M-TAP Dance: Targeting PRMT1 and PRMT5 Family Members to Push Cancer Cells Over the Edge.

Abstract:

:In this issue of Cancer Cell, Fedoriw and colleagues characterize a potent reversible inhibitor of type I PRMTs, GSK3368715, with anti-proliferative effects on numerous cancer types. Using a combination of GSK3368715 with PRMT5 inhibitors, the authors show that a threshold of overall arginine methylation reduction needs to be achieved for synergistic anti-tumor activity.

journal_name

Cancer Cell

journal_title

Cancer cell

authors

Srour N,Mersaoui SY,Richard S

doi

10.1016/j.ccell.2019.06.004

subject

Has Abstract

pub_date

2019-07-08 00:00:00

pages

3-5

issue

1

eissn

1535-6108

issn

1878-3686

pii

S1535-6108(19)30295-8

journal_volume

36

pub_type

评论,杂志文章
  • The cyclin-like protein Spy1 regulates growth and division characteristics of the CD133+ population in human glioma.

    abstract::The heterogeneity of brain cancers, as most solid tumors, complicates diagnosis and treatment. Identifying and targeting populations of cells driving tumorigenesis is a top priority for the cancer biology field. This is not a trivial task; considerable variance exists in the driving mutations, identifying markers, and...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccr.2013.12.006

    authors: Lubanska D,Market-Velker BA,deCarvalho AC,Mikkelsen T,Fidalgo da Silva E,Porter LA

    更新日期:2014-01-13 00:00:00

  • Impairment of cytoplasmic eIF6 activity restricts lymphomagenesis and tumor progression without affecting normal growth.

    abstract::Eukaryotic Initiation Factor 6 (eIF6) controls translation by regulating 80S subunit formation. eIF6 is overexpressed in tumors. Here, we demonstrate that eIF6 inactivation delays tumorigenesis and reduces tumor growth in vivo. eIF6(+/-) mice resist to Myc-induced lymphomagenesis and have prolonged tumor-free survival...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccr.2011.04.018

    authors: Miluzio A,Beugnet A,Grosso S,Brina D,Mancino M,Campaner S,Amati B,de Marco A,Biffo S

    更新日期:2011-06-14 00:00:00

  • Gluing Proteins for Targeted Degradation.

    abstract::Targeted protein degradation is an emerging technology for drug development. An article published in Nature reported a novel mechanism of targeted protein degradation triggered by small-molecule-induced polymerization of the oncogenic transcription factor BCL6. ...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccell.2020.12.020

    authors: Naito M,Murata S

    更新日期:2021-01-11 00:00:00

  • Kidney cancer: now available in a new flavor.

    abstract::The role of the von Hippel-Lindau tumor suppressor protein (pVHL) in kidney cancer has provided a rationale for treating this disease with hypoxia-inducible factor (HIF) antagonists. In this issue, Simon and coworkers show that the molecular signature of VHL(-/-) kidney cancers is profoundly influenced by whether they...

    journal_title:Cancer cell

    pub_type: 评论,杂志文章

    doi:10.1016/j.ccr.2008.11.005

    authors: Kaelin WG Jr

    更新日期:2008-12-09 00:00:00

  • Dynein light chain 1, a p21-activated kinase 1-interacting substrate, promotes cancerous phenotypes.

    abstract::We identified dynein light chain 1 (DLC1) as a physiologic substrate of p21-activated kinase 1 (Pak1). Pak1-DLC1 interaction plays an essential role in cell survival, which depends on Pak1's phosphorylation of DLC1 on Ser88. Pak1 associates with the complex of DLC1 and BimL, a proapoptotic BH3-only protein, and phosph...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccr.2004.05.022

    authors: Vadlamudi RK,Bagheri-Yarmand R,Yang Z,Balasenthil S,Nguyen D,Sahin AA,den Hollander P,Kumar R

    更新日期:2004-06-01 00:00:00

  • p62, Upregulated during Preneoplasia, Induces Hepatocellular Carcinogenesis by Maintaining Survival of Stressed HCC-Initiating Cells.

