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Molecular Cancer Research Highlights February 2019 * Volume 17 * Number 2 Selected Articles from This Issue Protein-protein interaction network involving genes associated with GO:receptor activity Pan-Cancer Metastasis Correlates TGFBR3 ACVR2A NR2C2 NR2F1 AHR HNF4G HNF4A GRIK5 ARNT CALCRL CRCP ASGR1 TLR4 TLR5 GRID2 et al. DLG3 MED13 CFI TSHR ASGR2 TNFRSF4 CD226 Chen and Zhang Page 476 TLR1 ERBB4 MED17 SEC63 TLR10 AGER GRIA2 NR0B2 MED30 GLP1R LHCGR DERL1 TNFRSF9 ITGB2 KCNJ1 ESRRG NR5A2 Chen and Zhang and colleagues describe a systematic analysis SEC62 SORL1 MERTK BMPR2 GPR183 TRAM1 BMPR1A CFTR KCNH2 GPC6 of molecular correlates of metastasis using The Cancer Genome NRP1 PTPRR EPHB6 CD80 MED14 MED1 PPARA CELSR2 NCAM1 RYK CD86 Atlas (TCGA) datasets across 11 different cancer types, with data PPARG STRA6 EPNA3 LRP2 EFNB2 INTS6 CD28 PIGR ESRRB involving mRNA, microRNA, protein, and DNA methylation. NR4A2 THRAP3 TFRC GRM5 CD79B FLT1 ATP6AP2 NTRK1 INSRR NR3C1 XPR1 While some differential expression patterns associated with FCGR2C KDR ITGB1 CD79A CD3G AMOT ITGA4 IL2RA INSR PTPRC metastasis may be shared across multiple cancer types, each NR2F2 CD4 FZD4 DDR2 CXCR5 CD36 CD46 ITGAV ITGB6 VTN one also shows a metastasis signature that is distinct. When DLG1 CXCR4 CD1D IFNAR1 CALM3 GRM7 CNR1 FZD5 CD55 HCRTR1 combining TCGA data with that from multiple independent ADRB1 GABRR1 CSF1R NPC1 CR2 GABRR2 F2R F2 KCNQ5 CD47 LIFR ANTXR2 MET CD97 GP1BA fi LRP6 CR1 P2RX2 ABCC9 IL6ST pro ling datasets of metastatic tumors, the resulting catalog of FLT4 OSMR PTPRH P2RX4 KCNJ8 CUL5 GHR PTPRB gene-level alterations, according to cancer type, provides a Higher expression in metastasis versus primary for given cancer type BRCA CESC CRC ESCA HNSC PAAD PCPG PRAD SARC SKCM THCA resource for future studies. Fas Expression and Colon PCDH7 Modulates PDCD4 Suppresses Cancer Immune Evasion KrasG12D-Driven Lung Prostate Cancer Growth Tumorigenesis In Vivo and Castration Resistance Xiao et al. Page 420 Zhou et al. Page 594 Zennami et al. Page 618 Cytotoxic T lymphocytes (CTL) use the Protocadherins (PCDHs) are Prostate cancer can develop resistance to Fas-mediated apoptosis pathway as one of transmembrane proteins and members of anti-androgen therapy by reactiving the two effector mechanisms to suppress the Cadherin superfamily that play well- Androgen Receptor (AR) signaling. The tumors. Xiao et al. report here that the established roles in cell adhesion and critical processes that lie downstream of þ CD133 CD24loFaslo colon cancer cell regulation of signaling pathways. Both AR and contribute to tumor growth and subset exhibits decreased sensitivity to oncogenic and tumor suppressive roles therapeutic resistance remain to be fully FasL-induced apoptosis in vitro and have been assigned to PCDHs. However, defined. Zennami and colleagues increased resistance to both tumor-specific the roles of individual PCDHs in cancer identified PDCD4, a tumor suppressive CTL adoptive transfer and PD-1 blockade and the mechanisms through which their protein, as a key target of AR signaling in antibody immunotherapies in preclinical gain-of-function and loss-of-function prostate cancer cells. AR signaling mouse tumor models in vivo. Furthermore, drive tumorigenesis in vivo remain poorly suppresses PDCD4 expression, through Fas expression level is positively correlated understood. The current study establishes miR-21, leading to enhanced cell with colon cancer patient survival time. a critical oncogenic function for PCDH7 in proliferation, survival, tumorigenesis, and This study indicates that the lung cancer using a novel transgenic castration resistance. These results uncover þ CD133 CD24loFaslo colon cancer cells mouse model. Moreover, somatic genome PDCD4 loss as a new molecular may, at least in part, underlie colon cancer editing of Pcdh7 with CRISPR/Cas9 in mechanism of castration resistance and LSL-G12D fl/fl resistance to immune checkpoint Kras ; Tp53 mice support the suggest that pathways downstream of inhibitor immunotherapy. potential therapeutic efficacy of PCDH7 PDCD4 may be novel targets for therapy. inhibition for patients with lung cancer. www.aacrjournals.org 335 Downloaded from mcr.aacrjournals.org on October 1, 2021. © 2019 American Association for Cancer Research. Highlights of This Issue Mol Cancer Res 2019;17:335. Updated version Access the most recent version of this article at: http://mcr.aacrjournals.org/content/17/2/335 E-mail alerts Sign up to receive free email-alerts related to this article or journal. Reprints and To order reprints of this article or to subscribe to the journal, contact the AACR Publications Department at Subscriptions [email protected]. Permissions To request permission to re-use all or part of this article, use this link http://mcr.aacrjournals.org/content/17/2/335. Click on "Request Permissions" which will take you to the Copyright Clearance Center's (CCC) Rightslink site. Downloaded from mcr.aacrjournals.org on October 1, 2021. © 2019 American Association for Cancer Research. .
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