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[PMID]:29283339
[Au] Autor:Prabhu VV; Devaraj SN
[Ad] Endereço:Department of Biochemistry, University of Madras, Guindy campus, Chennai-600025, Tamil Nadu, India.
[Ti] Título:KAI1/CD82, Metastasis Suppressor Gene as a Therapeutic Target for Non-Small-Cell Lung Carcinoma.
[So] Source:J Environ Pathol Toxicol Oncol;36(3):269-275, 2017.
[Is] ISSN:2162-6537
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Lung cancer is the most frequent malignancy and the leading cause of cancer-related death worldwide; it is the second most common cancer, comprising 1.69 million deaths worldwide per year. Among these, 85% of lung cancers are non-small-cell lung carcinoma (NSCLC). Metastasis is common in NSCLC patients and are responsible for most deaths. Kang-Ai 1 (KAI1), a tumor metastasis suppressor gene also known as Cluster of Differentiation 82 (CD82), is a member of the membrane tetraspanin protein family, which are capable of inhibiting the metastatic process in NSCLC. KAI1/CD82 suppresses metastasis via multiple mechanisms regulating inhibition of cell motility, adhesion, fusion, and proliferation. KAI1 may attenuate signaling to shut down metastatic colonization through attenuation of epidermal growth factor receptor (EGFR) signaling and inhibition of the Wnt signaling pathways. In this review, we focus on the differential expression of KAI1/CD82, a tumor metastasis suppressor gene that can inhibit cancer invasion and cell metastasis during NSCLC. The differential expression of KAI1/CD82 could prove to be of novel therapeutic significance in treating malignant tumors and in reducing their metastatic potential.
[Mh] Termos MeSH primário: Carcinoma Pulmonar de Células não Pequenas/genética
Genes Supressores de Tumor
Proteína Kangai-1/genética
Neoplasias Pulmonares/genética
[Mh] Termos MeSH secundário: Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico
Carcinoma Pulmonar de Células não Pequenas/patologia
Genes p53
Seres Humanos
Proteína Kangai-1/antagonistas & inibidores
Proteína Kangai-1/fisiologia
Neoplasias Pulmonares/tratamento farmacológico
Neoplasias Pulmonares/patologia
Receptor do Fator de Crescimento Epidérmico/fisiologia
Via de Sinalização Wnt/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (CD82 protein, human); 0 (Kangai-1 Protein); EC 2.7.10.1 (Receptor, Epidermal Growth Factor)
[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:171229
[St] Status:MEDLINE
[do] DOI:10.1615/JEnvironPatholToxicolOncol.2017024619


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[PMID]:28880937
[Au] Autor:Zuidscherwoude M; Worah K; van der Schaaf A; Buschow SI; van Spriel AB
[Ad] Endereço:Department of Tumor Immunology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, The Netherlands.
[Ti] Título:Differential expression of tetraspanin superfamily members in dendritic cell subsets.
[So] Source:PLoS One;12(9):e0184317, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Dendritic cells (DCs), which are essential for initiating immune responses, are comprised of different subsets. Tetraspanins organize dendritic cell membranes by facilitating protein-protein interactions within the so called tetraspanin web. In this study we analyzed expression of the complete tetraspanin superfamily in primary murine (CD4+, CD8+, pDC) and human DC subsets (CD1c+, CD141+, pDC) at the transcriptome and proteome level. Different RNA and protein expression profiles for the tetraspanin genes across human and murine DC subsets were identified. Although RNA expression levels of CD37 and CD82 were not significantly different between human DC subsets, CD9 RNA was highly expressed in pDCs, while CD9 protein expression was lower. This indicates that relative RNA and protein expression levels are not always in agreement. Both murine CD8α+ DCs and its regarded human counterpart, CD141+ DCs, displayed relatively high protein levels of CD81. CD53 protein was highly expressed on human pDCs in contrast to the relatively low protein expression of most other tetraspanins. This study demonstrates that tetraspanins are differentially expressed by human and murine DC subsets which provides a valuable resource that will aid the understanding of tetraspanin function in DC biology.
