocellular Carcinoma by Regulating miRNA-22-3p/akt2 in vitro and in vivo [Retraction] 长非编码 RNA NEAT1 在体内外通过调控 miRNA-22-3p/akt2 促进肝细胞癌细胞增殖和侵袭并抑制其凋亡 [Retraction] (撤回)
IF 4 4区 医学 Q3 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Pub Date : 2024-05-07 DOI: 10.2147/ott.s476432
Xichang Zhou, Xiang Wang, Yizhou Zhou, Long Cheng, Youwei Zhang, Yangmei Zhang
Retraction for the article Long Noncoding RNA NEAT1 Promotes Cell Proliferation And Invasion And Suppresses Apoptosis In Hepatocellular Carcinoma By Regulating miRNA-22-3p/akt2 In Vitro And In Vivo
长非编码 RNA NEAT1 通过调控 miRNA-22-3p/akt2 体外和体内促进肝细胞癌细胞增殖和侵袭并抑制其凋亡》一文的撤稿决定
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引用次数: 0
Synchronous Multiple Primary Malignant Adenocarcinoma of the Descending Colon and Fungating Bleeding Adenocarcinoma of the Terminal Ileum Presenting Massive Rectal Bleeding: A Trap for the Unwary 降结肠同步多发性原发性恶性腺癌和末端回肠出血性腺癌并发大量直肠出血:不明真相者的陷阱
IF 4 4区 医学 Q3 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Pub Date : 2024-05-02 DOI: 10.2147/ott.s453682
Baicheng Li, Zhao Chen, Guangzhi Wang, Yaqing Liu, Shili Ning
Abstract: Primary cancer of the ileum is rare, and when it occurs in conjunction with primary colon cancer, it becomes even more infrequent and challenging to diagnose prior to surgical intervention. Primary small bowel cancers can be overlooked and may be misidentified as small bowel mesenchymal tumours or advanced metastases from colon cancer. We present an exceedingly uncommon case of ruptured primary ileal cancer combined with primary descending colon cancer presenting with gastrointestinal bleeding. Based on our understanding, instances of dual tumours concurrently occurring are exceedingly infrequent. In this patient, there was a preoperative suspicion of bleeding from colon cancer in the descending region. However, intraoperative exploration revealed that the location of the bleeding was a terminal ileal mass. Following the surgical intervention, the patient recovered satisfactorily. Intraoperative exploration of the entire gastrointestinal tract is therefore necessary in patients with gastrointestinal haemorrhage, especially in those who require urgent surgery without adequate preoperative investigations. If a mass is detected at the end of the ileum, intraoperative pathology should be performed if feasible. Subsequently, if the diagnosis reveals an adenocarcinoma, terminal ileocolic resection and right hemicolectomy are necessary for appropriate resection.

Keywords: multiple primary malignant neoplasms, gut bleeding, adenocarcinoma of the small bowel, descending colon cancer, gastrointestinal tumours, case report
摘要:回肠原发性癌症非常罕见,当它与原发性结肠癌同时发生时,就变得更加罕见,而且在手术干预前进行诊断也很困难。原发性小肠癌容易被忽视,可能被误认为是小肠间质瘤或结肠癌晚期转移瘤。我们介绍了一例极为罕见的原发性回肠癌破裂合并原发性降结肠癌并伴有消化道出血的病例。根据我们的了解,同时发生双重肿瘤的病例极为罕见。在这名患者中,术前怀疑是降结肠部位的结肠癌引起的出血。但术中探查发现,出血部位是回肠末端肿块。手术治疗后,患者恢复良好。因此,对于胃肠道出血患者,尤其是需要紧急手术但术前检查不充分的患者,术中有必要对整个胃肠道进行探查。如果在回肠末端发现肿块,应在可行的情况下进行术中病理检查。关键词:多发性原发性恶性肿瘤;肠道出血;小肠腺癌;降结肠癌;胃肠道肿瘤;病例报告
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引用次数: 0
Long Non-Coding RNA TRG-AS1 Promoted Proliferation and Invasion of Lung Cancer Cells Through the miR-224-5p/SMAD4 Axis [Retraction] 长非编码 RNA TRG-AS1 通过 miR-224-5p/SMAD4 轴促进肺癌细胞的增殖和侵袭 [撤稿]
IF 4 4区 医学 Q3 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Pub Date : 2024-04-18 DOI: 10.2147/ott.s474055
Mengyan Zhang, Weiguo Zhu, Mansour Haeryfar, Sumei Jiang, Xiang Jiang, Wei Chen, Jiancheng Li
Retraction for the article Long Non-Coding RNA TRG-AS1 Promoted Proliferation and Invasion of Lung Cancer Cells Through the miR-224-5p/SMAD4 Axis
撤销长非编码 RNA TRG-AS1 通过 miR-224-5p/SMAD4 轴促进肺癌细胞增殖和侵袭的文章
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引用次数: 0
Investigating the Cell Origin and Liver Metastasis Factors of Colorectal Cancer by Single-Cell Transcriptome Analysis 通过单细胞转录组分析研究结直肠癌的细胞起源和肝转移因素
IF 4 4区 医学 Q3 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Pub Date : 2024-04-17 DOI: 10.2147/ott.s454295
Zhilin Sha, Qingxiang Gao, Lei Wang, Ni An, Yingjun Wu, Dong Wei, Tong Wang, Chen Liu, Yang Shen
Background: Colorectal cancer (CRC) is one of the deadliest causes of death by cancer worldwide. Liver metastasis (LM) is the main cause of death in patients with CRC. Therefore, identification of patients with the greatest risk of liver metastasis is critical for early treatment and reduces the mortality of patients with colorectal cancer liver metastases.
