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[PMID]:27596143
[Au] Autor:Jiang MC
[Ad] Endereço:Targetrust Biotech. Ltd., No. 510 Zhongzheng Rd, Xinzhuang Dist, New Taipei City, 24205, Taiwan. jiangmwd@gmail.com.
[Ti] Título:CAS (CSE1L) signaling pathway in tumor progression and its potential as a biomarker and target for targeted therapy.
[So] Source:Tumour Biol;37(10):13077-13090, 2016 Oct.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CSE1L (chromosome segregation 1-like protein), also named as CAS (cellular apoptosis susceptibility protein), is highly expressed in most cancer types. CSE1L/CAS is a multiple functional protein that plays roles in apoptosis, cell survival, chromosome assembly, nucleocytoplasmic transport, microvesicle formation, and cancer metastasis; some of the functions are explicitly correlated. CSE1L is also a cancer serum biomarker. The phosphorylation of CAS is regulated by the extracellular signal-regulated kinase (ERK). The RAS/RAF/MAPK/ERK signaling pathways are the essential targets of most targeted cancer drugs, thus serum phosphorylated CSE1L may be a potential biomarker for monitoring drug resistance in targeted therapy. CSE1L can regulate Ras-induced ERK phosphorylation. CSE1L also regulates the expression and phosphorylation of CREB (cAMP response element binding protein) and MITF (microphthalmia-associated transcription factor) and is thus involved in the melanogenesis and progression of melanoma. CAS is an exosome/microvesicle membrane protein. Tumor cells consistently secrete microvesicles and tumor-derived microvesicles may be accumulated around tumors. Therefore, microvesicle membrane CSE1L may be a potential target for the development of high-efficacy antibody-drug conjugates (ADCs) for cancer therapy. This review will focus on CSE1L expression in cancers, its relationship to Ras/ERK and cAMP/PKA signaling pathways in melanoma development, its potential for the development of ADCs and tumor imaging reagents, and secretory phosphorylated CSE1L for monitoring the emergence of drug resistance in targeted cancer therapy.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Biomarcadores/metabolismo
Proteína de Suscetibilidade a Apoptose Celular/metabolismo
Terapia de Alvo Molecular
Neoplasias/diagnóstico
Neoplasias/tratamento farmacológico
[Mh] Termos MeSH secundário: Seres Humanos
Neoplasias/metabolismo
Neoplasias/patologia
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Biomarkers); 0 (Cellular Apoptosis Susceptibility Protein)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160907
[St] Status:MEDLINE


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[PMID]:27521996
[Au] Autor:Pimiento JM; Neill KG; Henderson-Jackson E; Eschrich SA; Chen DT; Husain K; Shibata D; Coppola D; Malafa MP
[Ad] Endereço:Department of Gastrointestinal Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida.
[Ti] Título:Knockdown of CSE1L Gene in Colorectal Cancer Reduces Tumorigenesis in Vitro.
[So] Source:Am J Pathol;186(10):2761-8, 2016 Oct.
[Is] ISSN:1525-2191
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human cellular apoptosis susceptibility (chromosomal segregation 1-like, CSE1L) gene plays a role in nuclear-to-cytoplasm transport and chromosome segregation during mitosis, cellular proliferation, and apoptosis. CSE1L is involved in colon carcinogenesis. CSE1L gene expression was assessed with three data sets using Affymetrix U133 + gene chips on normal human colonic mucosa (NR), adenomas (ADs), and colorectal carcinoma (CRC). CSE1L protein expression in CRC, AD, and NR from the same patients was measured by immunohistochemistry using a tissue microarray. We evaluated CSE1L expression in CRC cells (HCT116, SW480, and HT29) and its biological functions. CSE1L mRNA was significantly increased in all AD and CRC compared with NR (P < 0.001 and P = 0.02, respectivly). We observed a change in CSE1L staining intensity and cellular localization by immunohistochemistry. CSE1L was significantly increased during the transition from AD to CRC when compared with NR in a CRC tissue microarray (P = 0.01 and P < 0.001). HCT116, SW480, and HT29 cells also expressed CSE1L protein. CSE1L knockdown by shRNA inhibited protein, resulting in decreased cell proliferation, reduced colony formation in soft agar, and induction of apoptosis. CSE1L protein is expressed early and across all stages of CRC development. shRNA knockdown of CSE1L was associated with inhibition of tumorigenesis in CRC cells. CSE1L may represent a potential target for treatment of CRC.