[Mh] Termos MeSH primário: Células Dendríticas/metabolismo
Tetraspaninas/metabolismo
[Mh] Termos MeSH secundário: Animais
Antígenos de Neoplasias/genética
Células Cultivadas
Citometria de Fluxo
Seres Humanos
Proteína Kangai-1/genética
Leucócitos Mononucleares/metabolismo
Camundongos
Ligação Proteica
RNA Mensageiro/genética
Tetraspanina 28/genética
Tetraspanina-25/genética
Tetraspaninas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Neoplasm); 0 (CD37 protein, human); 0 (Kangai-1 Protein); 0 (RNA, Messenger); 0 (Tetraspanin 28); 0 (Tetraspanin-25); 0 (Tetraspanins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170908
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184317


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[PMID]:28534512
[Au] Autor:Li W; Hu M; Wang C; Lu H; Chen F; Xu J; Shang Y; Wang F; Qin J; Yan Q; Krueger BJ; Renne R; Gao SJ; Lu C
[Ad] Endereço:State Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing, China.
[Ti] Título:A viral microRNA downregulates metastasis suppressor CD82 and induces cell invasion and angiogenesis by activating the c-Met signaling.
[So] Source:Oncogene;36(38):5407-5420, 2017 Sep 21.
[Is] ISSN:1476-5594
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Kaposi's sarcoma (KS) as the most common AIDS-associated malignancy is etiologically caused by KS-associated herpesvirus (KSHV). KS is a highly disseminated and vascularized tumor. KSHV encodes 12 pre-microRNAs that yield 25 mature microRNAs (miRNAs), but their roles in KSHV-induced tumor metastasis and angiogenesis remain largely unclear. KSHV-encoded miR-K12-6 (miR-K6) can generate two mature miRNAs, miR-K6-5p and miR-K6-3p. Recently, we have shown that miR-K6-3p induced cell migration and angiogenesis via directly targeting SH3 domain binding glutamate-rich protein (SH3BGR). Here, by using mass spectrometry, bioinformatics analysis and luciferase reporter assay, we showed that miR-K6-5p directly targeted the coding sequence of CD82 molecule (CD82), a metastasis suppressor. Ectopic expression of miR-K6-5p specifically inhibited the expression of endogenous CD82 and strongly promoted endothelial cells invasion and angiogenesis. Overexpression of CD82 significantly inhibited cell invasion and angiogenesis induced by miR-K6-5p. Mechanistically, CD82 directly interacted with c-Met to inhibit its activation. MiR-K6-5p directly repressed CD82, relieving its inhibition on c-Met activation and inducing cell invasion and angiogenesis. Lack of miR-K6 abrogated KSHV suppression of CD82 resulting in compromised KSHV activation of c-Met pathway, and KSHV induction of cell invasion and angiogenesis. In conclusion, our data show that by reducing CD82, KSHV miR-K6-5p expedites cell invasion and angiogenesis by activating the c-Met pathway. Our findings illustrate that KSHV miRNAs may be critical for the dissemination and angiogenesis of KSHV-induced malignant tumors.
[Mh] Termos MeSH primário: Herpesvirus Humano 8/genética
Proteína Kangai-1/genética
MicroRNAs/metabolismo
Proteínas Proto-Oncogênicas c-met/metabolismo
Xeroderma Pigmentoso/irrigação sanguínea
[Mh] Termos MeSH secundário: Animais
Regulação para Baixo
Células HEK293
Xenoenxertos
Células Endoteliais da Veia Umbilical Humana
Seres Humanos
Proteína Kangai-1/biossíntese
Proteína Kangai-1/metabolismo
Masculino
Camundongos
Camundongos Nus
MicroRNAs/genética
Invasividade Neoplásica
Metástase Neoplásica
Neovascularização Patológica/genética
Neovascularização Patológica/metabolismo
Proteínas Proto-Oncogênicas c-met/genética
Transdução de Sinais
Transfecção
Xeroderma Pigmentoso/genética
Xeroderma Pigmentoso/metabolismo
Xeroderma Pigmentoso/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD82 protein, human); 0 (Kangai-1 Protein); 0 (MicroRNAs); EC 2.7.10.1 (MET protein, human); EC 2.7.10.1 (Proto-Oncogene Proteins c-met)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171122
[Lr] Data última revisão:
171122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170524
[St] Status:MEDLINE
[do] DOI:10.1038/onc.2017.139


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[PMID]:28431527
[Au] Autor:Zhu B; Zhou L; Yu L; Wu S; Song W; Gong X; Wang D
[Ad] Endereço:Department of Pathology, the First Affiliated Hospital of Bengbu Medical College, Bengbu Medical College, No.287, Changhuai Road, Bengbu, Anhui Province, China.
