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- 1. 糸球体半月体形成の機序 mechanisms of glomerular crescent formation
- 2. 胃癌の病理および分子学的病因 pathology and molecular pathogenesis of gastric cancer
- 3. 子宮癌肉腫の臨床的特徴、診断、病期分類、および治療 clinical features diagnosis staging and treatment of uterine carcinosarcoma
- 4. 前立腺肥大症の疫学および病因 epidemiology and pathogenesis of benign prostatic hyperplasia
- 5. 悪性肝腫瘍の病理 pathology of malignant liver tumors
- Synergistic effect of lung tumor-associated dendritic cell-derived HB-EGF and CXCL5 on cancer progression.
- Kuo PL1, Huang MS, Hung JY, Chou SH, Chiang SY, Huang YF, Yang CJ, Tsai MJ, Chang WA, Hsu YL.Author information 1Institute of Clinical Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan; Department of Medical Research, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan; Cancer Center, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan.AbstractThe interaction between cancer cells and their microenvironment is a paradoxical cycle that exacerbates cancer progression and results in metastasis. Our study investigated the mechanism underlying the synergistic enhancement of release of soluble factors from tumor-associated dendritic cells and its effect on cancer development. The combination of HB-EGF (heparin-binding EGF-like growth factor) and CXCL5 (CXCL5/epithelial neutrophil-activating peptide-78) produced a strong synergistic effect on cancer proliferation, epithelial-mesenchymal transition, migration and invasion. CXCL5 not only potentiated the classical EGFR pathway and the AKT and ERK/RSK1/2 signaling pathways but also increased the phosphorylation of heat shock protein 27 (HSP27), which was slightly increased in A549 cells treated with either HB-EGF or CXCL5 only. Phosphorylated HSP27 stabilized sustained AKT activity by direct interaction, leading to enhanced tumor spheroid formation. Knockdown of HSP27 by shRNA decreased HB-EGF plus CXCL5-mediated tumor spheroid formation in a three-dimensional culture system, suggesting that AKT/HSP27 was required for HB-EGF/CXCL5-mediated cancer progression. Inhibiting RSK also reduces the modulation of c-Fos phosphorylation, Snail upregulation and cell migration by HB-EGF plus CXCL5, suggesting a synergistic effect of ERK/RSK and HB-EGF plus CXCL5 on cell migration. In mice, CXCL5 antibody synergistically enhances the efficiency of the tyrosine kinase inhibitor, gefitinib, without increasing its toxicity. These results provide evidence that elucidates potential cross-points between extracellular signals affecting lung cancer progression. Targeting CXCL5 may provide therapeutic benefits for lung cancer chemotherapy or immunotherapy.
- International journal of cancer. Journal international du cancer.Int J Cancer.2014 Jul 1;135(1):96-108. doi: 10.1002/ijc.28673. Epub 2014 Jan 8.
- The interaction between cancer cells and their microenvironment is a paradoxical cycle that exacerbates cancer progression and results in metastasis. Our study investigated the mechanism underlying the synergistic enhancement of release of soluble factors from tumor-associated dendritic cells and it
- PMID 24346967
- Protumorigenic effects of Snail-expression fibroblasts on colon cancer cells.
- Herrera A1, Herrera M, Alba-Castellón L, Silva J, García V, Loubat-Casanovas J, Alvarez-Cienfuegos A, Miguel García J, Rodriguez R, Gil B, Ma Jesús Citores, Ma Jesús Larriba, Ignacio Casal J, de Herreros AG, Bonilla F, Peña C.Author information 1Department of Medical Oncology, Hospital Universitario Puerta de Hierro de Majadahonda, Majadahonda, Madrid, Spain.AbstractSnail1 is a transcriptional factor that plays an important role in epithelial-mesenchymal transition and in the acquisition of invasive properties by epithelial cells. In colon tumors, Snail1 expression in the stroma correlates with lower specific survival of cancer patients. However, the role(s) of Snail1 expression in stroma and its association with patients' survival have not been determined. We used human primary carcinoma-associated fibroblasts (CAFs) or normal fibroblasts (NFs) and fibroblast cell lines to analyze the effects of Snail1 expression on the protumorigenic capabilities in colon cancer cells. Snail1 expression was higher in CAFs than in NFs and, as well as α-SMA, a classic marker of activated CAFs. Moreover, in tumor samples from 50 colon cancer patients, SNAI1 expression was associated with expression of other CAF markers, such as α-SMA and fibroblast activation protein. Interestingly, coculture of CAFs with colon cells induced a significant increase in epithelial cell migration and proliferation, which was associated with endogenous SNAI1 expression levels. Ectopic manipulation of Snail1 in fibroblasts demonstrated that Snail1 expression controlled migration as well as proliferation of cocultured colon cancer cells in a paracrine manner. Furthermore, expression of Snail1 in fibroblasts was required for the coadjuvant effect of these cells on colon cancer cell growth and invasion when coxenografted in nude mice. Finally, cytokine profile changes, particularly MCP-3 expression, in fibroblasts are put forward as mediators of Snail1-derived effects on colon tumor cell migration. In summary, these studies demonstrate that Snail1 is necessary for the protumorigenic effects of fibroblasts on colon cancer cells.