    abstract::p62 is a ubiquitin-binding autophagy receptor and signaling protein that accumulates in premalignant liver diseases and most hepatocellular carcinomas (HCCs). Although p62 was proposed to participate in the formation of benign adenomas in autophagy-deficient livers, its role in HCC initiation was not explored. Here we...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccell.2016.04.006

    authors: Umemura A,He F,Taniguchi K,Nakagawa H,Yamachika S,Font-Burgada J,Zhong Z,Subramaniam S,Raghunandan S,Duran A,Linares JF,Reina-Campos M,Umemura S,Valasek MA,Seki E,Yamaguchi K,Koike K,Itoh Y,Diaz-Meco MT,Moscat J,K

    更新日期:2016-06-13 00:00:00

  • Tobacco smoke promotes lung tumorigenesis by triggering IKKbeta- and JNK1-dependent inflammation.

    abstract::Chronic exposure to tobacco smoke, which contains over 60 tumor-initiating carcinogens, is the major risk factor for development of lung cancer, accounting for a large portion of cancer-related deaths worldwide. It is well established that tobacco smoke is a tumor initiator, but we asked whether it also acts as a tumo...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccr.2009.12.008

    authors: Takahashi H,Ogata H,Nishigaki R,Broide DH,Karin M

    更新日期:2010-01-19 00:00:00

  • Breaking news on fragile sites in cancer.

    abstract::Chromosome rearrangements in B lymphocytes can be initiated by AID-associated double strand breaks (DSBs), with others arising by unclear mechanisms. A recent study by Barlow and colleagues in Cell reports on genomic regions, termed early replicating fragile sites, that may explain many AID-independent DSBs and create...

    journal_title:Cancer cell

    pub_type: 评论,杂志文章

    doi:10.1016/j.ccr.2013.01.017

    authors: Glover TW,Wilson TE

    更新日期:2013-02-11 00:00:00

  • Targeting the Vulnerability of Glutathione Metabolism in ARID1A-Deficient Cancers.

    abstract::ARID1A encodes an SWI/SNF chromatin-remodeling factor and is frequently mutated in various cancers. This study demonstrates that ARID1A-deficient cancer cells are specifically vulnerable to inhibition of the antioxidant glutathione (GSH) and the glutamate-cysteine ligase synthetase catalytic subunit (GCLC), a rate-lim...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccell.2018.12.009

    authors: Ogiwara H,Takahashi K,Sasaki M,Kuroda T,Yoshida H,Watanabe R,Maruyama A,Makinoshima H,Chiwaki F,Sasaki H,Kato T,Okamoto A,Kohno T

    更新日期:2019-02-11 00:00:00

  • FoxM1 promotes β-catenin nuclear localization and controls Wnt target-gene expression and glioma tumorigenesis.

    abstract::Wnt/β-catenin signaling is essential for stem cell regulation and tumorigenesis, but its molecular mechanisms are not fully understood. Here, we report that FoxM1 is a downstream component of Wnt signaling and is critical for β-catenin transcriptional function in tumor cells. Wnt3a increases the level and nuclear tran...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccr.2011.08.016

    authors: Zhang N,Wei P,Gong A,Chiu WT,Lee HT,Colman H,Huang H,Xue J,Liu M,Wang Y,Sawaya R,Xie K,Yung WK,Medema RH,He X,Huang S

    更新日期:2011-10-18 00:00:00

  • Next-generation genomic profiling of hepatocellular adenomas: a new era of individualized patient care.

    abstract::Hepatocellular adenomas (HCAs) are clinically relevant benign liver lesions that commonly occur in women on hormonal contraceptives. In this issue of Cancer Cell, Pilati and colleagues present an integrative multi-"omics"-based analysis of HCA and identify recurrent genetic alterations associated with adenoma-carcinom...

    journal_title:Cancer cell

    pub_type: 评论,杂志文章

    doi:10.1016/j.ccr.2014.03.032

    authors: Marquardt JU,Thorgeirsson SS

    更新日期:2014-04-14 00:00:00

  • Kit-activating mutations cooperate with Spi-1/PU.1 overexpression to promote tumorigenic progression during erythroleukemia in mice.

    abstract::The erythroleukemia developed by spi-1/PU.1 transgenic mice is a multistage process characterized by an early arrest of the proerythroblast differentiation followed later on by malignant transformation. Herein, we report the presence of acquired mutations in the SCF receptor gene (Kit) in 86% of tumors isolated during...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccr.2005.11.009

    authors: Kosmider O,Denis N,Lacout C,Vainchenker W,Dubreuil P,Moreau-Gachelin F

    更新日期:2005-12-01 00:00:00

  • PKCλ/ι Loss Induces Metabolic Reprogramming in Liver Cancer: Hitting Two Birds with One Stone?