[Mh] Termos MeSH primário: Adenoma/patologia
Carcinogênese/genética
Proteína de Suscetibilidade a Apoptose Celular/genética
Neoplasias Colorretais/genética
Regulação Neoplásica da Expressão Gênica
[Mh] Termos MeSH secundário: Adenoma/genética
Adenoma/metabolismo
Adulto
Idoso
Idoso de 80 Anos ou mais
Apoptose/genética
Linhagem Celular Tumoral
Núcleo Celular/metabolismo
Proliferação Celular
Proteína de Suscetibilidade a Apoptose Celular/metabolismo
Neoplasias Colorretais/metabolismo
Neoplasias Colorretais/patologia
Citoplasma/metabolismo
Células Epiteliais/metabolismo
Células Epiteliais/patologia
Feminino
Seres Humanos
Masculino
Meia-Idade
Transporte Proteico
Análise Serial de Tecidos
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cellular Apoptosis Susceptibility Protein)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171011
[Lr] Data última revisão:
171011
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160814
[St] Status:MEDLINE


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[PMID]:26892809
[Au] Autor:Holzer K; Drucker E; Oliver S; Winkler J; Eiteneuer E; Herpel E; Breuhahn K; Singer S
[Ad] Endereço:Institute of Pathology, University Hospital Heidelberg, 69120 Heidelberg, Germany.
[Ti] Título:Cellular apoptosis susceptibility (CAS) is overexpressed in thyroid carcinoma and maintains tumor cell growth: A potential link to the BRAFV600E mutation.
[So] Source:Int J Oncol;48(4):1679-87, 2016 Apr.
[Is] ISSN:1791-2423
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Thyroid carcinoma is among the most common malignant endocrine neoplasms with a rising incidence. Genetic alterations occurring in thyroid cancer frequently affect the RAS/RAF/MEK/ERK-pathway such as the oncogenic, kinase-activating BRAF(V600E) mutation. Nuclear transport receptors including importins and exportins represent an important part of the nuclear transport machinery providing nucleo-cytoplasmic exchange of macromolecules. The role of nuclear transport receptors in the development and progression of thyroid carcinomas is largely unknown. Here, we studied the expression and function of the exportin cellular apoptosis susceptibility (CAS) in thyroid carcinogenesis and its link to the BRAF(V600E) mutation. By using immunohistochemistry (IHC) we found significantly increased IHC scores of CAS in primary papillary (PTC) and medullary (MTC), but not in follicular (FTC) thyroid carcinoma compared to non-tumorous (NT) thyroid tissue. Interestingly, metastases of the aforementioned subtypes including FTC showed a strong CAS positivity. Among PTCs we observed that CAS immunoreactivity was significantly higher in the tumors harboring the BRAF(V600E) mutation. Furthermore, depletion of CAS by RNAi in the BRAF(V600E)-positive PTC cell line B-CPAP led to reduced tumor cell growth measured by crystal violet assays. This phenotype could be attributed to reduced proliferation and increased cell death as assayed by BrdU ELISAs and immunoblotting for PARP-cleavage, respectively. Finally, we found additive effects of CAS siRNA and vemurafenib treatment in B-CPAP cells. Collectively, these data suggest that CAS overexpression in thyroid carcinoma depends on the subtype and the disease stage. Our findings also indicate that CAS maintains PTC cell proliferation and survival. Targeting CAS could represent a potential therapeutic approach particularly in combination with BRAF inhibitors such as vemurafenib in BRAF(V600E)-positive tumors.
