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[PMID]: 28859290 [Au] Autor: Troester MA; Sun X; Allott EH; Geradts J; Cohen SM; Tse CK; Kirk EL; Thorne LB; Mathews M; Li Y; Hu Z; Robinson WR; Hoadley KA; Olopade OI; Reeder-Hayes KE; Earp HS; Olshan AF; Carey LA; Perou CM [Ad] Endereço: Department of Epidemiology, Lineberger Comprehensive Cancer Center; Department of Pathology and Lab Medicine, Department of Nutrition (EHA), and Department of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, NC; Dana Farber Cancer Institute, Harvard University, Boston, MA; Center [Ti] Título: Racial Differences in PAM50 Subtypes in the Carolina Breast Cancer Study. [So] Source: J Natl Cancer Inst;110(2), 2018 Feb 01. [Is] ISSN: 1460-2105 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Background: African American breast cancer patients have lower frequency of hormone receptor-positive (HR+)/human epidermal growth factor receptor 2 (HER2)-negative disease and higher subtype-specific mortality. Racial differences in molecular subtype within clinically defined subgroups are not well understood. Methods: Using data and biospecimens from the population-based Carolina Breast Cancer Study (CBCS) Phase 3 (2008-2013), we classified 980 invasive breast cancers using RNA expression-based PAM50 subtype and recurrence (ROR) score that reflects proliferation and tumor size. Molecular subtypes (Luminal A, Luminal B, HER2-enriched, and Basal-like) and ROR scores (high vs low/medium) were compared by race (blacks vs whites) and age (≤50 years vs > 50 years) using chi-square tests and analysis of variance tests. Results: Black women of all ages had a statistically significantly lower frequency of Luminal A breast cancer (25.4% and 33.6% in blacks vs 42.8% and 52.1% in whites; younger and older, respectively). All other subtype frequencies were higher in black women (case-only odds ratio [OR] = 3.11, 95% confidence interval [CI] = 2.22 to 4.37, for Basal-like; OR = 1.45, 95% CI = 1.02 to 2.06, for Luminal B; OR = 2.04, 95% CI = 1.33 to 3.13, for HER2-enriched). Among clinically HR+/HER2- cases, Luminal A subtype was less common and ROR scores were statistically significantly higher among black women. Conclusions: Multigene assays highlight racial disparities in tumor subtype distribution that persist even in clinically defined subgroups. Differences in tumor biology (eg, HER2-enriched status) may be targetable to reduce disparities among clinically ER+/HER2- cases. [Mh] Termos MeSH primário: Afroamericanos Neoplasias da Mama/química Neoplasias da Mama/etnologia Grupo com Ancestrais do Continente Europeu RNA Neoplásico/análise Receptor ErbB-2/análise Receptores Estrogênicos/análise Receptores de Progesterona/análise [Mh] Termos MeSH secundário: Adulto Idoso Neoplasias da Mama/genética Neoplasias da Mama/patologia Proliferação Celular Feminino Seres Humanos Meia-Idade Recidiva Carga Tumoral Adulto Jovem [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (RNA, Neoplasm); 0 (Receptors, Estrogen); 0 (Receptors, Progesterone); EC 2.7.10.1 (ERBB2 protein, human); EC 2.7.10.1 (Receptor, ErbB-2) [Em] Mês de entrada: 1709 [Cu] Atualização por classe: 180308 [Lr] Data última revisão: 180308 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170902 [St] Status: MEDLINE [do] DOI: 10.1093/jnci/djx135

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[PMID]: 29421439 [Au] Autor: Li B; Mao R; Liu C; Zhang W; Tang Y; Guo Z [Ad] Endereço: Department of Interventional Therapy, Tianjin Medical University Cancer Institute and Hospital, Chinese National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin 300060, China. Electronic address: libao_gr6688@163.com. [Ti] Título: LncRNA FAL1 promotes cell proliferation and migration by acting as a CeRNA of miR-1236 in hepatocellular carcinoma cells. [So] Source: Life Sci;197:122-129, 2018 Mar 15. [Is] ISSN: 1879-0631 [Cp] País de publicação: Netherlands [La] Idioma: eng [Ab] Resumo: BACKGROUND: Long non-coding RNAs (LncRNAs) have been demonstrated to play crucial role in tumor growth and metastasis for hepatocellular carcinoma (HCC). LncRNA FAL1 has been indicated to promote