    abstract::In this issue of Cancer Cell, Kudo et al. identify a novel tumor suppressor role for PKCλ/ι in hepatocellular carcinoma. Loss of PKCλ/ι in obesity-driven liver cancer results in cellular metabolic reprogramming that induces two reciprocally sustainable processes, oxidative phosphorylation and autophagy, which promote ...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccell.2020.07.003

    authors: Ramadori P,Li X,Heikenwalder M

    更新日期:2020-08-10 00:00:00

  • PDEF promotes luminal differentiation and acts as a survival factor for ER-positive breast cancer cells.

    abstract::Breast cancer is a heterogeneous disease and can be classified based on gene expression profiles that reflect distinct epithelial subtypes. We identify prostate-derived ETS factor (PDEF) as a mediator of mammary luminal epithelial lineage-specific gene expression and as a factor required for tumorigenesis in a subset ...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccr.2013.04.026

    authors: Buchwalter G,Hickey MM,Cromer A,Selfors LM,Gunawardane RN,Frishman J,Jeselsohn R,Lim E,Chi D,Fu X,Schiff R,Brown M,Brugge JS

    更新日期:2013-06-10 00:00:00

  • Radiotherapy complements immune checkpoint blockade.

    abstract::Adaptive immune resistance ablates effective anti-tumor immune responses. In a recent issue of Nature, Victor and colleagues describe that anti-PD-L1 combats adaptive immune resistance upon localized radiation plus anti-CTLA-4 therapy. The superior activity of radiation and dual immune checkpoint blockade is mediated ...

    journal_title:Cancer cell

    pub_type: 评论,杂志文章

    doi:10.1016/j.ccell.2015.03.015

    authors: Ngiow SF,McArthur GA,Smyth MJ

    更新日期:2015-04-13 00:00:00

  • Senesce to Survive: YAP-Mediated Dormancy Escapes EGFR/MEK Inhibition.

    abstract::Therapeutic resistance is a major challenge in cancer treatment. In this issue of Cancer Cell, Kurppa et al. demonstrated that a senescence-like state enables lung cancer cells to survive dual inhibition of EGFR and MEK. This was mediated by the YAP/TEAD pathway, which drives epigenomic reprogramming and EMT to counte...

    journal_title:Cancer cell

    pub_type: 评论,杂志文章

    doi:10.1016/j.ccell.2019.12.008

    authors: Bado I,Zhang XH

    更新日期:2020-01-13 00:00:00

  • Large-Scale Characterization of Drug Responses of Clinically Relevant Proteins in Cancer Cell Lines.

    abstract::Perturbation biology is a powerful approach to modeling quantitative cellular behaviors and understanding detailed disease mechanisms. However, large-scale protein response resources of cancer cell lines to perturbations are not available, resulting in a critical knowledge gap. Here we generated and compiled perturbed...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccell.2020.10.008

    authors: Zhao W,Li J,Chen MM,Luo Y,Ju Z,Nesser NK,Johnson-Camacho K,Boniface CT,Lawrence Y,Pande NT,Davies MA,Herlyn M,Muranen T,Zervantonakis IK,von Euw E,Schultz A,Kumar SV,Korkut A,Spellman PT,Akbani R,Slamon DJ,Gray

    更新日期:2020-12-14 00:00:00

  • Haploinsufficiency of SAMD9L, an endosome fusion facilitator, causes myeloid malignancies in mice mimicking human diseases with monosomy 7.

    abstract::Monosomy 7 and interstitial deletion of 7q (-7/7q-) are well-recognized nonrandom chromosomal abnormalities frequently found among patients with myelodysplastic syndromes (MDSs) and myeloid leukemias. We previously identified candidate myeloid tumor suppressor genes (SAMD9, SAMD9-like = SAMD9L, and Miki) in the 7q21.3...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccr.2013.08.011

    authors: Nagamachi A,Matsui H,Asou H,Ozaki Y,Aki D,Kanai A,Takubo K,Suda T,Nakamura T,Wolff L,Honda H,Inaba T

    更新日期:2013-09-09 00:00:00

  • Does CSF1R Blockade Turn into Friendly Fire?

