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Thioredoxin-interacting protein (TXNIP) is a substrate of the NEDD4-like E3 ubiquitin-protein ligase WWP1 in cellular redox state regulation of acute myeloid leukemia cells. 在急性髓性白血病细胞的细胞氧化还原状态调控过程中,硫氧还蛋白相互作用蛋白(TXNIP)是类似 NEDD4 的 E3 泛素蛋白连接酶 WWP1 的底物。
IF 6.6 2区 医学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2025-01-01 Epub Date: 2024-10-04 DOI: 10.1002/1878-0261.13722
Sara Giovannini, Yanan Li, Rosalba Pecorari, Claudia Fierro, Claudia Fiorilli, Federica Corigliano, Valeria Moriconi, Ji Zhou, Anna De Antoni, Artem Smirnov, Sara Rinalducci, Anna Maria Timperio, Massimiliano Agostini, Jinping Zhang, Yufang Shi, Eleonora Candi, Gerry Melino, Francesca Bernassola

The HECT-type E3 ubiquitin WWP1 (also known as NEDD4-like E3 ubiquitin-protein ligase WWP1) acts as an oncogenic factor in acute myeloid leukemia (AML) cells. WWP1 overexpression in AML confers a proliferative advantage to leukemic blasts (abnormal immature white blood cells) and counteracts apoptotic cell death and differentiation. In an effort to elucidate the molecular basis of WWP1 oncogenic activities, we identified WWP1 as a previously unknown negative regulator of thioredoxin-interacting protein (TXNIP)-mediated reactive oxygen species (ROS) production in AML cells. TXNIP inhibits the disulfide reductase enzymatic activity of thioredoxin (Trx), impairing its antioxidant function and, ultimately, leading to the disruption of cellular redox homeostasis. In addition, TXNIP restricts cell growth and survival by blocking glucose uptake and metabolism. Here, we found that WWP1 directly interacts with TXNIP, thus promoting its ubiquitin-dependent proteasomal proteolysis. As a result, accumulation of TXNIP in response to WWP1 inactivation in AML blasts reduces Trx activity and increases ROS production, hence inducing cellular oxidative stress. Increased ROS generation in WWP1-depleted cells culminates in DNA strand breaks and subsequent apoptosis. Coherently with TXNIP stabilization following WWP1 inactivation, we also observed an impairment of both glucose up-take and consumption. Hence, a contribution to the increased cell death observed in WWP1-depleted cells also possibly arises from the attenuation of glucose up-take and glycolytic flux resulting from TXNIP accumulation. Future studies are needed to establish whether TXNIP-dependent deregulation of redox homeostasis in WWP1-overexpressing blasts may affect the response of leukemic cells to chemotherapeutic drugs.

HECT 型 E3 泛素 WWP1(又称 NEDD4-like E3 泛素蛋白连接酶 WWP1)是急性髓性白血病(AML)细胞中的致癌因子。WWP1 在急性髓性白血病中的过表达使白血病细胞(异常的未成熟白细胞)具有增殖优势,并抵消细胞凋亡和分化。为了阐明 WWP1 致癌活性的分子基础,我们发现 WWP1 是以前未知的硫氧还蛋白相互作用蛋白(TXNIP)介导的急性髓性白血病细胞活性氧(ROS)产生的负调控因子。TXNIP会抑制硫氧还原酶(Trx)的酶活性,损害其抗氧化功能,最终导致细胞氧化还原平衡的破坏。此外,TXNIP 还会阻碍葡萄糖的摄取和代谢,从而限制细胞的生长和存活。在这里,我们发现 WWP1 直接与 TXNIP 相互作用,从而促进其泛素依赖性蛋白酶体蛋白水解。因此,在急性髓细胞白血病细胞中,WWP1 失活后 TXNIP 的积累会降低 Trx 活性,增加 ROS 的产生,从而诱发细胞氧化应激。在去除了 WWP1 的细胞中,ROS 生成的增加最终导致 DNA 链断裂和细胞凋亡。WWP1 失活后,TXNIP 趋于稳定,与此同时,我们还观察到葡萄糖的吸收和消耗都受到了影响。因此,在去除了 WWP1 的细胞中观察到的细胞死亡增加的一个原因也可能是 TXNIP 积累导致葡萄糖摄取和糖酵解通量减弱。未来还需要进行研究,以确定依赖于 TXNIP 的氧化还原平衡失调是否会影响白血病细胞对化疗药物的反应。
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引用次数: 0
RETRACTION: Targeting MYCN IRES in MYCN-amplified Neuroblastoma With Mir-375 Inhibits Tumor Growth and Sensitizes Tumor Cells to Radiation. 撤回:用Mir-375靶向MYCN IRES在MYCN扩增的神经母细胞瘤中抑制肿瘤生长并使肿瘤细胞对辐射敏感。
IF 6.6 2区 医学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2025-01-01 Epub Date: 2024-12-03 DOI: 10.1002/1878-0261.13775

