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  1 / 7921 MEDLINE  
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[PMID]:28460475
[Au] Autor:Song JM; Molla K; Anandharaj A; Cornax I; O Sullivan MG; Kirtane AR; Panyam J; Kassie F
[Ad] Endereço:Masonic Cancer Center, University of Minnesota, Minneapolis, MN 55455, USA.
[Ti] Título:Triptolide suppresses the in vitro and in vivo growth of lung cancer cells by targeting hyaluronan-CD44/RHAMM signaling.
[So] Source:Oncotarget;8(16):26927-26940, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Higher levels of hyaluronan (HA) and its receptors CD44 and RHAMM have been associated with poor prognosis and metastasis in NSCLC. In the current study, our goal was to define, using cellular and orthotopic lung tumor models, the role of HA-CD44/RHAMM signaling in lung carcinogenesis and to assess the potential of triptolide to block HA-CD44/RHAMM signaling and thereby suppress the development and progression of lung cancer. Triptolide reduced the viability of five non-small cell lung cancer (NSCLC) cells, the proliferation and self-renewal of pulmospheres, and levels of HA synthase 2 (HAS2), HAS3, HA, CD44, RHAMM, EGFR, Akt and ERK, but increased the cleavage of caspase 3 and PARP. Silencing of HAS2, CD44 or RHAMM induced similar effects. Addition of excess HA to the culture media completely abrogated the effects of triptolide and siRNAs targeting HAS2, CD44, or RHAMM. In an orthotopic lung cancer model in nude rats, intranasal administration of liposomal triptolide (400 µg/kg) for 8 weeks significantly reduced lung tumor growth as determined by bioluminescence imaging, lung weight measurements and gross and histopathological analysis of tumor burden. Also, triptolide suppressed expressions of Ki-67, a marker for cell proliferation, HAS2, HAS3, HA, CD44, and RHAMM in lung tumors. Overall, our results provide a strong rationale for mitigating lung cancer by targeting the HA-CD44/RHAMM signaling axis.
[Mh] Termos MeSH primário: Antineoplásicos Alquilantes/farmacologia
Diterpenos/farmacologia
Proteínas da Matriz Extracelular/metabolismo
Receptores de Hialuronatos/antagonistas & inibidores
Receptores de Hialuronatos/metabolismo
Neoplasias Pulmonares/metabolismo
Fenantrenos/farmacologia
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Modelos Animais de Doenças
Compostos de Epóxi/farmacologia
Inativação Gênica
Seres Humanos
Receptores de Hialuronatos/genética
Hialuronan Sintases/genética
Hialuronan Sintases/metabolismo
Neoplasias Pulmonares/tratamento farmacológico
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/patologia
Masculino
RNA Interferente Pequeno/genética
Ratos
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Alkylating); 0 (CD44 protein, human); 0 (Diterpenes); 0 (Epoxy Compounds); 0 (Extracellular Matrix Proteins); 0 (Hyaluronan Receptors); 0 (Phenanthrenes); 0 (RNA, Small Interfering); 0 (hyaluronan-mediated motility receptor); 19ALD1S53J (triptolide); EC 2.4.1.212 (Hyaluronan Synthases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15879


  2 / 7921 MEDLINE  
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[PMID]:28468593
[Au] Autor:Ikemoto H; Lingasamy P; Anton Willmore AM; Hunt H; Kurm K; Tammik O; Scodeller P; Simón-Gracia L; Kotamraju VR; Lowy AM; Sugahara KN; Teesalu T
[Ad] Endereço:1 Laboratory of Cancer Biology, Institute of Biomedicine and Translational Medicine, University of Tartu, Tartu, Estonia.
[Ti] Título:Hyaluronan-binding peptide for targeting peritoneal carcinomatosis.