[Mh] Termos MeSH primário: Carcinoma Papilar/patologia
Proteína de Suscetibilidade a Apoptose Celular/metabolismo
Mutação
Proteínas Proto-Oncogênicas B-raf/genética
Neoplasias da Glândula Tireoide/patologia
Regulação para Cima
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Carcinoma Papilar/genética
Carcinoma Papilar/metabolismo
Linhagem Celular Tumoral
Proliferação Celular
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Masculino
Meia-Idade
Metástase Neoplásica
Neoplasias da Glândula Tireoide/genética
Neoplasias da Glândula Tireoide/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cellular Apoptosis Susceptibility Protein); EC 2.7.11.1 (BRAF protein, human); EC 2.7.11.1 (Proto-Oncogene Proteins B-raf)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160220
[St] Status:MEDLINE
[do] DOI:10.3892/ijo.2016.3388


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[PMID]:26668314
[Au] Autor:Monian P; Jiang X
[Ad] Endereço:From the Cell Biology Program and Gerstner Sloan Kettering Graduate School of Biomedical Sciences, Memorial Sloan Kettering Cancer Center, New York, New York 10065.
[Ti] Título:The Cellular Apoptosis Susceptibility Protein (CAS) Promotes Tumor Necrosis Factor-related Apoptosis-inducing Ligand (TRAIL)-induced Apoptosis and Cell Proliferation.
[So] Source:J Biol Chem;291(5):2379-88, 2016 Jan 29.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A signature event during the cell intrinsic apoptotic pathway is mitochondrial outer membrane permeabilization, leading to formation of the apoptosome, a caspase activation complex. The cellular apoptosis susceptibility protein (CAS) can facilitate apoptosome assembly by stimulating nucleotide exchange on Apaf-1 following binding of cytochrome c. We report here that CAS expression itself is up-regulated during tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis, and knockdown of CAS renders cells resistant to TRAIL. We find that TRAIL induces up-regulation of CAS in a posttranscriptional, caspase-8-dependent manner through degradation of cIAP1, an E3 ligase that targets CAS for ubiquitin-dependent proteasomal degradation. We identified a novel signaling pathway whereby caspase-8 engages a feedforward cascade that leads to CAS up-regulation and amplifies the apoptotic signal. Furthermore, in silico analysis revealed that expression of CAS is up-regulated at both the mRNA and DNA levels in human breast tumors, consistent with its role in promoting cell proliferation. Overexpression of various oncogenes led to CAS up-regulation in non-transformed cells. Intriguingly, oncogene-induced CAS up-regulation also resulted in greater susceptibility to TRAIL-induced cell death, consistent with its proapoptotic function. These findings suggest that CAS plays contrasting roles in proliferation and apoptosis and that overexpression of CAS in tumors could serve as a potential biomarker to guide therapeutic choices.
[Mh] Termos MeSH primário: Apoptose
Proliferação Celular
Proteína de Suscetibilidade a Apoptose Celular/metabolismo
Regulação Neoplásica da Expressão Gênica
Ligante Indutor de Apoptose Relacionado a TNF/metabolismo
[Mh] Termos MeSH secundário: Apoptossomas
Fator Apoptótico 1 Ativador de Proteases/metabolismo
Caspase 8/metabolismo
Linhagem Celular Tumoral
Sobrevivência Celular
Células HEK293
Células HT29
Seres Humanos
Proteínas Inibidoras de Apoptose/metabolismo
Membranas Mitocondriais/metabolismo
Permeabilidade
RNA Interferente Pequeno/metabolismo
Transdução de Sinais
Ubiquitina/metabolismo
Ubiquitina-Proteína Ligases/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (APAF1 protein, human); 0 (Apoptosomes); 0 (Apoptotic Protease-Activating Factor 1); 0 (Cellular Apoptosis Susceptibility Protein); 0 (Inhibitor of Apoptosis Proteins); 0 (RNA, Small Interfering); 0 (TNF-Related Apoptosis-Inducing Ligand); 0 (TNFSF10 protein, human); 0 (Ubiquitin); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 3.4.22.- (CASP8 protein, human); EC 3.4.22.- (Caspase 8)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:170129
[Lr] Data última revisão:
170129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151216
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M115.685008


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[PMID]:26331446
[Au] Autor:Lee WR; Shen SC; Wu PR; Chou CL; Shih YH; Yeh CM; Yeh KT; Jiang MC
[Ad] Endereço:Department of Dermatology, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan.