Retraction: H. Zhang, T. Liu, S. Yi, L. Gu, and M. Zhou, "Targeting MYCN IRES in MYCN-amplified Neuroblastoma With Mir-375 Inhibits Tumor Growth and Sensitizes Tumor Cells to Radiation," Molecular Oncology 9, no. 7 (2015): 1301-1311, https://doi.org/10.1016/j.molonc.2015.03.005. The above article, published online on 24 March 2015 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Kevin Ryan; FEBS Press; and John Wiley & Sons Ltd. The retraction has been agreed upon following an investigation into concerns raised by a third party, which revealed inappropriate image section duplications within the article (Figure 5B) and between this (Figures 3B and 4B) and another article published by the same group of authors in a different scientific context. The authors were unable to provide a satisfactory explanation and the original raw data, which has led the editors to lose confidence in the data presented. Therefore, the editors consider the conclusions substantially compromised and are retracting the paper.

引用本文:张宏,刘涛,易淑娟,顾丽,周敏,“靶向MYCN IRES的Mir-375抑制肿瘤生长和肿瘤细胞对辐射的敏感性”,中国生物医学工程学报,第9期。上述文章于2015年3月24日在Wiley online Library (wileyonlinelibrary.com)上发表,经主编Kevin Ryan同意撤回;2月出版社;及约翰威利父子有限公司。在对第三方提出的问题进行调查后,已同意撤回,该第三方发现文章中(图5B)以及这篇文章(图3B和4B)与同一组作者在不同科学背景下发表的另一篇文章之间存在不适当的图像部分重复。作者无法提供令人满意的解释和原始数据,这导致编辑对所提供的数据失去信心。因此,编辑们认为这些结论在很大程度上受到了损害,正在撤回这篇论文。
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引用次数: 0
Simultaneous detection of eight cancer types using a multiplex droplet digital PCR assay. 使用多重液滴数字 PCR 检测法同时检测八种癌症类型。
IF 6.6 2区 医学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2025-01-01 Epub Date: 2024-09-06 DOI: 10.1002/1878-0261.13708
Isabelle Neefs, Nele De Meulenaere, Thomas Vanpoucke, Janah Vandenhoeck, Dieter Peeters, Marc Peeters, Guy Van Camp, Ken Op de Beeck

DNA methylation biomarkers have emerged as promising tools for cancer detection. Common methylation patterns across tumor types allow multi-cancer detection. Droplet digital PCR (ddPCR) has gained considerable attention for methylation detection. However, multi-cancer detection using multiple targets in ddPCR has never been performed before. Therefore, we developed a multiplex ddPCR assay for multi-cancer detection. Based on previous data analyses using The Cancer Genome Atlas (TCGA), we selected differentially methylated targets for eight frequent tumor types (lung, breast, colorectal, prostate, pancreatic, head and neck, liver, and esophageal cancer). Three targets were validated using ddPCR in 103 tumor and 109 normal adjacent fresh frozen samples. Two distinct ddPCR assays were successfully developed. Output data from both assays is combined to obtain a read-out from the three targets together. Our overall ddPCR assay has a cross-validated area under the curve (cvAUC) of 0.948. Performance between distinct cancer types varies, with sensitivities ranging from 53.8% to 100% and specificities ranging from 80% to 100%. Compared to previously published single-target parameters, we show that combining targets can drastically increase sensitivity and specificity, while lowering DNA input. In conclusion, we are the first to report a multi-cancer methylation ddPCR assay, which allows for highly accurate tumor predictions.