the progression of various cancers. However, the role of lncRNA FAL1 in HCC was poorly understood. METHODS: The expression levels of lncRNA FAL1 in HCC tissues and cells were determined by RT-qPCR. The roles of lncRNA FAL1 on HCC cells were investigated by MTT, colony formation, transwell, RT-qPCR, and Western blotting. The miRNA binding sites of lncRNA FAL1 was predicted using RegRNA 2.0 and miR-1236 was validated to target lncRNA FAL1 by luciferase reporter assays and RT-qPCR. Finally, the expression levels of lncRNA FAL1 in serum exosome of HCC patients was also investigated and the role of exosome-mediated lncRNA FAL1 was further investigated by co-culturing with HCC cells. RESULTS: This study first showed that lncRNA FAL1 was up-regulated in HCC tissues and functioned as an oncogene in HCC. LncRNA FAL1 could accelerate cell proliferation and metastasis as a ceRNA mechanism by competitively binding to miR-1236. Moreover, lncRNA FAL1 was also up-regulated in serum exosome of HCC patients and could transfer lncRNA FAL1 to HCC cells to increase their abilities of cell proliferation and migration. CONCLUSIONS: Taken together, this study indicated that lncRNA FAL1 functions as an oncogenic in HCC and may be a novel diagnostic biomarker or a novel target for the treatment of HCC in future. [Mh] Termos MeSH primário: Carcinoma Hepatocelular/metabolismo Movimento Celular Proliferação Celular Regulação Neoplásica da Expressão Gênica Neoplasias Hepáticas/metabolismo MicroRNAs/biossíntese RNA Longo não Codificante/biossíntese RNA Neoplásico/biossíntese Regulação para Cima [Mh] Termos MeSH secundário: Carcinoma Hepatocelular/genética Carcinoma Hepatocelular/patologia Exossomos/genética Exossomos/metabolismo Exossomos/patologia Feminino Células Hep G2 Seres Humanos Neoplasias Hepáticas/genética Neoplasias Hepáticas/patologia Masculino MicroRNAs/genética RNA Longo não Codificante/genética RNA Neoplásico/genética [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (MIRN1236 microRNA, human); 0 (MicroRNAs); 0 (RNA, Long Noncoding); 0 (RNA, Neoplasm); 0 (focally amplified long noncoding RNA on chromosome 1, human) [Em] Mês de entrada: 1803 [Cu] Atualização por classe: 180301 [Lr] Data última revisão: 180301 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 180209 [St] Status: MEDLINE

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[PMID]: 29459023 [Au] Autor: Shen Y; Feng Y; Chen H; Huang L; Wang F; Bai J; Yang Y; Wang J; Zhao W; Jia Y; Peng Y; Lei X; He A [Ad] Endereço: Department of Hematology, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China. [Ti] Título: Focusing on long non-coding RNA dysregulation in newly diagnosed multiple myeloma. [So] Source: Life Sci;196:133-142, 2018 Mar 01. [Is] ISSN: 1879-0631 [Cp] País de publicação: Netherlands [La] Idioma: eng [Ab] Resumo: AIMS: Multiple myeloma (MM) is an incurable hematological cancer with a higher rate of relapse. Alterations in the function of long non-coding RNAs (lncRNAs) promote the progression and metastasis of cancer. We carry out this study to explore the expression profile of differently expressed lncRNAs in newly diagnosed MM. MAIN METHODS: The Bone marrows we analyzed were obtained from five MM and five IDA patients (serving as controls). Arraystar Human LncRNA Array V4.0 was used to profile expression of lncRNAs and mRNAs. Gene ontology (GO) and pathway analysis were utilized to understand the biological roles of differently expressed genes, while Database for Annotation, Visualization and Integrated Discovery (DAVID) was used for constructing the lncRNA-mRNA co-expression network. Quantitative polymerase chain reaction (qRT-PCR) was performed to confirm the expressions of dysregulated lncRNAs. KEY FINDINGS: Bioinformatic analysis of the lncRNA expression identified >3000 dysregulated lncRNAs (difference ≥ 2-fold) in MM samples. GO and pathway analysis revealed that ECM-receptor and cell cycle pathway-related genes were significantly associated with MM. Four dysregulated lncRNAs were confirmed by qRT-PCR. Among them, the expression of ST3GAL6-AS1, LAMA5-AS1and RP11-175D17.3wereassociated with stage and risk status