[Ti] Título:CSE1L Links cAMP/PKA and Ras/ERK pathways and regulates the expressions and phosphorylations of ERK1/2, CREB, and MITF in melanoma cells.
[So] Source:Mol Carcinog;55(11):1542-1552, 2016 Nov.
[Is] ISSN:1098-2744
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The Ras/ERK (extracellular signal-regulated protein kinase) and cAMP/PKA (protein kinase A) pathways are essential for the transcriptional activities of CREB (cAMP response element binding protein) and MITF (microphthalmia-associated transcription factor) in melanogenesis and the progression of melanoma. However, the interaction between Ras/ERK and cAMP/PKA pathways in the melanogenesis and progression of melanoma is not fully known. Here, we report that CSE1L (chromosome segregation 1-like protein) regulates cAMP/PKA-induced CREB and MITF expressions as well as Ras-induced ERK1/2 phosphorylation. IBMX, a cAMP/PKA activator, treatment induced CSE1L phosphorylation and augmented Ras-induced ERK1/2 phosphorylation. CSE1L knockdown by CSE1L shRNA expression vectors inhibited Ras-induced ERK1/2 phosphorylation and melanogenesis in melanoma cells. CSE1L overexpression increased phospho-CREB expression; CSE1L knockdown also inhibited Ras-induced phospho-CREB, MITF, and tyrosinase expressions, regardless of the presence of IBMX. This study identifies CSE1L links and controls the Ras/ERK and cAMP/PKA pathways in the melanogenesis of melanoma cells. Melanomas frequently develop drug resistance via paradoxical activation of Ras/Raf/MEK/ERK or alternatively activated Ras/ERK and cAMP/PKA pathways. Thus CSE1L may be a potential target for treating melanomas that harbor Ras mutations or are resistant to drugs targeting Raf/MEK/ERK. © 2015 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Proteína de Suscetibilidade a Apoptose Celular/metabolismo
Sistema de Sinalização das MAP Quinases
Melanoma/metabolismo
Neoplasias Cutâneas/metabolismo
[Mh] Termos MeSH secundário: 1-Metil-3-Isobutilxantina/farmacologia
Idoso
Idoso de 80 Anos ou mais
Animais
Linhagem Celular Tumoral
Feminino
Seres Humanos
Masculino
Melanoma/patologia
Camundongos
Meia-Idade
Mutação
Transplante de Neoplasias
Fosforilação
Neoplasias Cutâneas/patologia
Proteínas ras/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cellular Apoptosis Susceptibility Protein); EC 3.6.5.2 (ras Proteins); TBT296U68M (1-Methyl-3-isobutylxanthine)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170517
[Lr] Data última revisão:
170517
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150903
[St] Status:MEDLINE
[do] DOI:10.1002/mc.22407


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[PMID]:26278417
[Au] Autor:Yuksel UM; Turker I; Dilek G; Dogan L; Gulcelik MA; Oksuzoglu B
[Ad] Endereço:Department of Surgery, Oncology Training and Research Hospital, Ankara, Turkey.
[Ti] Título:Does CSE1L Overexpression Affect Distant Metastasis Development in Breast Cancer?
[So] Source:Oncol Res Treat;38(9):431-4, 2015.