[So] Source:Tumour Biol;39(5):1010428317701628, 2017 May.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Peritoneal carcinomatosis results from dissemination of solid tumors in the peritoneal cavity, and is a common site of metastasis in patients with carcinomas of gastrointestinal or gynecological origin. Peritoneal carcinomatosis treatment is challenging as poorly vascularized, disseminated peritoneal micro-tumors are shielded from systemic anticancer drugs and drive tumor regrowth. Here, we describe the identification and validation of a tumor homing peptide CKRDLSRRC (IP3), which upon intraperitoneal administration delivers payloads to peritoneal metastases. IP3 peptide was identified by in vivo phage display on a mouse model of peritoneal carcinomatosis of gastric origin (MKN-45P), using high-throughput sequencing of the peptide-encoding region of phage genome as a readout. The IP3 peptide contains a hyaluronan-binding motif, and fluorescein-labeled IP3 peptide bound to immobilized hyaluronan in vitro. After intraperitoneal administration in mice bearing peritoneal metastases of gastric and colon origin, IP3 peptide homed robustly to macrophage-rich regions in peritoneal tumors, including poorly vascularized micro-tumors. Finally, we show that IP3 functionalization conferred silver nanoparticles the ability to home to peritoneal tumors of gastric and colonic origin, suggesting that it could facilitate targeted delivery of nanoscale payloads to peritoneal tumors. Collectively, our study suggests that the IP3 peptide has potential applications for targeting drugs, nanoparticles, and imaging agents to peritoneal tumors.
[Mh] Termos MeSH primário: Carcinoma/tratamento farmacológico
Receptores de Hialuronatos/administração & dosagem
Peptídeos/administração & dosagem
Neoplasias Peritoneais/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Bacteriófagos/genética
Carcinoma/genética
Carcinoma/patologia
Linhagem Celular Tumoral
Modelos Animais de Doenças
Sistemas de Liberação de Medicamentos
Seres Humanos
Receptores de Hialuronatos/genética
Camundongos
Nanopartículas/administração & dosagem
Nanopartículas/química
Metástase Neoplásica
Peptídeos/genética
Cavidade Peritoneal/patologia
Neoplasias Peritoneais/genética
Neoplasias Peritoneais/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hyaluronan Receptors); 0 (Peptides)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317701628


  3 / 7921 MEDLINE  
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[PMID]:27776018
[Au] Autor:Vartanian A; Baryshnikova M; Burova O; Afanasyeva D; Misyurin V; Belyаvsky A; Shprakh Z
[Ad] Endereço:Department of Experimental Diagnosis and Therapy of Tumors, N.N. Blokhin Russian Cancer Research Center, Moscow, Russia.
[Ti] Título:Inhibitor of vasculogenic mimicry restores sensitivity of resistant melanoma cells to DNA-damaging agents.
[So] Source:Melanoma Res;27(1):8-16, 2017 Feb.
[Is] ISSN:1473-5636
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The increasing incidence of melanoma makes this cancer an important public health problem. Therapeutic resistance is still a major obstacle to the therapy of patients with metastatic melanomas. The aim of this study was to develop the melanoma cell line resistant to DNA-alkylating agents and to elucidate the mechanisms involved in acquired drug resistance. We established a unique melanoma subline Mel MeR resistant to DNA-alkylating drug aranoza by continuous stepwise selection of the Mel Me/WT cell line with increasing concentrations of this drug. Mel MeR cells were also cross-resistant to streptozotocin or cisplatin. Here, we show that aranoza-resistant melanoma cells modulate the ABC transporter activity, upregulate the expression of PRAME, adopt a vascular-related phenotype and engage in vasculogenic mimicry. LCS1269, a vasculogenic mimicry low-molecular-weight inhibitor, reverses the sensitivity of resistant melanoma cells to DNA-damaging agents. In this study, we provide experimental evidence that LCS1269 might be considered as a new potential anticancer agent capable of overcoming multidrug resistance for DNA-damaging agents in melanoma.