[Ti] Título:Evaluation of the correlation of vasculogenic mimicry, ALDH1, KAI1 and microvessel density in the prediction of metastasis and prognosis in colorectal carcinoma.
[So] Source:BMC Surg;17(1):47, 2017 Apr 21.
[Is] ISSN:1471-2482
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Metastasis and recurrence are the most common reasons for treatment failure of colorectal carcinoma (CRC). Vasculogenic mimicry (VM, blood supply formation often seen in highly aggressive tumors), Aldehyde dehydrogenase 1 (ALDH1, a biomarker of cancer stem cells), KAI1 (a suppressor gene of tumor metastasis) are all valuable factors for metastasis and prognosis in diverse human cancers. However, the correlation of VM, ALDH1, KAI1 and microvessel density (MVD) in CRC is unclear. In this study, we analyzed the correlations among VM, ALDH1, KAI1 and MVD, as well as their respective correlations with clinicopathological parameters and survival in CRC. METHODS: The level of VM, ALDH1, KAI1 and MVD in 204 whole tissue samples of CRC were examined by immunhistochemistry. Clinical data was also collected. RESULTS: Levels of VM, ALDH1 and MVD were significantly higher, and levels of KAI1 significantly lower, in CRC tissues than in normal colorectal tissues. Levels of VM, ALDH1 and MVD were positively associated with invasion of depth, lymph node metastasis (LNM), distant metastasis and tumor-node-metastasis (TNM) stages, and negatively with patients' overall survival (OS). Levels of KAI1 was negatively correlated with invasion of depth, LNM, distant metastasis and TNM stages, and the KAI1 positive expression subgroup had significantly longer OS than did the KAI1- subgroup. In multivariate analysis, high levels of VM, ALDH1 and KAI1, as well as TNM stages were independently correlated with lower OS in patients with CRC. CONCLUSIONS: VM, MVD and the expression of ALDH1 and KAI1 may represent promising metastatic and prognostic biomarkers, as well as potential therapeutic targets for CRC.
[Mh] Termos MeSH primário: Neoplasias Colorretais/patologia
Isoenzimas/metabolismo
Microvasos/metabolismo
Retinal Desidrogenase/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Feminino
Seres Humanos
Proteína Kangai-1/metabolismo
Metástase Linfática
Masculino
Meia-Idade
Recidiva Local de Neoplasia
Prognóstico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD82 protein, human); 0 (Isoenzymes); 0 (Kangai-1 Protein); EC 1.2.1.- (aldehyde dehydrogenase 1); EC 1.2.1.36 (Retinal Dehydrogenase)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170423
[St] Status:MEDLINE
[do] DOI:10.1186/s12893-017-0246-6


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[PMID]:28368419
[Au] Autor:Di Giacomo V; Tian TV; Mas A; Pecoraro M; Batlle-Morera L; Noya L; Martín-Caballero J; Ruberte J; Keyes WM
[Ad] Endereço:Gene Regulation, Stem Cells and Cancer Program, Centre for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Barcelona, Spain.
[Ti] Título:ΔNp63α promotes adhesion of metastatic prostate cancer cells to the bone through regulation of CD82.
[So] Source:Oncogene;36(31):4381-4392, 2017 Aug.
[Is] ISSN:1476-5594
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:ΔNp63α is a critical mediator of epithelial development and stem cell function in a variety of tissues including the skin and breast, while overexpression of ΔNp63α acts as an oncogene to drive tumor formation and cancer stem cell properties in squamous cell carcinoma. However, with regards to the prostate, while ΔNp63α is expressed in the basal stem cells of the mature gland, during adenocarcinoma development, its expression is lost and its absence is used to clinically diagnose the malignant state. Surprisingly, here we identify a sub-population of bone metastatic prostate cancer cells in the PC3 cell line that express ΔNp63α. Interestingly, we discovered that ΔNp63α favors adhesion and stem-like growth of these cells in the bone microenvironment. In addition, we show that these properties require expression of the target gene CD82. Together, this work uncovers a population of bone metastatic prostate cancer cells that express ΔNp63α, and provides important information about the mechanisms of bone metastatic colonization. Finally, we identify metastasis-promoting properties for the tetraspanin family member CD82.