DNA 甲基化生物标志物已成为一种很有前途的癌症检测工具。不同类型肿瘤的共同甲基化模式可用于多种癌症检测。液滴数字 PCR(ddPCR)在甲基化检测方面已经获得了相当多的关注。然而,在 ddPCR 中使用多靶点进行多癌症检测还从未有过。因此,我们开发了一种用于多癌检测的多重 ddPCR 检测方法。根据之前使用癌症基因组图谱(TCGA)进行的数据分析,我们选择了八种常见肿瘤类型(肺癌、乳腺癌、结直肠癌、前列腺癌、胰腺癌、头颈部癌、肝癌和食管癌)的不同甲基化靶点。在 103 个肿瘤样本和 109 个邻近的正常新鲜冷冻样本中使用 ddPCR 验证了三个靶点。成功开发了两种不同的 ddPCR 检测方法。两种检测方法的输出数据合并在一起,可获得三个靶点的读数。我们的整体 ddPCR 检测的交叉验证曲线下面积(cvAUC)为 0.948。不同癌症类型之间的性能各不相同,灵敏度从 53.8% 到 100% 不等,特异性从 80% 到 100% 不等。与之前公布的单一靶标参数相比,我们发现结合靶标可以大幅提高灵敏度和特异性,同时降低 DNA 输入。总之,我们首次报道了一种多癌症甲基化 ddPCR 检测方法,该方法可实现高度准确的肿瘤预测。
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引用次数: 0
ENL mutation and AML: a new model that reveals oncogenic condensate's function in leukemogenesis. ENL突变与急性髓细胞性白血病:揭示致癌凝聚物在白血病发生过程中功能的新模型。
IF 6.6 2区 医学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2025-01-01 Epub Date: 2024-09-26 DOI: 10.1002/1878-0261.13731
Zhong Fan, Yanan Jiang, Xiaotian Zhang

Precise regulation of gene expression is essential for proper development and the maintenance of homeostasis in organisms. Studies have shown that some transcriptional regulatory proteins influence gene expression through the formation of dynamic, locally concentrated assemblies known as condensates, while dysregulation of transcriptional condensates was associated with several cancers, such as Ewing sarcoma and AML [Wang Y et al. (2023) Nat Chem Biol 19, 1223-1234; Chandra B et al. (2022) Cancer Discov 12, 1152-1169]. Mutations in the histone acetylation "reader" eleven-nineteen-leukemia (ENL) have been shown to form discrete condensates at endogenous genomic targets, but it remains unclear how ENL mutations drive tumorigenesis and whether it is correlated with their condensate formation property. Liu et al. now show, using a conditional knock-in mouse model, that ENL YEATS domain mutation is a bona fide oncogenic driver for AML. This mutant ENL forms condensates in hematopoietic stem/progenitor cells at the genomic loci of key leukemogenic genes, including Meis1 and Hoxa cluster genes, and disrupting condensate formation via mutagenesis impairs its chromatin and oncogenic function. Furthermore, they show that small-molecule inhibition of the acetyl-binding activity displaces ENL mutant condensates from oncogenic target loci, and this inhibitor significantly impairs the onset and progression of AML driven by mutant ENL in vivo.

基因表达的精确调控对于生物体的正常发育和维持平衡至关重要。研究表明,一些转录调控蛋白通过形成动态的、局部集中的集合体(称为凝聚体)来影响基因表达,而转录凝聚体的失调与多种癌症有关,如尤文肉瘤和急性髓细胞性白血病[Wang Y et al. (2023) Nat Chem Biol 19, 1223-1234;Chandra B et al. (2022) Cancer Discov 12, 1152-1169]。组蛋白乙酰化 "阅读器 "十一-十九-白血病(ENL)突变已被证明可在内源性基因组靶点形成离散的凝集物,但ENL突变如何驱动肿瘤发生以及是否与其凝集物形成特性相关仍不清楚。Liu等人现在利用条件性基因敲入小鼠模型表明,ENL YEATS结构域突变是急性髓细胞性白血病的真正致癌驱动因子。这种突变的ENL在造血干细胞/祖细胞中关键致白血病基因(包括Meis1和Hoxa簇基因)的基因组位点上形成凝集物,通过诱变破坏凝集物的形成会损害其染色质和致癌功能。此外,他们还发现,抑制乙酰结合活性的小分子抑制剂可将ENL突变凝集素从致癌靶基因座上置换下来,这种抑制剂可显著抑制突变ENL驱动的AML在体内的发生和发展。
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引用次数: 0
RETRACTION: Long Noncoding RNA ZNF667-AS1 Reduces Tumor Invasion and Metastasis in Cervical Cancer by Counteracting Microrna-93-3p-Dependent PEG3 Downregulation. 返回:长非编码 RNA ZNF667-AS1 通过抵消 microRNA-93-3p 依赖性 PEG3 的下调作用,减少宫颈癌的肿瘤侵袭和转移。
IF 6.6 2区 医学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2025-01-01 Epub Date: 2024-11-27 DOI: 10.1002/1878-0261.13777