[Mh] Termos MeSH primário: Antineoplásicos Alquilantes/farmacologia
Carbazóis/farmacologia
Linhagem Celular Tumoral
Resistência a Medicamentos Antineoplásicos
Glicosídeos/farmacologia
Melanoma/tratamento farmacológico
Melanoma/metabolismo
Metilnitrosoureia/análogos & derivados
Neovascularização Patológica/prevenção & controle
[Mh] Termos MeSH secundário: Membro 1 da Subfamília B de Cassetes de Ligação de ATP/metabolismo
Antígenos de Neoplasias/genética
Apoptose/efeitos dos fármacos
Antígeno CD24/metabolismo
Resistência a Medicamentos Antineoplásicos/genética
Endoglina/metabolismo
Corantes Fluorescentes/metabolismo
Expressão Gênica/efeitos dos fármacos
Seres Humanos
Receptores de Hialuronatos/metabolismo
Molécula 1 de Adesão Intercelular/metabolismo
Masculino
Melanoma/irrigação sanguínea
Melanoma/genética
Metilnitrosoureia/farmacologia
Meia-Idade
Proteínas de Neoplasias/genética
Células-Tronco Neoplásicas/metabolismo
Proteínas Nucleares/genética
Fenótipo
Fosfoproteínas Fosfatases/genética
Proteínas Proto-Oncogênicas c-kit/metabolismo
Rodamina 123/metabolismo
Tetraspanina 30/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ABCB5 protein, human); 0 (ATP-Binding Cassette, Sub-Family B, Member 1); 0 (Antigens, Neoplasm); 0 (Antineoplastic Agents, Alkylating); 0 (CD24 Antigen); 0 (CD24 protein, human); 0 (CD44 protein, human); 0 (CD63 protein, human); 0 (Carbazoles); 0 (ENG protein, human); 0 (Endoglin); 0 (Fluorescent Dyes); 0 (GAGE1 protein, human); 0 (Glycosides); 0 (Hyaluronan Receptors); 0 (LCS1269); 0 (Neoplasm Proteins); 0 (Nuclear Proteins); 0 (PRAME protein, human); 0 (Tetraspanin 30); 0 (aranoza); 126547-89-5 (Intercellular Adhesion Molecule-1); 1N3CZ14C5O (Rhodamine 123); 684-93-5 (Methylnitrosourea); EC 2.7.10.1 (Proto-Oncogene Proteins c-kit); EC 3.1.3.16 (CTDSP1 protein, human); EC 3.1.3.16 (Phosphoprotein Phosphatases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1097/CMR.0000000000000308


  4 / 7921 MEDLINE  
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[PMID]:29355544
[Au] Autor:Li X; Zhou N; Wang J; Liu Z; Wang X; Zhang Q; Liu Q; Gao L; Wang R
[Ad] Endereço:Key Laboratory of Pharmacology, Chifeng University, Hongshan, Chifeng, Inner Mongolia 024000, China.
[Ti] Título:Quercetin suppresses breast cancer stem cells (CD44 /CD24 ) by inhibiting the PI3K/Akt/mTOR-signaling pathway.
[So] Source:Life Sci;196:56-62, 2018 Mar 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: Cancer stem cells (CSCs) are considered the prime source of cancer recurrence, metastasis, and progression and represent important targets for developing novel anticancer agents and therapeutic strategies. The aim of this study was to investigate the effect of treating breast CSCs with the anticancer flavonoid, quercetin. MAIN METHODS: We examined changes in the cluster of differentiation CD44 /CD24 CSC population and behavior using the breast cancer cell line MCF-7. KEY FINDINGS: Our results indicated that cell viability, clone formation, mammosphere generation, and nude mice tumor metastasis were inhibited in the CD44 /CD24 population and that MCF-7 cells exhibited G1-phase arrest after quercetin treatment. Additionally, CyclinD1 and B cell lymphoma-2 expression were suppressed and Bcl-2-like protein-4 expression was enhanced after quercetin treatment. We also observed that estrogen receptor α and phosphatidylinositol-3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling were downregulated concurrently with the inhibition of CD44 /CD24 viability and clone formation. Our findings suggested that quercetin treatment promoted weaker malignant activity associated with CSCs relative to that observed in normal cancer cells through its inhibition of the PI3K/Akt/mTOR-signaling pathway. SIGNIFICANCE: These results indicated that CSCs are potential therapeutic targets for quercetin treatment of breast cancer.
