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Genome-wide CRISPR screening reveals novel therapeutic targets in RIT1-driven lung cancer. 全基因组CRISPR筛选揭示了RIT1-驱动的癌症的新治疗靶点。
IF 2.1 Q3 ONCOLOGY
Molecular and Cellular Oncology
Pub Date : 2021-11-16 DOI: 10.1080/23723556.2021.2000318
Amanda K Riley, Alice H Berger

In recent work, we performed CRISPR/Cas9 screening in RIT1 (Ras-like in all tissues)-mutant cancer cells. We found that RIT1-mutant cells are vulnerable to loss of mitotic regulators, and mutant RIT1 synergizes with YAP1 (yes-associated protein 1) in oncogenesis. These findings can be leveraged to identify targeted therapies for RIT1-mutant cancer.

在最近的工作中，我们在RIT1（所有组织中的Ras-like）突变癌症细胞中进行了CRISPR/Cas9筛选。我们发现RIT1突变细胞容易失去有丝分裂调节因子，并且突变RIT1在致癌过程中与YAP1（yes相关蛋白1）协同作用。这些发现可用于确定RIT1-毛特癌症的靶向治疗。
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引用次数: 0
Epigenetic condensates regulate chromatin activity and tumorigenesis. 表观遗传凝聚体调节染色质活性和肿瘤发生。
IF 2.1 Q3 ONCOLOGY
Molecular and Cellular Oncology
Pub Date : 2021-11-09 eCollection Date: 2021-01-01 DOI: 10.1080/23723556.2021.1997040
Bi Shi, Wei Li, Hao Jiang

Alterations of epigenetic modulators are extensively associated with cancer, but their key molecular activities in cancer regulation are often unclear. We discovered that lysine demethylase 6A (KDM6A, also known as UTX) suppresses cancer by forming liquid-like condensates with lysine methyltransferase 2D (KMT2D, also known as MLL4) and regulating chromatin activity at multiple levels.

表观遗传调节剂的改变与癌症广泛相关，但其在癌症调控中的关键分子活动往往不清楚。我们发现赖氨酸去甲基化酶6A (KDM6A，也称为UTX)通过与赖氨酸甲基转移酶2D (KMT2D，也称为MLL4)形成液体状凝聚体并在多个水平上调节染色质活性来抑制癌症。
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引用次数: 0
A therapeutic window for preventive therapy in NF1-associated optic pathway glioma nf1相关视神经胶质瘤预防性治疗的治疗窗口期
IF 2.1 Q3 ONCOLOGY
Molecular and Cellular Oncology
Pub Date : 2021-11-02 DOI: 10.1080/23723556.2021.1989262
Yuan Zhu, Wang Zheng, Emmanuelle S. Jecrois, Brianna R. Pierce, Daniel M. Treisman
ABSTRACT Pediatric low-grade gliomas (pLGGs) are almost universally driven by abnormal activation of RAS-mediated MEK-ERK/MAPK signaling pathway. pLGGs predominantly occur in children, suggesting that they originate in an ERK-dependent neural stem/progenitor population(s) transiently present in the developing brain. Our recent preclinical study reveals a cell-lineage-of-origin and develops a chemopreventative therapeutic strategy.
儿童低级别胶质瘤(pLGGs)几乎普遍由ras介导的MEK-ERK/MAPK信号通路异常激活驱动。pLGGs主要发生在儿童中，这表明它们起源于短暂存在于发育中的大脑中的erk依赖性神经干/祖细胞群。我们最近的临床前研究揭示了细胞谱系的起源，并开发了一种化学预防治疗策略。
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引用次数: 1
Interdisciplinary team science to understand and intercept rare cancers 跨学科团队科学理解和拦截罕见癌症
IF 2.1 Q3 ONCOLOGY
Molecular and Cellular Oncology
Pub Date : 2021-11-02 DOI: 10.1080/23723556.2021.1997331
S. Fröhling
ABSTRACT For most rare cancers, precision oncology approaches are not established because these entities are poorly understood and their investigation requires the collaboration of many centers. The MASTER precision oncology network demonstrates that clinical whole-genome/exome and RNA sequencing yield molecular mechanism-aware treatments that benefit a substantial proportion of patients with advanced rare cancers and will prepare the ground for future clinical trials.