[Mh] Termos MeSH primário: Neoplasias Ósseas/secundário
Proteína Kangai-1/fisiologia
Neoplasias da Próstata/patologia
Fatores de Transcrição/fisiologia
Proteínas Supressoras de Tumor/fisiologia
[Mh] Termos MeSH secundário: Animais
Adesão Celular
Linhagem Celular Tumoral
Regulação da Expressão Gênica
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD82 protein, human); 0 (Kangai-1 Protein); 0 (TP63 protein, human); 0 (Transcription Factors); 0 (Tumor Suppressor Proteins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170404
[St] Status:MEDLINE
[do] DOI:10.1038/onc.2017.42


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[PMID]:28260006
[Au] Autor:Chai J; Du L; Ju J; Ma C; Shen Z; Yang X; Liang L; Ni Q; Sun M
[Ad] Endereço:Department of Oral and Maxillofacial Surgery, School of Stomatology, Xi'an Medical University, Xi'an, Shaanxi 710021, P.R. China.
[Ti] Título:Overexpression of KAI1/CD82 suppresses in vitro cell growth, migration, invasion and xenograft growth in oral cancer.
[So] Source:Mol Med Rep;15(4):1527-1532, 2017 Apr.
[Is] ISSN:1791-3004
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:KAI1/CD82 is a metastatic suppressor gene in human prostate cancer and several other types of cancer in humans. The present study aimed to examine the role of the overexpression of KAI1 in the progression of oral cancer. Human KAI1/CD82 cDNA was transfected into OSCC­15 and 293T cell lines, and its effects on OSCC­15 cell proliferation, invasion and apoptosis were assessed by performing a 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide assay, Matrigel invasion and Annexin V­FITC staining, respectively. In addition, a xenograft model was used to assess the effect of KAI1/CD82 on the in vivo growth of tumors. The overexpression of KAI1/CD82 inhibited the proliferation and invasion of OSCC-15 cells. It also enhanced the apoptotic rate of the OSCC­15 cells. Furthermore, the overexpression of KAI1/CD82 inhibited tumor growth in the xenograft model. The results demonstrated that the overexpression of KAI1/CD82 significantly inhibited the proliferation and invasion of human oral cancer cells, and inhibited tumor growth in the xenograft model. Therefore, KAI1/CD82 may be considered as a potential therapeutic target in oral cancer.
[Mh] Termos MeSH primário: Movimento Celular
Proteína Kangai-1/metabolismo
Neoplasias Bucais/metabolismo
Neoplasias Bucais/patologia
Ensaios Antitumorais Modelo de Xenoenxerto
[Mh] Termos MeSH secundário: Animais
Apoptose
Linhagem Celular Tumoral
Proliferação Celular
Proteínas de Fluorescência Verde/metabolismo
Seres Humanos
Masculino
Camundongos Endogâmicos BALB C
Camundongos Nus
Invasividade Neoplásica
Plasmídeos/metabolismo
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD82 protein, human); 0 (Kangai-1 Protein); 0 (enhanced green fluorescent protein); 147336-22-9 (Green Fluorescent Proteins)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170306
[St] Status:MEDLINE
[do] DOI:10.3892/mmr.2017.6186


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[PMID]:28252644
[Au] Autor:Xu L; Hou Y; Tu G; Chen Y; Du YE; Zhang H; Wen S; Tang X; Yin J; Lang L; Sun K; Yang G; Tang X; Liu M
[Ad] Endereço:Key Laboratory of Laboratory Medical Diagnostics, Chinese Ministry of Education, Chongqing Medical University, Chongqing 400016, China.
[Ti] Título:Nuclear Drosha enhances cell invasion via an EGFR-ERK1/2-MMP7 signaling pathway induced by dysregulated miRNA-622/197 and their targets LAMC2 and CD82 in gastric cancer.
[So] Source:Cell Death Dis;8(3):e2642, 2017 Mar 02.