[Mh] Termos MeSH primário: Antioxidantes/farmacologia
Antígeno CD24/efeitos dos fármacos
Receptores de Hialuronatos/efeitos dos fármacos
Proteína Oncogênica v-akt/antagonistas & inibidores
Fosfatidilinositol 3-Quinases/antagonistas & inibidores
Quercetina/farmacologia
Transdução de Sinais/efeitos dos fármacos
Serina-Treonina Quinases TOR/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Feminino
Fase G1/efeitos dos fármacos
Seres Humanos
Células MCF-7
Camundongos Nus
Proteínas Proto-Oncogênicas c-bcl-2/antagonistas & inibidores
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (CD24 Antigen); 0 (CD44 protein, human); 0 (Hyaluronan Receptors); 0 (Proto-Oncogene Proteins c-bcl-2); 9IKM0I5T1E (Quercetin); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.1.1 (MTOR protein, human); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.11.1 (Oncogene Protein v-akt)
[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:180123
[St] Status:MEDLINE


  5 / 7921 MEDLINE  
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[PMID]:29298343
[Au] Autor:Choi YJ; Park SJ; Park YS; Park HS; Yang KM; Heo K
[Ad] Endereço:Research Center, Dongnam Institute of Radiological & Medical Sciences, Busan, Republic of Korea.
[Ti] Título:EpCAM peptide-primed dendritic cell vaccination confers significant anti-tumor immunity in hepatocellular carcinoma cells.
[So] Source:PLoS One;13(1):e0190638, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cancer stem-like cells (CSCs) may play a key role in tumor initiation, self-renewal, differentiation, and resistance to current treatments. Dendritic cells (DCs) play a vital role in host immune reactions as well as antigen presentation. In this study, we explored the suitability of using CSC peptides as antigen sources for DC vaccination against human breast cancer and hepatocellular carcinoma (HCC) with the aim of achieving CSC targeting and enhancing anti-tumor immunity. CD44 is used as a CSC marker for breast cancer and EpCAM is used as a CSC marker for HCC. We selected CD44 and EpCAM peptides that bind to HLA-A2 molecules on the basis of their binding affinity, as determined by a peptide-T2 binding assay. Our data showed that CSCs express high levels of tumor-associated antigens (TAAs) as well as major histocompatibility complex (MHC) molecules. Pulsing DCs with CD44 and EpCAM peptides resulted in the efficient generation of mature DCs (mDCs), thus enhancing T cell stimulation and generating potent cytotoxic T lymphocytes (CTLs). The activation of CSC peptide-specific immune responses by the DC vaccine in combination with standard chemotherapy may provide better clinical outcomes in advanced carcinomas.
[Mh] Termos MeSH primário: Vacinas Anticâncer/uso terapêutico
Carcinoma Hepatocelular/terapia
Células Dendríticas/imunologia
Molécula de Adesão da Célula Epitelial/administração & dosagem
Neoplasias Hepáticas/terapia
Fragmentos de Peptídeos/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Vacinas Anticâncer/imunologia
Carcinoma Hepatocelular/imunologia
Linhagem Celular Tumoral
Ensaio de Imunoadsorção Enzimática
Molécula de Adesão da Célula Epitelial/química
Feminino
Antígeno HLA-A2/imunologia
Xenoenxertos
Seres Humanos
Receptores de Hialuronatos/imunologia
Neoplasias Hepáticas/imunologia
Camundongos
Camundongos Endogâmicos BALB C
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cancer Vaccines); 0 (EPCAM protein, human); 0 (Epithelial Cell Adhesion Molecule); 0 (HLA-A2 Antigen); 0 (Hyaluronan Receptors); 0 (Peptide Fragments)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180104
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190638


  6 / 7921 MEDLINE  
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[PMID]:29374695
[Au] Autor:Matuura H; Miyamoto M; Takano M; Soyama H; Aoyama T; Yoshikawa T; Kato K; Sakamoto T; Kuwahara M; Takasaki K; Ishibashi H; Iwahashi H; Tsuda H; Furuya K
[Ad] Endereço:Department of Obstetrics and Gynecology, National Defense Medical College Hospital, Tokorozawa, Japan.
[Ti] Título:Low Expression of CD44 Is an Independent Factor of Poor Prognosis in Ovarian Mucinous Carcinoma.