Retraction: Y.-J. Li, Z. Yang, Y.-Y. Wang, and Y. Wang, "Long Noncoding RNA ZNF667-AS1 Reduces Tumor Invasion and Metastasis in Cervical Cancer by Counteracting Microrna-93-3p-Dependent PEG3 Downregulation," Molecular Oncology 13, no. 11 (2019): 2375-2392, https://doi.org/10.1002/1878-0261.12565. The above article, published online on 17 October 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Kevin Ryan; FEBS Press; and John Wiley & Sons Ltd. The retraction has been agreed upon following an investigation into concerns raised by a third party, which revealed implausible Western blot data (Figures 5B, L, G and Q), and an image duplication in Figure 6B. The authors' failure to respond with the original raw data has led the editors to lose confidence in the data presented. Therefore, the editors consider the conclusions substantially compromised and are retracting the paper.

撤回:Li Y-J, Yang Z, Wang Y-Y, Wang Y.长非编码RNA ZNF667-AS1通过对抗microRNA-93-3p依赖的PEG3下调减少宫颈癌的肿瘤侵袭和转移Mol Oncol.2019;13(11):2375-2392. https://doi.org/10.1002/1878-0261.12565 上述文章于2019年10月17日在线发表于Wiley Online Library (wileyonlinelibrary.com),经期刊主编Kevin Ryan、FEBS Press和John Wiley & Sons Ltd.协议撤回。在对第三方提出的疑虑进行调查后,作者同意撤稿。第三方提出的疑虑揭示了难以置信的 Western 印迹数据(图 5B,L,G,Q)和图 6B 中的图像重复。由于作者未能提供原始数据,编辑对所提供的数据失去了信心。因此,编辑认为该论文的结论大打折扣,并撤回该论文。
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引用次数: 0
APOBEC3C-mediated NF-κB activation enhances clear cell renal cell carcinoma progression. APOBEC3C 介导的 NF-κB 激活可促进透明细胞肾细胞癌的进展。
IF 6.6 2区 医学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2025-01-01 Epub Date: 2024-08-26 DOI: 10.1002/1878-0261.13721
Nora Hase, Danny Misiak, Helge Taubert, Stefan Hüttelmaier, Michael Gekle, Marcel Köhn

Renowned as the predominant form of kidney cancer, clear cell renal cell carcinoma (ccRCC) exhibits susceptibility to immunotherapies due to its specific expression profile as well as notable immune cell infiltration. Despite this, effectively treating metastatic ccRCC remains a significant challenge, necessitating a more profound comprehension of the underlying molecular mechanisms governing its progression. Here, we unveil that the enhanced expression of the RNA-binding protein DNA dC → dU-editing enzyme APOBEC-3C (APOBEC3C; also known as A3C) in ccRCC tissue and ccRCC-derived cell lines serves as a catalyst for tumor growth by amplifying nuclear factor-kappa B (NF-κB) activity. By employing RNA-sequencing and cell-based assays in ccRCC-derived cell lines, we determined that A3C is a stress-responsive factor and crucial for cell survival. Furthermore, we identified that A3C binds and potentially stabilizes messenger RNAs (mRNAs) encoding positive regulators of the NF-κB pathway. Upon A3C depletion, essential subunits of the NF-κB family are abnormally restrained in the cytoplasm, leading to deregulation of NF-κB target genes. Our study illuminates the pivotal role of A3C in promoting ccRCC tumor development, positioning it as a prospective target for future therapeutic strategies.