[Is] ISSN:2041-4889
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Drosha is an RNA III-like enzyme that has an aberrant expression in some tumors. Our previous studies showed the aberrant Drosha in gastric tumors. However, the roles of nuclear Drosha, the main regulator of microRNA (miRNA) biogenesis, in gastric cancer (GC) progression remain poorly understood. In this study, we demonstrated that nuclear Drosha is significantly associated with cell invasion of GC and that Drosha silence impedes the tumor invasion. Knockdown of Drosha led to a set of dysregulated miRNAs in GC cells. Multiple targets of these miRNAs were the members in cell migration, invasion and metastasis-associated signaling (e.g. ECM-receptor interaction, focal adhesion, p53 signaling and MAPK signaling pathway) revealed by bioinformatics analysis. LAMC2 (a key element of ECM-receptor signaling) and CD82 (a suppressor of p53 signaling) are the targets of miR-622 and miR-197, respectively. High levels of LAMC2 and low levels of CD82 were significantly related to the worse outcome for GC patients. Furthermore, overexpression of LAMC2 and knockdown of CD82 markedly promoted GC cell invasion and activated EGFR/ERK1/2-MMP7 signaling via upregulation of the expression of phosphorylated (p)-EGFR, p-ERK1/2 and MMP7. Our findings suggest that nuclear Drosha potentially has a role in the development of GC.
[Mh] Termos MeSH primário: Proteína Kangai-1/metabolismo
Laminina/metabolismo
Sistema de Sinalização das MAP Quinases/fisiologia
Metaloproteinase 7 da Matriz/metabolismo
MicroRNAs/metabolismo
Receptor do Fator de Crescimento Epidérmico/metabolismo
Ribonuclease III/metabolismo
Neoplasias Gástricas/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Movimento Celular/fisiologia
Regulação Neoplásica da Expressão Gênica/fisiologia
Seres Humanos
Invasividade Neoplásica/patologia
Metástase Neoplásica/patologia
Fosforilação/fisiologia
Transdução de Sinais/fisiologia
Neoplasias Gástricas/patologia
Regulação para Cima/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD82 protein, human); 0 (Kangai-1 Protein); 0 (LAMC2 protein, human); 0 (Laminin); 0 (MicroRNAs); EC 2.7.10.1 (EGFR protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 3.1.26.3 (DROSHA protein, human); EC 3.1.26.3 (Ribonuclease III); EC 3.4.24.23 (MMP7 protein, human); EC 3.4.24.23 (Matrix Metalloproteinase 7)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170303
[St] Status:MEDLINE
[do] DOI:10.1038/cddis.2017.5


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[PMID]:27813113
[Au] Autor:Lee J; Lee MS; Jeoung DI; Kim YM; Lee H
[Ad] Endereço:Department of Biological Sciences, College of Natural Sciences, Kangwon National University, Chunchon, Republic of Korea.
[Ti] Título:Promoter CpG-Site Methylation of the KAI1 Metastasis Suppressor Gene Contributes to Its Epigenetic Repression in Prostate Cancer.
[So] Source:Prostate;77(4):350-360, 2017 Mar.