[So] Source:Anticancer Res;38(2):717-722, 2018 02.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:AIM: To determine whether CD44, which is associated with tumor growth and metastasis, is related to carcinogenesis and prognosis in ovarian mucinous carcinomas (MACs). MATERIALS AND METHODS: Tissue blocks from 71 patients with benign mucinous ovarian tumors were used in the study: 35 were from patients with borderline mucinous ovarian tumors, and 60 from patients with MACs. Immunochemical analysis was performed to evaluate the expression of CD44 and examine its association with tumorigenesis and survival. RESULTS: Compared to benign tumors, borderline tumors had high CD44 expression levels (p=0.047). Conversely, MACs had lower expression than borderline tumors (p=0.032). Progression-free and overall survival of patients with MAC with low CD44 expression were worse than those of patients with high expression (p=0.04 and p=0.02, respectively). CONCLUSION: Malignant transformation of mucinous tumors is associated with changes in CD44 expression, with low expression level being a prognostic factor in MAC.
[Mh] Termos MeSH primário: Adenocarcinoma Mucinoso/metabolismo
Adenocarcinoma Mucinoso/mortalidade
Receptores de Hialuronatos/metabolismo
Neoplasias Ovarianas/metabolismo
Neoplasias Ovarianas/mortalidade
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Idoso de 80 Anos ou mais
Biomarcadores Tumorais/metabolismo
Feminino
Seres Humanos
Meia-Idade
Análise Multivariada
Prognóstico
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (CD44 protein, human); 0 (Hyaluronan Receptors)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180129
[St] Status:MEDLINE


  7 / 7921 MEDLINE  
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[PMID]:29269483
[Au] Autor:Huang H; Zhang J; Harvey SE; Hu X; Cheng C
[Ad] Endereço:Division of Hematology and Oncology, Department of Medicine, Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611, USA.
[Ti] Título:RNA G-quadruplex secondary structure promotes alternative splicing via the RNA-binding protein hnRNPF.
[So] Source:Genes Dev;31(22):2296-2309, 2017 11 15.
[Is] ISSN:1549-5477
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:It is generally thought that splicing factors regulate alternative splicing through binding to RNA consensus sequences. In addition to these linear motifs, RNA secondary structure is emerging as an important layer in splicing regulation. Here we demonstrate that RNA elements with G-quadruplex-forming capacity promote exon inclusion. Destroying G-quadruplex-forming capacity while keeping G tracts intact abrogates exon inclusion. Analysis of RNA-binding protein footprints revealed that G quadruplexes are enriched in heterogeneous nuclear ribonucleoprotein F (hnRNPF)-binding sites and near hnRNPF-regulated alternatively spliced exons in the human transcriptome. Moreover, hnRNPF regulates an epithelial-mesenchymal transition (EMT)-associated CD44 isoform switch in a G-quadruplex-dependent manner, which results in inhibition of EMT. Mining breast cancer TCGA (The Cancer Genome Atlas) data sets, we demonstrate that hnRNPF negatively correlates with an EMT gene signature and positively correlates with patient survival. These data suggest a critical role for RNA G quadruplexes in regulating alternative splicing. Modulation of G-quadruplex structural integrity may control cellular processes important for tumor progression.
[Mh] Termos MeSH primário: Processamento Alternativo
Quadruplex G
Ribonucleoproteínas Nucleares Heterogêneas Grupo F-H/metabolismo
RNA/química
[Mh] Termos MeSH secundário: Neoplasias da Mama/metabolismo
Neoplasias da Mama/mortalidade
Linhagem Celular
Transição Epitelial-Mesenquimal
Éxons
Feminino
Seres Humanos
Receptores de Hialuronatos/genética
Invasividade Neoplásica
RNA/metabolismo
Precursores de RNA/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Heterogeneous-Nuclear Ribonucleoprotein Group F-H); 0 (Hyaluronan Receptors); 0 (RNA Precursors); 63231-63-0 (RNA)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180202
[Lr] Data última revisão:
180202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171223
[St] Status:MEDLINE
[do] DOI:10.1101/gad.305862.117


  8 / 7921 MEDLINE  
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[PMID]:29172759
[Au] Autor:Wang S; Shao M; Zhong Z; Wang A; Cao J; Lu Y; Wang Y; Zhang J
[Ad] Endereço:a State Key Laboratory of Quality Research in Chinese Medicine , Institute of Chinese Medical Sciences, University of Macau , Macau , China.