    abstract::In this issue of Cancer Cell, Kumar et al. describe how CSF1R blockade induces not only an expected deprivation of tumor-associated macrophages, but also an accumulation of tumor-infiltrating polymorphonuclear mononuclear cells caused by Cxcl-1 released from cancer-associated fibroblasts. ...

    journal_title:Cancer cell

    pub_type: 评论,杂志文章

    doi:10.1016/j.ccell.2017.10.012

    authors: Greten TF

    更新日期:2017-11-13 00:00:00

  • EGFR phosphorylates tumor-derived EGFRvIII driving STAT3/5 and progression in glioblastoma.

    abstract::EGFRvIII, a frequently occurring mutation in primary glioblastoma, results in a protein product that cannot bind ligand, but signals constitutively. Deducing how EGFRvIII causes transformation has been difficult because of autocrine and paracrine loops triggered by EGFRvIII alone or in heterodimers with wild-type EGFR...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccr.2013.09.004

    authors: Fan QW,Cheng CK,Gustafson WC,Charron E,Zipper P,Wong RA,Chen J,Lau J,Knobbe-Thomsen C,Weller M,Jura N,Reifenberger G,Shokat KM,Weiss WA

    更新日期:2013-10-14 00:00:00

  • A tell-tail sign of chromatin: histone mutations drive pediatric glioblastoma.

    abstract::Recent genomic analyses of pediatric glioblastoma, a poorly understood tumor with dismal outcome, have identified mutations in histone H3 variants that affect critical amino acids in the tail. The findings extend discoveries of chromatin regulator inactivation and gain-of-function mutations by documenting alteration o...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccr.2012.03.001

    authors: Rheinbay E,Louis DN,Bernstein BE,Suvà ML

    更新日期:2012-03-20 00:00:00

  • Oncogenic BRAF regulates oxidative metabolism via PGC1α and MITF.

    abstract::Activating mutations in BRAF are the most common genetic alterations in melanoma. Inhibition of BRAF by small molecules leads to cell-cycle arrest and apoptosis. We show here that BRAF inhibition also induces an oxidative phosphorylation gene program, mitochondrial biogenesis, and the increased expression of the mitoc...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccr.2013.02.003

    authors: Haq R,Shoag J,Andreu-Perez P,Yokoyama S,Edelman H,Rowe GC,Frederick DT,Hurley AD,Nellore A,Kung AL,Wargo JA,Song JS,Fisher DE,Arany Z,Widlund HR

    更新日期:2013-03-18 00:00:00

  • Twist1-induced invadopodia formation promotes tumor metastasis.

    abstract::The Twist1 transcription factor is known to promote tumor metastasis and induce Epithelial-Mesenchymal Transition (EMT). Here, we report that Twist1 is capable of promoting the formation of invadopodia, specialized membrane protrusions for extracellular matrix degradation. Twist1 induces PDGFRα expression, which in tu...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccr.2011.01.036

    authors: Eckert MA,Lwin TM,Chang AT,Kim J,Danis E,Ohno-Machado L,Yang J

    更新日期:2011-03-08 00:00:00

  • CD4(+) T cells regulate pulmonary metastasis of mammary carcinomas by enhancing protumor properties of macrophages.

    abstract::During breast cancer development, increased presence of leukocytes in neoplastic stroma parallels disease progression; however, the functional significance of leukocytes in regulating protumor versus antitumor immunity in the breast remains poorly understood. Utilizing the MMTV-PyMT model of mammary carcinogenesis, we...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccr.2009.06.018

    authors: DeNardo DG,Barreto JB,Andreu P,Vasquez L,Tawfik D,Kolhatkar N,Coussens LM

    更新日期:2009-08-04 00:00:00

  • Smoothened variants explain the majority of drug resistance in basal cell carcinoma.

    abstract::Advanced basal cell carcinomas (BCCs) frequently acquire resistance to Smoothened (SMO) inhibitors through unknown mechanisms. Here we identify SMO mutations in 50% (22 of 44) of resistant BCCs and show that these mutations maintain Hedgehog signaling in the presence of SMO inhibitors. Alterations include four ligand ...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccell.2015.02.002

    authors: Atwood SX,Sarin KY,Whitson RJ,Li JR,Kim G,Rezaee M,Ally MS,Kim J,Yao C,Chang AL,Oro AE,Tang JY

    更新日期:2015-03-09 00:00:00

  • Inhibition of mitochondrial translation as a therapeutic strategy for human acute myeloid leukemia.