透明细胞肾细胞癌(ccRCC)是肾癌的主要形式,由于其特殊的表达谱和明显的免疫细胞浸润,它很容易受到免疫疗法的影响。尽管如此,有效治疗转移性 ccRCC 仍是一项重大挑战,需要更深入地了解其进展的潜在分子机制。在这里,我们揭示了RNA结合蛋白DNA dC → dU编辑酶APOBEC-3C(APOBEC3C,又称A3C)在ccRCC组织和ccRCC衍生细胞系中的表达增强,通过扩大核因子卡巴B(NF-κB)的活性而成为肿瘤生长的催化剂。通过对ccRCC衍生细胞系进行RNA测序和基于细胞的检测,我们确定A3C是一种应激反应因子,对细胞存活至关重要。此外,我们还发现 A3C 与编码 NF-κB 通路正调控因子的信使 RNA(mRNA)结合并可能使其稳定。A3C耗竭后,NF-κB家族的重要亚基在细胞质中受到异常抑制,导致NF-κB靶基因失调。我们的研究揭示了A3C在促进ccRCC肿瘤发展中的关键作用,并将其定位为未来治疗策略的前瞻性靶点。
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引用次数: 0
Nongenetic evolution of the tumor: from challenges to new therapeutic opportunities. 肿瘤的非遗传进化:从挑战到新的治疗机遇。
IF 6.6 2区 医学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2025-01-01 Epub Date: 2024-10-18 DOI: 10.1002/1878-0261.13753
Elisa Oricchio

The ability of cancer cells to change and adapt poses a critical challenge to identifying curative solutions. Tumor evolution has been extensively studied from a genetic perspective, to guide clinicians in selecting the most appropriate therapeutic option based on a patient's mutational profile. However, several studies reported that tumors can evolve toward more aggressive stages or become resistant to therapies without changing their genetic makeup. Indeed, several cell-intrinsic and cell-extrinsic mechanisms contribute to tumor evolution. In this viewpoint, I focus on how chromatin, epigenetic, and transcriptional changes contribute to tumor evolution, allowing cancer cells to transition to different cell states and bypass response to therapies. Although tumor nongenetic evolution is harder to trace and predict, understanding its principles might open new therapeutic opportunities.

癌细胞的变化和适应能力对确定治疗方案提出了严峻的挑战。人们从基因角度对肿瘤演变进行了广泛研究,以指导临床医生根据患者的突变特征选择最合适的治疗方案。然而,有几项研究报告称,肿瘤可以向更具侵袭性的阶段发展,或者在不改变基因构成的情况下对疗法产生抗药性。事实上,一些细胞内在和细胞外的机制促成了肿瘤的进化。在这一观点中,我将重点关注染色质、表观遗传和转录变化如何促进肿瘤进化,使癌细胞过渡到不同的细胞状态并绕过对疗法的反应。虽然肿瘤非遗传进化更难追踪和预测,但了解其原理可能会带来新的治疗机会。
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引用次数: 0
Assessments of prostate cancer cell functions highlight differences between a pan-PI3K/mTOR inhibitor, gedatolisib, and single-node inhibitors of the PI3K/AKT/mTOR pathway. 对前列腺癌细胞功能的评估凸显了泛 PI3K/mTOR 抑制剂 gedatolisib 与 PI3K/AKT/mTOR 通路单节点抑制剂之间的差异。
IF 6.6 2区 医学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2025-01-01 Epub Date: 2024-08-02 DOI: 10.1002/1878-0261.13703
Adrish Sen, Salmaan Khan, Stefano Rossetti, Aaron Broege, Ian MacNeil, Ann DeLaForest, Jhomary Molden, Laura Davis, Charles Iversrud, Megan Seibel, Ross Kopher, Stephen Schulz, Lance Laing