[Ti] Título:Co-delivery of gambogic acid and TRAIL plasmid by hyaluronic acid grafted PEI-PLGA nanoparticles for the treatment of triple negative breast cancer.
[So] Source:Drug Deliv;24(1):1791-1800, 2017 Nov.
[Is] ISSN:1521-0464
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-based combination therapy and gene therapy are new strategies to potentially overcome the limitations of TRAIL, however, the lack of efficient and low toxic vectors remains the major obstacle. In this study, we developed a hyaluronic acid (HA)-decorated polyethylenimine-poly(d,l-lactide-co-glycolide) (PEI-PLGA) nanoparticle (NP) system for targeted co-delivery of TRAIL plasmid (pTRAIL) and gambogic acid (GA) in triple-negative breast cancer (TNBC) therapy. GA was encapsulated into the core of the PEI-PLGA NPs while pTRAIL was adsorbed onto the positive NP surface via charge adsorption. The coating of HA on PEI-PLGA NPs functions as a targeting ligand by binding to CD44 receptor of TNBC cells and a shell to neutralize the excess positive charge of inner NPs. The resultant pTRAIL and GA co-loaded HA-coated PEI-PLGA NPs exhibited spherical shape (121.5 nm) and could promote the internalization of loaded cargoes into TNBC cells through the CD44-dependent endocytic pathway. The dual drug-loaded NPs significantly augmented apoptotic cell death in vitro and inhibited TNBC tumor growth in vivo. This multifunctional NP system efficiently co-delivered GA and pTRAIL, thus representing a promising strategy to treat TNBC and bringing forth a platform strategy for co-delivery of therapeutic DNA and chemotherapeutic agents in combinatorial TNBC therapy.
[Mh] Termos MeSH primário: Ácido Hialurônico/administração & dosagem
Ácido Láctico/administração & dosagem
Nanopartículas/administração & dosagem
Plasmídeos/administração & dosagem
Polietilenoimina/administração & dosagem
Ácido Poliglicólico/administração & dosagem
Ligante Indutor de Apoptose Relacionado a TNF/administração & dosagem
Neoplasias de Mama Triplo Negativas/tratamento farmacológico
Xantonas/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/administração & dosagem
Linhagem Celular Tumoral
Portadores de Fármacos/administração & dosagem
Seres Humanos
Receptores de Hialuronatos/metabolismo
Células MCF-7
Camundongos
Neoplasias de Mama Triplo Negativas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Drug Carriers); 0 (Hyaluronan Receptors); 0 (TNF-Related Apoptosis-Inducing Ligand); 0 (Xanthones); 0 (polylactic acid-polyglycolic acid copolymer); 26009-03-0 (Polyglycolic Acid); 33X04XA5AT (Lactic Acid); 8N585K83U2 (gambogic acid); 9002-98-6 (Polyethyleneimine); 9004-61-9 (Hyaluronic Acid)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180130
[Lr] Data última revisão:
180130
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1080/10717544.2017.1406558


  9 / 7921 MEDLINE  
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[PMID]:27775742
[Au] Autor:Kingsmore KM; Logsdon DK; Floyd DH; Peirce SM; Purow BW; Munson JM
[Ad] Endereço:Department of Biomedical Engineering, University of Virginia School of Medicine, Charlottesville, VA 22908, USA.
[Ti] Título:Interstitial flow differentially increases patient-derived glioblastoma stem cell invasion via CXCR4, CXCL12, and CD44-mediated mechanisms.
[So] Source:Integr Biol (Camb);8(12):1246-1260, 2016 12 05.