of MM. On the basis of GEO public database analysis, LAMA5-AS1 was related with an overall survival rate of MM patients. SIGNIFICANCE: These results reveal the feasible functions of lncRNAs in pathogenesis of MM. Further studies are required to explore whether these lncRNAs could serve as candidate therapeutic targets and new molecular biomarkers for MM. [Mh] Termos MeSH primário: Mieloma Múltiplo/genética RNA Longo não Codificante/biossíntese [Mh] Termos MeSH secundário: Adulto Idoso Células da Medula Óssea/efeitos dos fármacos Biologia Computacional Progressão da Doença Regulação para Baixo/efeitos dos fármacos Feminino Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos Redes Reguladoras de Genes/efeitos dos fármacos Seres Humanos Masculino Meia-Idade Mieloma Múltiplo/tratamento farmacológico Reação em Cadeia da Polimerase RNA Longo não Codificante/efeitos dos fármacos RNA Longo não Codificante/genética RNA Mensageiro/biossíntese RNA Mensageiro/genética RNA Neoplásico/biossíntese RNA Neoplásico/genética Taxa de Sobrevida Adulto Jovem [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (RNA, Long Noncoding); 0 (RNA, Messenger); 0 (RNA, Neoplasm) [Em] Mês de entrada: 1802 [Cu] Atualização por classe: 180226 [Lr] Data última revisão: 180226 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 180221 [St] Status: MEDLINE

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[PMID]: 29192829 [Au] Autor: Liu G; Thannickal VJ [Ad] Endereço: 1 Department of Medicine University of Alabama at Birmingham Birmingham, Alabama. [Ti] Título: The Lung Likes the Little Fella miR-29. [So] Source: Am J Respir Cell Mol Biol;57(6):637-638, 2017 12. [Is] ISSN: 1535-4989 [Cp] País de publicação: United States [La] Idioma: eng [Mh] Termos MeSH primário: Hipertensão Pulmonar/metabolismo Fibrose Pulmonar Idiopática/metabolismo Neoplasias Pulmonares/metabolismo Pulmão/metabolismo MicroRNAs/metabolismo RNA Neoplásico/metabolismo [Mh] Termos MeSH secundário: Animais Seres Humanos Hipertensão Pulmonar/genética Hipertensão Pulmonar/patologia Fibrose Pulmonar Idiopática/genética Fibrose Pulmonar Idiopática/patologia Pulmão/patologia Neoplasias Pulmonares/genética Neoplasias Pulmonares/patologia MicroRNAs/genética RNA Neoplásico/genética [Pt] Tipo de publicação: EDITORIAL [Nm] Nome de substância: 0 (MIRN29 microRNA, human); 0 (MicroRNAs); 0 (RNA, Neoplasm) [Em] Mês de entrada: 1802 [Cu] Atualização por classe: 180221 [Lr] Data última revisão: 180221 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 171202 [St] Status: MEDLINE [do] DOI: 10.1165/rcmb.2017-0266ED

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[PMID]: 29324844 [Au] Autor: Barakat DJ; Suresh R; Barberi T; Pienta KJ; Simons BW; Friedman AD [Ad] Endereço: Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America. [Ti] Título: Absence of myeloid Klf4 reduces prostate cancer growth with pro-atherosclerotic activation of tumor myeloid cells and infiltration of CD8 T cells. [So] Source: PLoS One;13(1):e0191188, 2018. [Is] ISSN: 1932-6203 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: The microenvironment of prostate cancer often includes abundant tumor-associated macrophages (TAMs), with their acquisition of an M2 phenotype correlating with local aggressiveness and metastasis. Tumor-derived M-CSF contributes to TAM M2 polarization, and M-CSF receptor inhibition slows prostate cancer growth in model systems. As additional cytokines can direct TAM M2 polarization, targeting downstream transcription factors could avoid resistance. Klf4 and C/EBPß each contribute to monocyte development, and reduced expression of macrophage Klf4 or C/EBPß favors their adoption of a pro-inflammatory M1 state. We find that a Hi-Myc C57BL/6 prostate cancer line grows more slowly in syngeneic Klf4(f/f);Lys-Cre compared with Klf4(f/f) mice when inoculated subcutaneously, but grows equally rapidly in C/EBPß(f/f);Lys-Cre and C/EBPß(f/f) hosts. In the absence of myeloid Klf4, TAMs have reduced expression of surface mannose receptor and Fizz1 mRNA, both M2 markers. Global gene expression analysis further revealed activation of pro-inflammatory, pro-atherosclerotic