[Is] ISSN:2296-5262
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: CSE1L (chromosome segregation 1-like) is the human homologue to the yeast gene CSE1, and is related to invasion and metastasis in cancer progression. The aim of this study was to investigate the potential role of CSE1L expression in distant metastasis of breast cancer. PATIENTS AND METHODS: A total of 71 breast cancer patients were included in this study. Clinical characteristics and CSE1L status were evaluated. Immunohistochemistry was performed on formalin-fixed, paraffin-embedded archival breast tumor tissue. The results of CSE1L staining were analyzed according to the percentage of immunoreactive cells. RESULTS: 34 patients had distant metastasis and 37 did not. The mean age of the patients was 50.5 ± 12.1 years. Age, tumor size, and hormone receptor status were similar in patients with distant metastasis and in those without. A statistically significant relationship was found between nuclear CSE1L expression and distant metastasis of breast cancer. Lymph node metastasis and nuclear grade were other factors affecting distant metastasis. CONCLUSION: There is a relationship between nuclear CSE1L overexpression and distant metastasis in breast cancer. CSE1L status may therefore become a valuable prognostic tool in the future.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/metabolismo
Neoplasias da Mama/diagnóstico
Neoplasias da Mama/metabolismo
Carcinoma/metabolismo
Carcinoma/secundário
Proteína de Suscetibilidade a Apoptose Celular/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Carcinoma/diagnóstico
Feminino
Seres Humanos
Meia-Idade
Prognóstico
Reprodutibilidade dos Testes
Sensibilidade e Especificidade
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Cellular Apoptosis Susceptibility Protein)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:150930
[Lr] Data última revisão:
150930
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150818
[St] Status:MEDLINE
[do] DOI:10.1159/000438501


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[PMID]:26123175
[Au] Autor:Okimoto S; Sun J; Fukuto A; Horikoshi Y; Matsuda S; Matsuda T; Ikura M; Ikura T; Machida S; Kurumizaka H; Miyamoto Y; Oka M; Yoneda Y; Kiuchi Y; Tashiro S
[Ad] Endereço:Department of Cellular Biology, Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima, 734-8551, Japan.
[Ti] Título:hCAS/CSE1L regulates RAD51 distribution and focus formation for homologous recombinational repair.
[So] Source:Genes Cells;20(9):681-94, 2015 Sep.
[Is] ISSN:1365-2443
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Homologous recombinational repair (HR) is one of the major repair systems for DNA double-strand breaks. RAD51 is a key molecule in HR, and the RAD51 concentration in the cell nucleus increases after DNA damage induction. However, the mechanism that regulates the intracellular distribution of RAD51 is still unclear. Here, we show that hCAS/CSE1L associates with RAD51 in human cells. We found that hCAS/CSE1L negatively regulates the nuclear protein level of RAD51 under normal conditions. hCAS/CSE1L is also required to repress the DNA damage-induced focus formation of RAD51. Moreover, we show that hCAS/CSE1L plays roles in the regulation of the HR activity and in chromosome stability. These findings suggest that hCAS/CSE1L is responsible for controlling the HR activity by directly interacting with RAD51.
[Mh] Termos MeSH primário: Proteína de Suscetibilidade a Apoptose Celular/metabolismo
Recombinação Homóloga
Rad51 Recombinase/metabolismo
Reparo de DNA por Recombinação
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Núcleo Celular/metabolismo
Aberrações Cromossômicas
Quebras de DNA de Cadeia Dupla
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cellular Apoptosis Susceptibility Protein); EC 2.7.7.- (RAD51 protein, human); EC 2.7.7.- (Rad51 Recombinase)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:150903
[Lr] Data última revisão:
150903
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150701
[St] Status:MEDLINE
[do] DOI:10.1111/gtc.12262


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[PMID]:26070816
[Au] Autor:Lee WR; Shen SC; Shih YH; Chou CL; Tseng JT; Chin SY; Liu KH; Chen YC; Jiang MC
[Ad] Endereço:Department of Dermatology, Shuang Ho Hospital, Taipei Medical University, New Taipei, Taiwan. wrlee@tmu.edu.tw.
[Ti] Título:Early decline in serum phospho-CSE1L levels in vemurafenib/sunitinib-treated melanoma and sorafenib/lapatinib-treated colorectal tumor xenografts.
[So] Source:J Transl Med;13:191, 2015 Jun 13.