Metastatic castration-resistant prostate cancer (mCRPC) is characterized by loss of androgen receptor (AR) sensitivity and oncogenic activation of the PI3K/AKT/mTOR (PAM) pathway. Loss of the PI3K regulator PTEN is frequent during prostate cancer (PC) initiation, progression, and therapeutic resistance. Co-targeting the PAM/AR pathways is a promising mCRPC treatment strategy but is hampered by reciprocal negative feedback inhibition or feedback relief. Most PAM inhibitors selectively spare (or weakly inhibit) one or more key nodes of the PAM pathway, potentiating drug resistance depending on the PAM pathway mutation status of patients. We posited that gedatolisib, a uniformly potent inhibitor of all class I PI3K isoforms, as well as mTORC1 and mTORC2, would be more effective than inhibitors targeting single PAM pathway nodes in PC cells. Using a combination of functional and metabolic assays, we evaluated a panel of PC cell lines with different PTEN/PIK3CA status for their sensitivity to multi-node PAM inhibitors (PI3K/mTOR: gedatolisib, samotolisib) and single-node PAM inhibitors (PI3Kα: alpelisib; AKT: capivasertib; mTOR: everolimus). Gedatolisib induced anti-proliferative and cytotoxic effects with greater potency and efficacy relative to the other PAM inhibitors, independent of PTEN/PIK3CA status. The superior effects of gedatolisib were likely associated with more effective inhibition of critical PAM-controlled cell functions, including cell cycle, survival, protein synthesis, oxygen consumption rate, and glycolysis. Our results indicate that potent and simultaneous blockade of all class I PI3K isoforms, mTORC1, and mTORC2 could circumvent PTEN-dependent resistance. Gedatolisib, as a single agent and in combination with other therapies, reported promising preliminary efficacy and safety in various solid tumor types. Gedatolisib is currently being evaluated in a Phase 1/2 clinical trial in combination with darolutamide in patients with mCRPC previously treated with an AR inhibitor, and in a Phase 3 clinical trial in combination with palbociclib and fulvestrant in patients with HR+/HER2- advanced breast cancer.

转移性去势抵抗性前列腺癌(mCRPC)的特点是丧失对雄激素受体(AR)的敏感性以及 PI3K/AKT/mTOR (PAM) 通路的致癌激活。PI3K调节因子PTEN的缺失经常发生在前列腺癌(PC)的发病、进展和治疗耐受过程中。联合靶向 PAM/AR 通路是一种很有前景的 mCRPC 治疗策略,但受到相互负反馈抑制或反馈缓解的阻碍。大多数 PAM 抑制剂会选择性地放过(或弱化抑制)PAM 通路的一个或多个关键节点,从而根据患者的 PAM 通路突变状况增强耐药性。我们认为,吉达托利西布是一种对所有I类PI3K同工酶以及mTORC1和mTORC2都具有相同效力的抑制剂,它比针对PC细胞中单一PAM通路节点的抑制剂更有效。我们采用功能和代谢测定相结合的方法,评估了一组具有不同 PTEN/PIK3CA 状态的 PC 细胞系对多节点 PAM 抑制剂(PI3K/mTOR:gedatolisib、samotolisib)和单节点 PAM 抑制剂(PI3Kα:alpelisib;AKT:capivasertib;mTOR:everolimus)的敏感性。与其他PAM抑制剂相比,Gedatolisib具有更强的抗增殖和细胞毒性作用,与PTEN/PIK3CA状态无关。gedatolisib的卓越效果可能与更有效地抑制PAM控制的关键细胞功能有关,包括细胞周期、存活、蛋白质合成、耗氧量和糖酵解。我们的研究结果表明,同时强效阻断所有 I 类 PI3K 同工酶、mTORC1 和 mTORC2 可以规避 PTEN 依赖性耐药性。据报道,Gedatolisib作为单药或与其他疗法联用,在各种实体瘤类型中具有良好的初步疗效和安全性。目前,Gedatolisib 正与 darolutamide 联用,在曾接受过 AR 抑制剂治疗的 mCRPC 患者中进行 1/2 期临床试验;与 palbociclib 和 fulvestrant 联用,在 HR+/HER2- 晚期乳腺癌患者中进行 3 期临床试验。
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引用次数: 0
Dynamic methylation and expression of alternative promoters for oestrogen receptor alpha in cell line models of fulvestrant resistance. 氟维司群耐药细胞系模型中雌激素受体 alpha 替代启动子的动态甲基化和表达。
IF 6.6 2区 医学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2025-01-01 Epub Date: 2024-08-06 DOI: 10.1002/1878-0261.13713
Juliane Albrecht, Mirjam Müller, Völundur Hafstað, Kamila Kaminska, Johan Vallon-Christersson, Gabriella Honeth, Helena Persson