pathways. Analysis of tumor-infiltrating lymphocytes (TILs) demonstrated markedly increased activated CD8 T cell numbers, and CD8 T cell depletion obviated the inhibitory effect of myeloid Klf4 deletion on prostate cancer growth. These findings suggest that reducing expression or activity of the Klf4 transcription factor in tumor myeloid cells may contribute to prostate cancer therapy. [Mh] Termos MeSH primário: Fatores de Transcrição Kruppel-Like/deficiência Neoplasias da Próstata/metabolismo Neoplasias da Próstata/patologia [Mh] Termos MeSH secundário: Animais Aterosclerose/etiologia Proteína beta Intensificadora de Ligação a CCAAT/deficiência Proteína beta Intensificadora de Ligação a CCAAT/genética Antígeno CD11c/metabolismo Linfócitos T CD8-Positivos/imunologia Linfócitos T CD8-Positivos/patologia Linhagem Celular Tumoral Fatores de Transcrição Kruppel-Like/genética Lectinas Tipo C/metabolismo Linfócitos do Interstício Tumoral Macrófagos/imunologia Macrófagos/metabolismo Macrófagos/patologia Masculino Lectinas de Ligação a Manose/metabolismo Camundongos Camundongos Endogâmicos C57BL Camundongos Transgênicos Células Mieloides/imunologia Células Mieloides/metabolismo Células Mieloides/patologia Neoplasias da Próstata/genética RNA Mensageiro/genética RNA Mensageiro/metabolismo RNA Neoplásico/genética RNA Neoplásico/metabolismo Receptores de Superfície Celular/metabolismo Microambiente Tumoral [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S. [Nm] Nome de substância: 0 (CCAAT-Enhancer-Binding Protein-beta); 0 (CD11c Antigen); 0 (GKLF protein); 0 (Kruppel-Like Transcription Factors); 0 (Lectins, C-Type); 0 (Mannose-Binding Lectins); 0 (RNA, Messenger); 0 (RNA, Neoplasm); 0 (Receptors, Cell Surface); 0 (mannose receptor) [Em] Mês de entrada: 1802 [Cu] Atualização por classe: 180220 [Lr] Data última revisão: 180220 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 180112 [St] Status: MEDLINE [do] DOI: 10.1371/journal.pone.0191188

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[PMID]: 29217194 [Au] Autor: Kong Q; Qiu M [Ad] Endereço: Department of Oncology, Affiliated Hospital of Jining Medical College, Jining, 272029, Shangdong province, China. [Ti] Título: Long noncoding RNA SNHG15 promotes human breast cancer proliferation, migration and invasion by sponging miR-211-3p. [So] Source: Biochem Biophys Res Commun;495(2):1594-1600, 2018 01 08. [Is] ISSN: 1090-2104 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Long non-coding RNAs (lncRNA) have been demonstrated to act as essential regulators in the development and progression of breast cancer. In our study, we found that long noncoding RNA SNHG15 was highly expressed in breast cancer tissues and cell lines. And the expression of SNHG15 was correlated with TNM stage, lymphnode metastasis and survival in breast cancer patients. SNHG15 knockdown significantly inhibited the proliferation and induced apoptosis in breast cancer cells in vitro and in vivo. Besides, SNHG15 downregulation suppressed cell migration and invasion in MCF-7 and BT-20 cells, and inhibited epithelial-mesenchymal transition (EMT). In mechanism, we found that SNHG15 acted as a competing endogenous RNA to sponge miR-211-3p, which was downregulated in breast cancers and inhibited cell proliferation and migration. Our results showed that there was a negative correlation between SNHG15 and miR-211-3p expression in breast cancer patients. Collectively, we, for the first time, revealed the functions of SNHG15 and miR-211-3p in breast cancer. [Mh] Termos MeSH primário: Neoplasias da Mama/genética Neoplasias da Mama/patologia MicroRNAs/genética RNA Longo não Codificante/genética [Mh] Termos MeSH secundário: Animais Apoptose/genética Neoplasias da Mama/metabolismo Linhagem Celular Tumoral Movimento Celular/genética Proliferação Celular/genética Progressão da Doença Transição Epitelial-Mesenquimal/genética Feminino Regulação Neoplásica da Expressão Gênica Técnicas de Silenciamento de Genes Xenoenxertos Seres Humanos Células MCF-7 Camundongos Camundongos Endogâmicos BALB C Camundongos Nus MicroRNAs/metabolismo Invasividade Neoplásica/genética Transplante de Neoplasias RNA Longo não Codificante/antagonistas & inibidores RNA Longo não Codificante/metabolismo RNA Neoplásico/antagonistas & inibidores RNA Neoplásico/genética RNA Neoplásico/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (MIRN211 microRNA, human); 0 (MicroRNAs); 0 (RNA, Long Noncoding); 0 (RNA, Neoplasm); 0 (SNHG16 lncRNA, human) [Em] Mês de entrada: 1802 [Cu] Atualização por classe: 180220 [Lr] Data última revisão: 180220 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 171209 [St] Status: MEDLINE