Methods: Initially, we characterized cell composition through single-cell transcriptome analysis. Subsequently, we employed copy number variation (CNV) and pseudotime analysis to delineate the cellular origins of LM and identify LM-related epithelial cells (LMECs). The LM-index was constructed using machine learning algorithms to forecast the relative abundance of LMECs, reflecting the risk of LM. Furthermore, we analyzed drug sensitivity and drug targeted gene expression in LMECs and patients with a high risk of LM. Finally, functional experiments were conducted to determine the biological roles of metastasis-related gene in vitro.
Results: Single-cell RNA sequencing analysis revealed different immune landscapes between primary CRC and LM tumor. LM originated from chromosomal variants with copy number loss of chr1 and chr6p and copy number gain of chr7 and chr20q. We identified the LMECs cluster and found LM-associated pathways such as Wnt/beta-catenin signaling and KRAS signaling. Subsequently, we identified ten metastasis-associated genes, including SOX4, and established the LM-index, which correlates with poorer prognosis, higher stage, and advanced age. Furthermore, we screened two drugs as potential candidates for treating LM, including Linsitinib_1510, Lapatinib_1558. Immunohistochemistry results demonstrated significantly elevated SOX4 expression in tumor samples compared to normal samples. Finally, in vitro experiments verified that silencing SOX4 significantly inhibited tumor cell migration and invasion.
Conclusion: This study reveals the possible cellular origin and driving factors of LM in CRC at the single cell level, and provides a reference for early detection of CRC patients with a high risk of LM.

背景:结肠直肠癌(CRC)是全球最致命的癌症死因之一。肝转移(LM)是导致 CRC 患者死亡的主要原因。因此,识别肝转移风险最大的患者对于早期治疗和降低结直肠癌肝转移患者的死亡率至关重要:最初,我们通过单细胞转录组分析确定了细胞组成的特征。随后,我们利用拷贝数变异(CNV)和伪时间分析来确定肝转移瘤的细胞起源,并识别与肝转移瘤相关的上皮细胞(LMECs)。我们利用机器学习算法构建了 LM 指数,以预测 LMEC 的相对丰度,从而反映出 LM 的风险。此外,我们还分析了 LMEC 和 LM 高危患者的药物敏感性和药物靶向基因表达。最后,我们进行了功能实验,以确定转移相关基因在体外的生物学作用:结果:单细胞RNA测序分析表明,原发性CRC和LM肿瘤的免疫景观不同。LM起源于染色体变异,chr1和chr6p拷贝数丢失,chr7和chr20q拷贝数增大。我们确定了 LMECs 群,并发现了与 LM 相关的通路,如 Wnt/beta-catenin 信号转导和 KRAS 信号转导。随后,我们确定了包括 SOX4 在内的十个转移相关基因,并建立了 LM 指数,该指数与较差的预后、较高的分期和高龄相关。此外,我们还筛选出两种治疗 LM 的潜在候选药物,包括 Linsitinib_1510、Lapatinib_1558。免疫组化结果显示,与正常样本相比,肿瘤样本中SOX4的表达明显升高。最后,体外实验验证了沉默SOX4能显著抑制肿瘤细胞的迁移和侵袭:结论:这项研究从单细胞水平揭示了乳腺癌可能的细胞起源和驱动因素,为早期发现乳腺癌高危人群提供了参考。
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引用次数: 0
Targeting of KDM5A by miR-421 in Human Ovarian Cancer Suppresses the Progression of Ovarian Cancer Cells [Retraction] 在人类卵巢癌中用 miR-421 靶向 KDM5A 可抑制卵巢癌细胞的进展 [撤回论文]
IF 4 4区 医学 Q3 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Pub Date : 2024-04-17 DOI: 10.2147/ott.s474059
Fang Ren, Christina Shrestha, Huirong Shi, Fangfang Sun, Minghui Zhang, Yuan Cao, Gailing Li
Retraction for the article Targeting of KDM5A by miR-421 in Human Ovarian Cancer Suppresses the Progression of Ovarian Cancer Cells
撤回《miR-421 在人类卵巢癌中靶向 KDM5A 可抑制卵巢癌细胞的进展》一文的决定
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引用次数: 0
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OncoTargets and therapy
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