摘要对于大多数罕见的癌症，由于对这些实体的了解不多，并且它们的研究需要多个中心的合作，因此没有建立精确的肿瘤学方法。MASTER精准肿瘤学网络表明，临床全基因组/外显子组和RNA测序产生了分子机制感知治疗，使相当一部分晚期罕见癌症患者受益，并将为未来的临床试验奠定基础。
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引用次数: 0
Greasy GLUT1 maintains glioblastoma malignancy 油腻的GLUT1维持胶质母细胞瘤的恶性
IF 2.1 Q3 ONCOLOGY
Molecular and Cellular Oncology
Pub Date : 2021-11-02 DOI: 10.1080/23723556.2021.2009423
Caiyun Liu, Xinjian Li
ABSTRACT How cancer cells absorb enough glucose to support their rapid growth is poorly understood. We have recently demonstrated that palmitoyl transferase DHHC9 palmitoylates glucose transporter GLUT1 at Cys207 to maintain GLUT1 plasma membrane localization. DHHC9-mediated GLUT1 palmitoylation supports glycolysis, proliferation, colony formation, and tumorigenicity of glioblastoma cells.
癌细胞如何吸收足够的葡萄糖以支持其快速生长尚不清楚。我们最近证明棕榈酰转移酶DHHC9棕榈酰化葡萄糖转运蛋白GLUT1在Cys207，以维持GLUT1质膜定位。dhhc9介导的GLUT1棕榈酰化支持胶质母细胞瘤细胞的糖酵解、增殖、集落形成和致瘤性。
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引用次数: 0
The perfect PTEN – transcriptional regulation by PTEN dictates sarcoma identity PTEN的完美转录调控决定了肉瘤的特性
IF 2.1 Q3 ONCOLOGY
Molecular and Cellular Oncology
Pub Date : 2021-11-02 DOI: 10.1080/23723556.2021.2002120
C. G. Langdon, M. Hatley
ABSTRACT Fusion-negative rhabdomyosarcoma (FN-RMS) is molecularly heterogeneous with few universal alterations except for Phosphatase and tensin homolog (PTEN) promoter hypermethylation. We demonstrate that losing Pten in FN-RMS engages an aberrant transcriptional program key in tumor maintenance and cell identity. These results highlight the importance between transcriptional state, cell of origin, and genetic perturbation in tumorigenesis.
摘要融合阴性横纹肌肉瘤（FN-RMS）是一种分子异质性肿瘤，除了磷酸酶和张力蛋白同源物（PTEN）启动子超甲基化外，几乎没有普遍的改变。我们证明，在FN-RMS中失去Pten参与了一个异常转录程序，这是肿瘤维持和细胞身份的关键。这些结果强调了转录状态、起源细胞和遗传干扰在肿瘤发生中的重要性。
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引用次数: 1
ZNF768: controlling cellular senescence and proliferation with ten fingers ZNF768：用十指控制细胞衰老和增殖
IF 2.1 Q3 ONCOLOGY
Molecular and Cellular Oncology
Pub Date : 2021-11-02 DOI: 10.1080/23723556.2021.1985930
Romain Villot, Audrey Poirier, R. Devillers, A. Kolnoguz, S. Elowe, V. Manem, P. Joubert, Frédérick A. Mallette, M. Laplante
ABSTRACT We recently identified Zinc-finger protein 768 (ZNF768) as a novel transcription factor controlling cell fate decision downstream of Rat sarcoma virus (RAS). We showed that ZNF768 depletion impairs cell cycle progression and triggers cellular senescence, while its overexpression allows cells to bypass oncogene-induced senescence. Elevated ZNF768 levels is common in tumors, suggesting that ZNF768 may help to escape cellular senescence, sustain proliferation and promote malignant transformation. Here, we discuss these recent findings and highlight key questions emerging from our work.