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[PMID]: 29278708 [Au] Autor: Suzuki S; Hoshino H; Yoshida K; Nakanishi J; Tsuchiya-Hirata S; Kobuke S; Haruyama N; Nishimura F; Shiba H [Ad] Endereço: Department of Biological Endodontics, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, 734-8553, Japan. Electronic address: suzukis@hiroshima-u.ac.jp. [Ti] Título: Genome-wide identification of chromatin-enriched RNA reveals that unspliced dentin matrix protein-1 mRNA regulates cell proliferation in squamous cell carcinoma. [So] Source: Biochem Biophys Res Commun;495(3):2303-2309, 2018 01 15. [Is] ISSN: 1090-2104 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Chromatin-enriched noncoding RNAs (ncRNAs) have emerged as key molecules in epigenetic processes by interacting with chromatin-associated proteins. Recently, protein-coding mRNA genes have been reported to be chromatin-tethered, similar with ncRNA. However, very little is known about whether chromatin-enriched mRNA is involved in the chromatin modification process. Here, we comprehensively examined chromatin-enriched RNA in squamous cell carcinoma (SQCC) cells by RNA subcellular localization analysis, which was a combination of RNA fractionation and RNA-seq. We identified 11 mRNAs as highly chromatin-enriched RNAs. Among these, we focused on the dentin matrix protein-1 (DMP-1) gene because its expression in SQCC cells has not been reported. Furthermore, we clarified that DMP-1 mRNA was retained in chromatin in its unspliced form in SQCC in vitro and in vivo. As the inhibition of the unspliced DMP-1 mRNA (unspDMP-1) expression resulted in decreased cellular proliferation in SQCC cells, we performed ChIP-qPCR to identify cell cycle-related genes whose expression was epigenetically modified by unspDMP-1, and found that the CDKN1B promoter became active in SQCC cells by inhibiting unspDMP-1 expression. This result was further validated by the increased CDKN1B gene expression in the cells treated with siRNA for unspDMP-1 and by restoration of the decreased cellular proliferation rate by simultaneously inhibiting CDKN1B expression in SQCC cells. Further, to examine whether unspDMP-1 was able to associate with the CDKN1B promoter region, SQCC cells stably expressing PP7-mCherry fusion protein were transiently transfected with the unspDMP-1 fused to 24 repeats of the PP7 RNA stem loop (unspDMP-1-24xPP7) and we found that unspDMP-1-24xPP7 was efficiently precipitated with the antibody against mCherry and was significantly enriched in the CDKN1B promoter region. Thus, unspDMP-1 is a novel chromatin-enriched RNA that epigenetically regulates cellular proliferation of SQCC. [Mh] Termos MeSH primário: Carcinoma de Células Escamosas/genética Carcinoma de Células Escamosas/patologia Proliferação Celular/genética Cromatina/genética Proteínas da Matriz Extracelular/genética Fosfoproteínas/genética RNA Neoplásico/genética RNA não Traduzido/genética [Mh] Termos MeSH secundário: Carcinoma de Células Escamosas/metabolismo Linhagem Celular Tumoral Mapeamento Cromossômico/métodos Seres Humanos MicroRNAs/genética [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Chromatin); 0 (DMP1 protein, human); 0 (Extracellular Matrix Proteins); 0 (MicroRNAs); 0 (Phosphoproteins); 0 (RNA, Neoplasm); 0 (RNA, Untranslated) [Em] Mês de entrada: 1802 [Cu] Atualização por classe: 180214 [Lr] Data última revisão: 180214 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 171227 [St] Status: MEDLINE