[Is] ISSN:1479-5876
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Although targeted therapies have improved the clinical outcomes of cancer treatment, tumors resistance to targeted drug are often detected too late and cause mortality. CSE1L is secreted from tumor and its phosphorylation is regulated by ERK1/2. ERK1/2 is located downstream of various growth factor receptors and kinases, the targets of most targeted drugs. Serum phospho-CSE1L may be a marker for monitoring the efficacy of targeted therapy. METHODS: We used mice tumor xenograft model to study the assay of serum phosphorylated CSE1L for early detecting the efficacy of targeted drugs. The phosphorylation status of CSE1L in vemurafenib and sorafenib treated tumor cells were assayed by immunoblotting with antibody against phosphorylated CSE1L. RESULTS: Ras activation increased phospho-CSE1L expression in B16F10 melanoma cells. Vemurafenib and sorafenib treatment did not significantly reduce the total CSE1L levels; however, they inhibited ERK1/2 and CSE1L phosphorylation in A375 melanoma cells and HT-29 colorectal cancer cells. In the melanoma xenograft model, serum phospho-CSE1L level declined 5 days after vemurafenib/sunitinib treatment and 3 days after sorafenib/lapatinib treatment in the HT-29 colon cancer xenograft model. Vemurafenib/sunitinib and sorafenib/lapatinib treatments resulted in tumor regression. CONCLUSIONS: Our results indicated that serum phospho-CSE1L is useful for early detecting the efficacy of targeted therapy in initial treatment and for monitoring emerging secondary drug resistance to facilitate timely therapeutic decision making.
[Mh] Termos MeSH primário: Proteína de Suscetibilidade a Apoptose Celular/sangue
Neoplasias Colorretais/tratamento farmacológico
Indóis/uso terapêutico
Melanoma/tratamento farmacológico
Niacinamida/análogos & derivados
Compostos de Fenilureia/uso terapêutico
Pirróis/uso terapêutico
Quinazolinas/uso terapêutico
Sulfonamidas/uso terapêutico
Ensaios Antitumorais Modelo de Xenoenxerto
[Mh] Termos MeSH secundário: Animais
Anticorpos Antineoplásicos/imunologia
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Neoplasias Colorretais/sangue
Neoplasias Colorretais/patologia
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Seres Humanos
Indóis/farmacologia
Masculino
Melanoma/sangue
Melanoma/patologia
Camundongos Endogâmicos NOD
Camundongos SCID
Niacinamida/farmacologia
Niacinamida/uso terapêutico
Compostos de Fenilureia/farmacologia
Fosforilação/efeitos dos fármacos
Pirróis/farmacologia
Quinazolinas/farmacologia
Sulfonamidas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies, Neoplasm); 0 (Cellular Apoptosis Susceptibility Protein); 0 (Indoles); 0 (Phenylurea Compounds); 0 (Pyrroles); 0 (Quinazolines); 0 (Sulfonamides); 0VUA21238F (lapatinib); 207SMY3FQT (vemurafenib); 25X51I8RD4 (Niacinamide); 9ZOQ3TZI87 (sorafenib); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); V99T50803M (sunitinib)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150614
[St] Status:MEDLINE
[do] DOI:10.1186/s12967-015-0553-6


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[PMID]:25973023
[Au] Autor:Chin SY; Wu PR; Shih YH; Yeh CM; Lee WR; Shen SC; Yeh KT; Jiang MC; Tseng JT
[Ad] Endereço:Department of Dermatology, Shuang Ho Hospital, Taipei Medical University New Taipei City, Taiwan ; Department of Dermatology, School of Medicine, College of Medicine, Taipei Medical University Taipei, Taiwan ; Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University Tai
[Ti] Título:High expression of cytoplasmic phosphorylated CSE1L in malignant melanoma but not in benign nevi: phosphorylated CSE1L for the discrimination between melanoma and benign nevi.
[So] Source:Int J Clin Exp Pathol;8(2):1393-401, 2015.