[Is] ISSN:1097-0045
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Repression of the KAI1 metastasis suppressor gene is closely associated with malignancy and poor prognosis in many human cancer types including prostate cancer. Since gene repression in human cancers frequently results from epigenetic alterations by DNA methylation and histone modifications, we examined whether the KAI1 gene becomes silenced through these epigenetic mechanisms in prostate cancer. METHODS: KAI1 mRNA and protein levels were determined by RT-PCR and immunoblotting analyses, respectively. Methylation status of the KAI1 promoter DNA in prostate cancer cell lines and tissues was evaluated by methylation-specific PCR analysis of bisulfite-modified genomic DNAs. Methylated CpG sites in the KAI1 promoter were identified by sequencing the PCR clones of the bisulfite-modified KAI1 promoter DNA. KAI1 protein levels in human prostate cancer tissue samples were examined by immunofluorescence staining of the tissues with an anti-KAI1 antibody. RESULTS: Among the three human prostate cancer cell lines examined, PC3 and DU145 cells exhibited markedly decreased levels of KAI1 mRNA and protein as compared to LNCaP cells, even though the exogenous KAI1 promoter not being methylated was normally functional in all these cell lines. Treatment of the low KAI1-expressing cell lines with a demethylating agent, 5'-aza-2'-deoxycytidine, significantly elevated KAI1 expression levels, implicating the involvement of DNA methylation in KAI1 downregulation. Methylation of CpG islands within the KAI1 promoter region was observed in the low KAI1-expressing cells, but not in the high KAI1-expressing cells. Also, methyl CpG-binding proteins such as MBD2 and MeCP2 were complexed to the KAI1 promoter in the low KAI1-expressing cells. Bisulfite sequencing analysis identified the intensively methylated CpG residues in the KAI1 promoter clones derived from prostate cancer cells and tissues with no or low KAI1 expression. As in prostate cancer cell lines, prostate cancer tissues from patients also displayed a negative association between KAI1 expression levels and methylation status of the KAI1 promoter. CONCLUSIONS: The present data suggest that the KAI1 gene might be repressed by epigenetic alterations through the promoter CpG-site methylation during prostate cancer progression. This epigenetic mechanism could provide a clue for understanding how the KAI1 gene was silenced in metastatic prostate cancers. Prostate 77: 350-360, 2017. © 2016 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Ilhas de CpG/fisiologia
Repressão Epigenética/fisiologia
Genes Supressores de Tumor/fisiologia
Proteína Kangai-1/metabolismo
Regiões Promotoras Genéticas/fisiologia
Neoplasias da Próstata/metabolismo
[Mh] Termos MeSH secundário: Sequência de Bases
Linhagem Celular Tumoral
Seres Humanos
Proteína Kangai-1/genética
Masculino
Neoplasias da Próstata/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD82 protein, human); 0 (Kangai-1 Protein)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161105
[St] Status:MEDLINE
[do] DOI:10.1002/pros.23274


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[PMID]:27053631
[Au] Autor:Ferrer-Mayorga G; Gómez-López G; Barbáchano A; Fernández-Barral A; Peña C; Pisano DG; Cantero R; Rojo F; Muñoz A; Larriba MJ
[Ad] Endereço:Department of Cancer Biology, Instituto de Investigaciones Biomédicas "Alberto Sols", Consejo Superior de Investigaciones Científicas, Universidad Autónoma de Madrid, IdiPAZ, Madrid, Spain.
[Ti] Título:Vitamin D receptor expression and associated gene signature in tumour stromal fibroblasts predict clinical outcome in colorectal cancer.
[So] Source:Gut;66(8):1449-1462, 2017 Aug.
[Is] ISSN:1468-3288
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Colorectal cancer (CRC) is a major health concern. Vitamin D deficiency is associated with high CRC incidence and mortality, suggesting a protective effect of vitamin D against this disease. Given the strong influence of tumour stroma on cancer progression, we investigated the potential effects of the active vitamin D metabolite 1α,25-dihydroxyvitamin D (1,25(OH) D ) on CRC stroma. DESIGN: Expression of vitamin D receptor (VDR) and two 1,25(OH) D target genes was analysed in 658 patients with CRC with prolonged clinical follow-up. 1,25(OH) D effects on primary cultures of patient-derived colon normal fibroblasts (NFs) and cancer-associated fibroblasts (CAFs) were studied using collagen gel contraction and migration assays and global gene expression analyses. Publicly available data sets (n=877) were used to correlate the 1,25(OH) D -associated gene signature in CAFs with CRC outcome. RESULTS: High VDR expression in tumour stromal fibroblasts was associated with better overall survival (OS) and progression-free survival in CRC, independently of its expression in carcinoma cells. 1,25(OH) D inhibited the protumoural activation of NFs and CAFs and imposed in CAFs a 1,25(OH) D -associated gene signature that correlated with longer OS and disease-free survival in CRC. Furthermore, expression of two genes from the signature, CD82 and S100A4, correlated with stromal VDR expression and clinical outcome in our cohort of patients with CRC. CONCLUSIONS: 1,25(OH) D has protective effects against CRC through the regulation of stromal fibroblasts. Accordingly, expression of VDR and 1,25(OH) D -associated gene signature in stromal fibroblasts predicts a favourable clinical outcome in CRC. Therefore, treatment of patients with CRC with VDR agonists could be explored even in the absence of VDR expression in carcinoma cells.