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[PMID]: 29175329 [Au] Autor: Yang X; Qu K; Tao J; Yin G; Han S; Liu Q; Sun H [Ad] Endereço: Department of Hepatobiliary Surgery, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, China. [Ti] Título: Inhibition of CIP2A attenuates tumor progression by inducing cell cycle arrest and promoting cellular senescence in hepatocellular carcinoma. [So] Source: Biochem Biophys Res Commun;495(2):1807-1814, 2018 01 08. [Is] ISSN: 1090-2104 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: CIP2A is a recent identified oncogene that inhibits protein phosphatase 2A (PP2A) and stabilizes c-Myc in cancer cells. To investigate the potential oncogenic role and prognostic value of CIP2A, we comprehensively analyzed the CIP2A expression levels in pan-cancer and observed high expression level of CIP2A in majority cancer types, including hepatocellular carcinoma (HCC). Based on a validation cohort including 60 HCC and 20 non-tumorous tissue samples, we further confirmed the high mRNA and protein expression levels of CIP2A in HCC, and found high CIP2A mRNA expression level was associated with unfavorable overall and recurrence-free survival in patients with HCC. Mechanistic investigations revealed that inhibition of CIP2A significantly attenuated cellular proliferation in vitro and tumourigenicity in vivo. Bioinformatic analysis suggested that CIP2A might be involved in regulating cell cycle. Our experimental data further confirmed CIP2A knockdown induced cell cycle arrest at G1 phase. We found accumulated cellular senescence in HCC cells with CIP2A knockdown, companying expression changes of senescence associated proteins (p21, CDK2, CDK4, cyclin D1, MCM7 and FoxM1). Mechanistically, CIP2A knockdown repressed FoxM1 expression and induced FoxM1 dephosphorylation. Moreover, inhibition of PP2A by phosphatase inhibitor rescued the repression of FoxM1. Taken together, our results showed that CIP2A was highly expressed in HCC. Inhibition of CIP2A induced cell cycle arrest and promoted cellular senescence via repressing FoxM1 transcriptional activity, suggesting a potential anti-cancer target for patients with HCC. [Mh] Termos MeSH primário: Carcinoma Hepatocelular/terapia Pontos de Checagem do Ciclo Celular/fisiologia Neoplasias Hepáticas/terapia Proteínas de Membrana/antagonistas & inibidores [Mh] Termos MeSH secundário: Autoantígenos/genética Autoantígenos/fisiologia Biomarcadores Tumorais/genética Carcinoma Hepatocelular/genética Carcinoma Hepatocelular/patologia Pontos de Checagem do Ciclo Celular/genética Linhagem Celular Tumoral Senescência Celular/genética Senescência Celular/fisiologia Progressão da Doença Proteína Forkhead Box M1/metabolismo Expressão Gênica Técnicas de Silenciamento de Genes Células Hep G2 Seres Humanos Neoplasias Hepáticas/genética Neoplasias Hepáticas/patologia Proteínas de Membrana/genética Proteínas de Membrana/fisiologia Oncogenes Prognóstico RNA Mensageiro/genética RNA Mensageiro/metabolismo RNA Neoplásico/genética RNA Neoplásico/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Autoantigens); 0 (Biomarkers, Tumor); 0 (FOXM1 protein, human); 0 (Forkhead Box Protein M1); 0 (KIAA1524 protein, human); 0 (Membrane Proteins); 0 (RNA, Messenger); 0 (RNA, Neoplasm) [Em] Mês de entrada: 1802 [Cu] Atualização por classe: 180212 [Lr] Data última revisão: 180212 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 171128 [St] Status: MEDLINE

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[PMID]: 29346397 [Au] Autor: Hildenbrand G; Metzler P; Pilarczyk G; Bobu V; Kriz W; Hosser H; Fleckenstein J; Krufczik M; Bestvater F; Wenz F; Hausmann M [Ad] Endereço: Kirchhoff-Institute for Physics, Faculty of Physics and Astronomy, Heidelberg University, Heidelberg, Germany. [Ti] Título: Dose enhancement effects of gold nanoparticles specifically targeting RNA in breast cancer cells. [So] Source: PLoS One;13(1):e0190183, 2018. [Is] ISSN: 1932-6203 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Localization microscopy has shown to be capable of systematic investigations on the arrangement and counting of cellular uptake of gold nanoparticles (GNP) with nanometer resolution. In this article, we show that the application of specially modified RNA targeting gold nanoparticles ("SmartFlares") can result in ring like shaped GNP arrangements around the cell nucleus. Transmission electron microscopy revealed GNP accumulation in vicinity to the intracellular membrane structures including them of the endoplasmatic reticulum. A quantification of the radio therapeutic dose enhancement as a proof of principle was conducted with γH2AX foci analysis: The application of both-SmartFlares and unmodified GNPs-lead to a significant dose enhancement with a factor of up to 1.2 times the dose deposition compared to non-treated breast cancer cells. This enhancement effect was even more pronounced for SmartFlares. Furthermore, it was shown that a magnetic field of 1 Tesla simultaneously applied during irradiation has no detectable influence on neither the structure nor the dose enhancement dealt by gold nanoparticles. [Mh] Termos MeSH primário: Neoplasias da Mama/patologia Ouro/química Nanopartículas Metálicas RNA Neoplásico/efeitos dos fármacos [Mh] Termos MeSH secundário: Neoplasias da Mama/genética Linhagem Celular Tumoral Seres Humanos Nanopartículas Metálicas/química [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (RNA, Neoplasm); 7440-57-5 (Gold) [Em] Mês de entrada: 1801 [Cu] Atualização por classe: 180129 [Lr] Data última revisão: 180129 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 180119 [St] Status: MEDLINE [do] DOI: 10.1371/journal.pone.0190183

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[PMID]: 29293502 [Au] Autor: Koplev S; Lin K; Dohlman AB; Ma'ayan A [Ad] Endereço: Department of Pharmacological Sciences, Mount Sinai Center for Bioinformatics, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY, United States of America. [Ti] Título: Integration of pan-cancer transcriptomics with RPPA proteomics reveals mechanisms of epithelial-mesenchymal transition. [So] Source: PLoS Comput Biol;14(1):e1005911, 2018 01. [Is] ISSN: 1553-7358 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Integrating data from multiple regulatory layers across cancer types could elucidate additional mechanisms of oncogenesis. Using antibody-based protein profiling of 736 cancer cell lines, along with matching transcriptomic data, we show that pan-cancer bimodality in the amounts of mRNA, protein, and protein phosphorylation reveals mechanisms related to the epithelial-mesenchymal transition (EMT). Based on the bimodal expression of E-cadherin, we define an EMT signature consisting of 239 genes, many of which were not previously associated with EMT. By querying gene expression signatures collected from cancer cell lines after small-molecule perturbations, we identify enrichment for histone deacetylase (HDAC) inhibitors as inducers of EMT, and kinase inhibitors as mesenchymal-to-epithelial transition (MET) promoters. Causal modeling of protein-based signaling identifies putative drivers of EMT. In conclusion, integrative analysis of pan-cancer proteomic and transcriptomic data reveals key regulatory mechanisms of oncogenic transformation. [Mh] Termos MeSH primário: Transição Epitelial-Mesenquimal/genética Neoplasias/genética Neoplasias/metabolismo [Mh] Termos MeSH secundário: Caderinas/genética Caderinas/metabolismo Carcinogênese Linhagem Celular Tumoral Biologia Computacional Transição Epitelial-Mesenquimal/efeitos dos fármacos Inibidores de Histona Desacetilases/farmacologia Seres Humanos Modelos Genéticos Modelos Estatísticos Neoplasias/patologia Fosforilação Análise Serial de Proteínas/estatística & dados numéricos Inibidores de Proteínas Quinases/farmacologia Proteômica RNA Mensageiro/genética RNA Mensageiro/metabolismo RNA Neoplásico/genética RNA Neoplásico/metabolismo Transcriptoma [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL [Nm] Nome de substância: 0 (CDH1 protein, human); 0 (Cadherins); 0 (Histone Deacetylase Inhibitors); 0 (Protein Kinase Inhibitors); 0 (RNA, Messenger); 0 (RNA, Neoplasm) [Em] Mês de entrada: 1801 [Cu] Atualização por classe: 180128 [Lr] Data última revisão: 180128 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 180103 [St] Status: MEDLINE [do] DOI: 10.1371/journal.pcbi.1005911

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