[Is] ISSN:1757-9708
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Glioblastoma (GBM) prognosis remains dismal due in part to the invasiveness of GBM cells. Interstitial fluid flow (IFF) has been shown to increase invasion of glioma cells in vitro through the CXCR4 receptor interacting with autologous, pericellular gradients of CXCL12 (autologous chemotaxis) or through the CD44 receptor interactions with the extracellular matrix (hyaluronan-mediated mechanotransduction). These mechanisms have not been examined together and thus we hypothesized that both mechanisms contribute to invasion in populations of cancer cells. Therefore, we examined IFF-stimulated CXCR4-, CXCL12-, and CD44-dependent invasion in patient-derived glioblastoma stem cells (GSCs). Using our 3D in vitro assay and correlative in vivo studies we demonstrated GSC lines show increased invasion with flow. This flow-stimulated invasion was reduced by blockade of CXCR4, CXCL12, and/or CD44, revealing that GSC invasion may be mediated simultaneously by both mechanisms. Characterization of CXCR4 , CXCL12 , and CD44 populations in four GSC lines revealed different percentages of protein positive subpopulations for each line. We developed an agent-based model to identify the contributions of each subpopulation to flow-stimulated invasion and validated the model through comparisons with experimental blocking studies. Clinically relevant radiation therapy increased flow-stimulated invasion in one GSC line. Our agent-based model predicted that IFF-stimulated invasion is driven primarily by CXCR4 CXCL12 populations, and, indeed our irradiated cells had an increase in this subpopulation. Together, these data indicate that different mechanisms govern the flow response across GSCs, but that within a single patient, there are subpopulations of GSCs that respond to flow via either CD44- or CXCR4-CXCL12 mechanisms.
[Mh] Termos MeSH primário: Quimiocina CXCL12/imunologia
Glioblastoma/imunologia
Glioblastoma/patologia
Receptores de Hialuronatos/imunologia
Mecanotransdução Celular/imunologia
Células-Tronco Neoplásicas/imunologia
Receptores CXCR4/imunologia
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Líquido Extracelular/imunologia
Seres Humanos
Invasividade Neoplásica
Células-Tronco Neoplásicas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CD44 protein, human); 0 (CXCL12 protein, human); 0 (CXCR4 protein, human); 0 (Chemokine CXCL12); 0 (Hyaluronan Receptors); 0 (Receptors, CXCR4)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180123
[Lr] Data última revisão:
180123
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE


  10 / 7921 MEDLINE  
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[PMID]:29277789
[Au] Autor:Spelt L; Sasor A; Ansari D; Hilmersson KS; Andersson R
[Ad] Endereço:Department of Surgery, Clinical Sciences Lund, Lund University and Skåne University Hospital, Lund, Sweden lidewij.spelt@med.lu.se.
[Ti] Título:The Prognostic Role of Cancer Stem Cell Markers for Long-term Outcome After Resection of Colonic Liver Metastases.
[So] Source:Anticancer Res;38(1):313-320, 2018 01.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: To assess the expression of cancer stem cell (CSC) markers CD44, CD133 and CD24 in colon cancer liver metastases and analyse their predictive value for overall survival (OS) and disease-free survival (DFS) after liver resection. MATERIALS AND METHODS: Patients operated on for colon cancer liver metastases were included. CSC marker expression was determined through immunohistochemistry analysis. OS and DFS were compared between marker-positive and marker-negative patients. Multivariate analysis was performed to select predictive variables for OS and DFS. RESULTS: CD133-positive patients had a worse DFS than CD133-negative patients, with a median DFS of 12 and 25 months (p=0.051). Multivariate analysis selected CD133 expression as a significant predictor for DFS. CD44 and CD24 were not found to predict OS or DFS. CONCLUSION: CD133 expression in colonic liver metastases is a negative prognostic factor for DFS after liver resection. In the future, CD133 could be used as a biomarker for risk stratification, and possibly for developing novel targeted therapy.
[Mh] Termos MeSH primário: Antígeno AC133/metabolismo
Antígeno CD24/metabolismo
Neoplasias do Colo/patologia
Receptores de Hialuronatos/metabolismo
Neoplasias Hepáticas/secundário
Células-Tronco Neoplásicas/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Biomarcadores Tumorais
Colo/patologia
Intervalo Livre de Doença
Feminino
Hepatectomia
Seres Humanos
Fígado/patologia
Fígado/cirurgia
Neoplasias Hepáticas/mortalidade
Neoplasias Hepáticas/cirurgia
Masculino
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AC133 Antigen); 0 (Biomarkers, Tumor); 0 (CD24 Antigen); 0 (CD24 protein, human); 0 (CD44 protein, human); 0 (Hyaluronan Receptors); 0 (PROM1 protein, human)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180104
[Lr] Data última revisão:
180104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171227
[St] Status:MEDLINE



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