Oestrogen receptor alpha (ER; gene symbol ESR1) is the most important prognostic and treatment-predictive biomarker in breast cancer. Drugs targeting oestrogen and ER for endocrine therapy of breast cancer include aromatase inhibitors, the selective ER modulator tamoxifen and the selective ER degrader fulvestrant. Tumours can develop resistance to endocrine therapy through several mechanisms, which is often linked to altered expression of ER. To investigate the role of promoter methylation in the regulation of ESR1 expression, we used bisulfite sequencing to measure methylation at CpG sites in alternative ER promoter regions for six cell line models of fulvestrant resistance. Both CpG methylation and expression of alternative first exons changed dynamically, with striking differences between cell lines that had stable or unstable resistance upon fulvestrant withdrawal. Methylation at some CpG sites was strongly negatively correlated with expression of specific first exons. In a breast tumour cohort, higher relative expression of upstream alternative first exons was associated with worse prognosis in post-menopausal women with ER-positive tumours who received endocrine therapy.

雌激素受体α(ER;基因符号 ESR1)是乳腺癌最重要的预后和治疗预测生物标志物。针对雌激素和ER的乳腺癌内分泌治疗药物包括芳香化酶抑制剂、选择性ER调节剂他莫昔芬和选择性ER降解剂氟维司群。肿瘤可通过多种机制对内分泌治疗产生耐药性,这通常与ER的表达改变有关。为了研究启动子甲基化在调控 ESR1 表达中的作用,我们使用亚硫酸氢盐测序法测量了六种氟维司群耐药细胞系模型中ER替代启动子区域 CpG 位点的甲基化情况。CpG甲基化和替代性第一外显子的表达都发生了动态变化,氟维司群停药后,耐药性稳定或不稳定的细胞系之间存在显著差异。某些 CpG 位点的甲基化与特定第一外显子的表达呈强负相关。在一个乳腺肿瘤队列中,上游替代性第一外显子的相对表达较高与绝经后接受内分泌治疗的ER阳性肿瘤妇女的预后较差有关。
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引用次数: 0
RETRACTION: Frequent Alterations of LOH11CR2A, PIG8 and CHEK1 Genes at Chromosomal 11q24.1-24.2 Region in Breast Carcinoma: Clinical and Prognostic Implications. 摘要:乳腺癌中11q24.1-24.2区域LOH11CR2A、PIG8和CHEK1基因的频繁改变:临床和预后意义。
IF 6.6 2区 医学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2025-01-01 Epub Date: 2024-12-03 DOI: 10.1002/1878-0261.13774

Retraction: S. Sinha, R.K. Singh, N. Bhattacharya, N. Mukherjee, S. Ghosh, N. Alam, A. Roy, S. Roychoudhury, and C.K. Panda, "Frequent Alterations of LOH11CR2A, PIG8 and CHEK1 Genes at Chromosomal 11q24.1-24.2 Region in Breast Carcinoma: Clinical and Prognostic Implications," Molecular Oncology 5, no. 5 (2011): 454-464, https://doi.org/10.1016/j.molonc.2011.06.005. The above article, published online on 7 July 2011 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Kevin M. Ryan; the Federation of European Biochemical Societies (FEBS); and John Wiley & Sons Ltd. Following publication, concerns were raised by a third party that portions of Figure 2 were duplicated, and Figures 5A and 5D were duplicated from an earlier publication by this research group. Internal investigation confirmed the duplications in these figures. The retraction has been agreed because of concerns that the images were manipulated, affecting the interpretation of the data and results presented.

引用本文:S. Sinha, R.K. Singh, N. Bhattacharya, N. Mukherjee, S. Ghosh, N. Alam, A. Roy, S. Roychoudhury, C.K. Panda,“乳腺癌11q24.1-24.2区LOH11CR2A、PIG8和CHEK1基因的频繁改变:临床和预后意义”,《分子肿瘤学》第5期,第2期。5 (2011): 454-464, https://doi.org/10.1016/j.molonc.2011.06.005上述文章于2011年7月7日在线发表在Wiley在线图书馆(wileyonlinelibrary.com)上,经该杂志主编Kevin M. Ryan同意撤回;欧洲生化学会联合会(FEBS);及约翰威利父子有限公司。在发表之后,第三方担心图2的部分内容被复制,图5A和图5D是从该研究小组早期发表的文章中复制的。内部调查证实了这些数字的重复。由于担心图像被篡改,影响了对所呈现的数据和结果的解释,因此同意撤稿。
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Molecular Oncology
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