[Mh] Termos MeSH primário: Calcitriol/farmacologia
Fibroblastos Associados a Câncer/metabolismo
Carcinoma/genética
Carcinoma/metabolismo
Neoplasias Colorretais/genética
Neoplasias Colorretais/metabolismo
Receptores de Calcitriol/metabolismo
Vitaminas/farmacologia
[Mh] Termos MeSH secundário: Carcinoma/química
Movimento Celular/efeitos dos fármacos
Células Cultivadas
Colágeno/efeitos dos fármacos
Neoplasias Colorretais/química
Intervalo Livre de Doença
Expressão Gênica/efeitos dos fármacos
Seres Humanos
Proteína Kangai-1/genética
Receptores de Calcitriol/análise
Proteína A4 de Ligação a Cálcio da Família S100/genética
Taxa de Sobrevida
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD82 protein, human); 0 (Kangai-1 Protein); 0 (Receptors, Calcitriol); 0 (S100 Calcium-Binding Protein A4); 0 (Vitamins); 142662-27-9 (S100A4 protein, human); 9007-34-5 (Collagen); FXC9231JVH (Calcitriol)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160408
[St] Status:MEDLINE
[do] DOI:10.1136/gutjnl-2015-310977


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[PMID]:27793161
[Au] Autor:Lu G; Zhou L; Zhang X; Zhu B; Wu S; Song W; Gong X; Wang D; Tao Y
[Ad] Endereço:Department of Emergence, The First Affiliated Hospital of Bengbu Medical College, No.287, Changhuai Road, Bengbu, China.
[Ti] Título:The expression of metastasis-associated in colon cancer-1 and KAI1 in gastric adenocarcinoma and their clinical significance.
[So] Source:World J Surg Oncol;14(1):276, 2016 Oct 28.
[Is] ISSN:1477-7819
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The most common reason for malignant tumor treatment failure is recurrence and metastasis. Metastasis-associated in colon cancer-1 (MACC1) was originally identified as a metastatic and prognostic biomarker for colon cancer and later other solid tumors. Kangai 1 (KAI1), a marker of suppressor of metastasis, is also associated with metastasis and poor prognosis in many tumors. However, the prognostic value of either MACC1 or KAI1 in gastric adenocarcinoma (GAC) is unclear. In this study, we explored the relationship between MACC1 and KAI1 expression, as well as their respective correlation with clinicopathological features, to determine if either could be helpful for improvement of survival prognosis in GAC patients. METHODS: The expression levels of both MACC1 and KAI1 in 325 whole-tissue sections of GAC were examined by immunohistochemistry. Clinical data was also collected. RESULTS: MACC1 was significantly overexpressed in GAC tissues when compared to levels in normal gastric tissues; KAI1 was significantly down-expressed in GAC tissues when compared to levels in normal gastric tissues. Investigation of association between MACC1 and KAI1 protein levels with clinicopathological parameters of GAC indicated association between the expression of each with tumor grade, lymph node metastasis, invasive depth, and TNM stages. The overall survival time of patients with MACC1- or KAI1-positive GAC tumors was significantly shorter or longer than that of those who were negative. Importantly, multivariate analysis suggested that positive expression of either MACC1 or KAI1, as well as TNM stage, could be independent prognostic factors for overall survival in patients with GAC. CONCLUSIONS: MACC1 and KAI1 may represent promising metastatic and prognostic biomarkers, as well as potential therapeutic targets, for GAC.
[Mh] Termos MeSH primário: Adenocarcinoma/secundário
Biomarcadores Tumorais/metabolismo
Proteína Kangai-1/metabolismo
Neoplasias Gástricas/patologia
Fatores de Transcrição/metabolismo
[Mh] Termos MeSH secundário: Adenocarcinoma/metabolismo
Adulto
Idoso
Estudos de Casos e Controles
Feminino
Seguimentos
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Técnicas Imunoenzimáticas
Metástase Linfática
Masculino
Meia-Idade
Gradação de Tumores
Invasividade Neoplásica
Estadiamento de Neoplasias
Prognóstico
Neoplasias Gástricas/metabolismo
Taxa de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (CD82 protein, human); 0 (Kangai-1 Protein); 0 (MACC1 protein, human); 0 (Transcription Factors)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161030
[St] Status:MEDLINE



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