[Is] ISSN:1936-2625
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Melanoma is difficult to treat when it has metastasized. Discrimination between melanoma and benign nevi in melanocytic lesions is crucial for identifying melanomas and consequently improving melanoma treatment and prognosis. The chromosome segregation 1-like (CSE1L) protein has been implicated in cancer progression and is regulated by phosphorylation by extracellular signal-regulated kinase 1/2 (ERK1/2) signaling, a critical pathway in melanoma progression. We studied phosphorylated CSE1L expression in human melanoma and benign nevi specimens. Immunohistochemistry with tissue microarray using antibody against phosphorylated CSE1L showed that melanomas exhibited considerable staining for phosphorylated CSE1L (100%, 34/34), whereas the benign nevi showed only faint staining (0%, 0/34). Melanomas mainly exhibited cytoplasmic phospho-CSE1L distribution, whereas the benign nevi mainly exhibited nuclear phospho-CSE1L distribution. Moreover, immunohistochemistry with anti-CSE1L antibody revealed that CSE1L mainly exhibited cytoplasmic/nuclear distribution and nuclear distribution was the dominant. Immunofluorescence with B16F10 melanoma cells showed cytoplasmic distribution of phospho-CSE1L and nuclear distribution of CSE1L. Our results indicated that nuclear CSE1L is mainly non-phosphorylated CSE1L and is involved in gene regulation and cytoplasmic CSE1L is mainly phosphorylated CSE1L and is involved in cytoplasmic signaling regulation in melanocytic tumorigenesis. Furthermore, immunohistochemical analysis of cytoplasmic phospho-CSE1L may aid in the diagnosis of melanoma.
[Mh] Termos MeSH primário: Proteína de Suscetibilidade a Apoptose Celular/metabolismo
Melanoma/diagnóstico
Nevo/diagnóstico
Neoplasias Cutâneas/diagnóstico
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Núcleo Celular/metabolismo
Citoplasma/metabolismo
Diagnóstico Diferencial
Feminino
Seres Humanos
Masculino
Melanoma/metabolismo
Melanoma/patologia
Camundongos
Nevo/metabolismo
Nevo/patologia
Fosforilação
Transdução de Sinais/fisiologia
Neoplasias Cutâneas/metabolismo
Neoplasias Cutâneas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cellular Apoptosis Susceptibility Protein)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150515
[St] Status:MEDLINE


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[PMID]:25791533
[Au] Autor:Yuksel UM; Dilek G; Dogan L; Gulcelik MA; Berberoglu U
[Ad] Endereço:Department of Surgery, Oncology Training and Research Hospital, Ankara - Turkey.
[Ti] Título:The relationship between CSE1L expression and axillary lymph node metastasis in breast cancer.
[So] Source:Tumori;101(2):194-8, 2015 Mar-Apr.
[Is] ISSN:2038-2529
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:AIM: CSE1L is the human homologue to the yeast gene CSE1 and CSE1L is a gene related to cancer progression. Thus, CSE1L may regulate the invasion and metastasis of breast cancer. The aim of this study is to show the relationship between CSE1L and axillary lymph node metastasis. METHODS: Sixty-six breast cancer patients were evaluated according to patient and tumor characteristics. Immunohistochemistry was carried out on formalin-fixed, paraffin-embedded archival breast tumor tissues. The results of CSE1L staining were analyzed according to the percentage of immunoreactive cells. RESULTS: There were 29 patients without axillary lymph node metastasis and 37 patients with nodal metastasis. The mean age of the patients was 50.6 ± 11.3 years. Age, tumor size, nuclear grade and hormone receptor status were similar in the axillary lymph node positive and negative groups. There was a statistically significant relationship between cytoplasmic CSE1L expression and axillary lymph node metastasis. However, nuclear CSE1L expression did not have any effect on axillary lymph node metastasis. CONCLUSIONS: Cytoplasmic CSE1L overexpression may be a valuable tool for prognosis of breast cancer in future.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/análise
Neoplasias da Mama/química
Neoplasias da Mama/patologia
Proteína de Suscetibilidade a Apoptose Celular/análise
Linfonodos/patologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Axila
Citoplasma/metabolismo
Progressão da Doença
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Imuno-Histoquímica
Metástase Linfática
Meia-Idade
Gradação de Tumores
Estadiamento de Neoplasias
Valor Preditivo dos Testes
Prognóstico
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Cellular Apoptosis Susceptibility Protein)
[Em] Mês de entrada:1507
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150321
[St] Status:MEDLINE
[do] DOI:10.5301/tj.5000239



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