我们最近发现锌指蛋白768 (ZNF768)是一种新的转录因子，可控制大鼠肉瘤病毒(RAS)下游的细胞命运决定。我们发现，ZNF768缺失会损害细胞周期进程并触发细胞衰老，而其过表达允许细胞绕过癌基因诱导的衰老。ZNF768水平升高在肿瘤中很常见，提示ZNF768可能有助于细胞逃避衰老、维持增殖和促进恶性转化。在这里，我们讨论了这些最近的发现，并强调了我们工作中出现的关键问题。
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引用次数: 2
Filling in the gaps in PARP inhibitor-induced synthetic lethality 填补PARP抑制剂诱导的合成致死率的空白
IF 2.1 Q3 ONCOLOGY
Molecular and Cellular Oncology
Pub Date : 2021-11-02 DOI: 10.1080/23723556.2021.2010512
Mariana Paes Dias, J. Jonkers
ABSTRACT Tumors with loss of breast cancer type 1 susceptibility protein (BRCA1) are homologous recombination (HR) deficient and hypersensitive to poly(ADP-ribose) polymerase inhibitors (PARPi). However, these tumors may restore HR and acquire PARPi resistance via loss of end-protection of DNA double-strand breaks. We found that loss of nuclear DNA ligase III resensitizes HR-restored BRCA1-deficient cells to PARPi by exposing post-replicative single-stranded DNA (ssDNA) gaps. Our work, and that of others, identifies ssDNA gaps as a key determinant of PARPi response.
乳腺癌1型易感蛋白(BRCA1)缺失的肿瘤是同源重组(HR)缺陷和对聚(adp -核糖)聚合酶抑制剂(PARPi)过敏的肿瘤。然而，这些肿瘤可能通过失去DNA双链断裂的末端保护而恢复HR并获得PARPi抗性。我们发现，核DNA连接酶III的缺失通过暴露复制后单链DNA (ssDNA)缺口，使hr修复的brca1缺陷细胞对PARPi重新敏感。我们和其他人的研究发现，ssDNA缺口是PARPi反应的关键决定因素。
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引用次数: 4
Novel insights into the RTK-dependent metastatic phenotype of KRAS-mutant lung adenocarcinoma KRAS突变型肺腺癌RTK依赖性转移表型的新见解
IF 2.1 Q3 ONCOLOGY
Molecular and Cellular Oncology
Pub Date : 2021-11-02 DOI: 10.1080/23723556.2021.2013723
Mariana Cooke
ABSTRACT In a recent study, our group identified RAC guanine nucleotide exchange factors (RAC-GEFs) driving motility signaling in KRAS mutant lung adenocarcinoma cells. The RAC-GEFs FARP1, ARHGEF39 and TIAM2 play fundamental roles in the formation of membrane ruffles in response to growth factor receptor stimulation.
摘要在最近的一项研究中，我们小组鉴定了在KRAS突变的肺腺癌细胞中驱动运动信号的RAC鸟嘌呤核苷酸交换因子（RAC GEFs）。RAC GEFs FARP1、ARHGEF39和TIAM2在响应生长因子受体刺激的膜褶皱的形成中发挥基本作用。
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引用次数: 1
SPF45/RBM17-dependent splicing and multidrug resistance to cancer chemotherapy SPF45/ rbm17依赖性剪接与肿瘤化疗多药耐药
IF 2.1 Q3 ONCOLOGY
Molecular and Cellular Oncology
Pub Date : 2021-11-02 DOI: 10.1080/23723556.2021.1996318
Kazuhiro Fukumura, J. Venables, A. Mayeda
ABSTRACT The early splicing complex A occupies at least eighty nucleotides of intron, in which U2AF covers the polypyrimidine tract. SPF45 (RBM17) functionally substitutes for U2AF on a subset of short introns. Since SPF45 expression confers resistance to various anticancer drugs, SPF45-dependent splicing may play a critical role in multidrug resistance.
早期剪接复合体A占据至少80个核苷酸的内含子，其中U2AF覆盖多嘧啶通道。SPF45 (RBM17)在短内含子的子集上功能替代U2AF。由于SPF45的表达赋予了多种抗癌药物的抗性，SPF45依赖性剪接可能在多药耐药中起关键作用。
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引用次数: 1
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