    abstract::To identify FDA-approved agents targeting leukemic cells, we performed a chemical screen on two human leukemic cell lines and identified the antimicrobial tigecycline. A genome-wide screen in yeast identified mitochondrial translation inhibition as the mechanism of tigecycline-mediated lethality. Tigecycline selective...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccr.2011.10.015

    authors: Skrtić M,Sriskanthadevan S,Jhas B,Gebbia M,Wang X,Wang Z,Hurren R,Jitkova Y,Gronda M,Maclean N,Lai CK,Eberhard Y,Bartoszko J,Spagnuolo P,Rutledge AC,Datti A,Ketela T,Moffat J,Robinson BH,Cameron JH,Wrana J,Eaves

    更新日期:2011-11-15 00:00:00

  • Sequential Therapy with PARP and WEE1 Inhibitors Minimizes Toxicity while Maintaining Efficacy.

    abstract::We demonstrate that concurrent administration of poly(ADP-ribose) polymerase (PARP) and WEE1 inhibitors is effective in inhibiting tumor growth but poorly tolerated. Concurrent treatment with PARP and WEE1 inhibitors induces replication stress, DNA damage, and abrogates the G2 DNA damage checkpoint in both normal and ...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccell.2019.05.001

    authors: Fang Y,McGrail DJ,Sun C,Labrie M,Chen X,Zhang D,Ju Z,Vellano CP,Lu Y,Li Y,Jeong KJ,Ding Z,Liang J,Wang SW,Dai H,Lee S,Sahni N,Mercado-Uribe I,Kim TB,Chen K,Lin SY,Peng G,Westin SN,Liu J,O'Connor MJ,Yap T

    更新日期:2019-06-10 00:00:00

  • Integrative genomic and proteomic analyses identify targets for Lkb1-deficient metastatic lung tumors.

    abstract::In mice, Lkb1 deletion and activation of Kras(G12D) results in lung tumors with a high penetrance of lymph node and distant metastases. We analyzed these primary and metastatic de novo lung cancers with integrated genomic and proteomic profiles, and have identified gene and phosphoprotein signatures associated with Lk...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccr.2010.04.026

    authors: Carretero J,Shimamura T,Rikova K,Jackson AL,Wilkerson MD,Borgman CL,Buttarazzi MS,Sanofsky BA,McNamara KL,Brandstetter KA,Walton ZE,Gu TL,Silva JC,Crosby K,Shapiro GI,Maira SM,Ji H,Castrillon DH,Kim CF,García-Echeve

    更新日期:2010-06-15 00:00:00

  • Metabolic activation of intrahepatic CD8+ T cells and NKT cells causes nonalcoholic steatohepatitis and liver cancer via cross-talk with hepatocytes.

    abstract::Hepatocellular carcinoma (HCC), the fastest rising cancer in the United States and increasing in Europe, often occurs with nonalcoholic steatohepatitis (NASH). Mechanisms underlying NASH and NASH-induced HCC are largely unknown. We developed a mouse model recapitulating key features of human metabolic syndrome, NASH, ...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccell.2014.09.003

    authors: Wolf MJ,Adili A,Piotrowitz K,Abdullah Z,Boege Y,Stemmer K,Ringelhan M,Simonavicius N,Egger M,Wohlleber D,Lorentzen A,Einer C,Schulz S,Clavel T,Protzer U,Thiele C,Zischka H,Moch H,Tschöp M,Tumanov AV,Haller D,Ung

    更新日期:2014-10-13 00:00:00

  • Hepatocyte necrosis induced by oxidative stress and IL-1 alpha release mediate carcinogen-induced compensatory proliferation and liver tumorigenesis.

    abstract::Hepatocyte I kappaB kinase beta (IKK beta) inhibits hepatocarcinogenesis by suppressing accumulation of reactive oxygen species (ROS) and liver damage, whereas JNK1 activation promotes ROS accumulation, liver damage, and carcinogenesis. We examined whether hepatocyte p38 alpha, found to inhibit liver carcinogenesis, a...

    journal_title:Cancer cell

    pub_type: 杂志文章

    doi:10.1016/j.ccr.2008.06.016

    authors: Sakurai T,He G,Matsuzawa A,Yu GY,Maeda S,Hardiman G,Karin M

    更新日期:2008-08-12 00:00:00