- International journal of cancer. Journal international du cancer.Int J Cancer.2014 Jun 15;134(12):2984-90. doi: 10.1002/ijc.28613. Epub 2013 Nov 29.
- Snail1 is a transcriptional factor that plays an important role in epithelial-mesenchymal transition and in the acquisition of invasive properties by epithelial cells. In colon tumors, Snail1 expression in the stroma correlates with lower specific survival of cancer patients. However, the role(s) of
- PMID 24242829
- GPI/AMF inhibition blocks the development of the metastatic phenotype of mature multi-cellular tumor spheroids.
- Gallardo-Pérez JC1, Rivero-Segura NA1, Marín-Hernández A1, Moreno-Sánchez R1, Rodríguez-Enríquez S2.Author information 1Departamento de Bioquímica, Instituto Nacional de Cardiología, Tlalpan, México DF 14080, México.2Departamento de Bioquímica, Instituto Nacional de Cardiología, Tlalpan, México DF 14080, México; Laboratorio de Medicina Traslacional, Instituto Nacional de Cancerología, México. Electronic address: email@example.com.AbstractEpithelial-mesenchymal transition (EMT) and cellular invasiveness are two pivotal processes for the development of metastatic tumor phenotypes. The metastatic profile of non-metastatic MCF-7 cells growing as multi-cellular tumor microspheroids (MCTSs) was analyzed by determining the contents of the EMT, invasive and migratory proteins, as well as their migration and invasiveness potential and capacity to secrete active cytokines such as the glucose phosphate isomerase/AMF (GPI/AMF). As for the control, the same analysis was also performed in MCF-7 and MDA-MB-231 (highly metastatic, MDA) monolayer cells, and in stage IIIB and IV human metastatic breast biopsies. The proliferative cell layers (PRL) of mature MCF-7 MCTSs, MDA monolayer cells and metastatic biopsies exhibited increased cellular contents (2-15 times) of EMT (β-catenin, SNAIL), migratory (vimentin, cytokeratin, and fibronectin) and invasive (MMP-1, VEGF) proteins versus MCF-7 monolayer cells, quiescent cell layers of mature MCF-7 MCTS and non-metastatic breast biopsies. The increase in metastatic proteins correlated with substantially elevated cellular abilities for migration (18-times) and invasiveness (13-times) and with the higher level (6-times) of the cytokine GPI/AMF in the extracellular medium of PRL, as compared to MCF-7 monolayer cells. Interestingly, the addition of the GPI/AMF inhibitors erythrose-4-phosphate or 6-phosphogluconate at micromolar doses significantly decreased its extracellular activity (>80%), with a concomitant diminution in the metastatic protein content and migratory tumor cell capacity, and with no inhibitory effect on tumor lactate production or toxicity on 3T3 mouse fibroblasts. The present findings provide new insights into the discovery of metabolic inhibitors to be used as complementary therapy against metastatic and aggressive tumors.
- Biochimica et biophysica acta.Biochim Biophys Acta.2014 Jun;1843(6):1043-53. doi: 10.1016/j.bbamcr.2014.01.013. Epub 2014 Jan 16.
- Epithelial-mesenchymal transition (EMT) and cellular invasiveness are two pivotal processes for the development of metastatic tumor phenotypes. The metastatic profile of non-metastatic MCF-7 cells growing as multi-cellular tumor microspheroids (MCTSs) was analyzed by determining the contents of the
- PMID 24440856
- Induction of palate epithelial mesenchymal transition by transforming growth factor β3 signaling
- Jalali Azadeh,Zhu Xiujuan,Liu ChangChih [他]
- Development, growth & differentiation 54(6), 633-648, 2012-08
- NAID 40019395360
- 樋口 千恵子
- 東京女子医科大学雑誌 82(E2), E388-E393, 2012-07-31
- … 動物実験では低pH, GDPの一つである3-deoxyglucosoneは腹膜中皮細胞のepithelial mesenchymal transition(EMT)を引き起こし、腹膜のコラーゲン産生亢進、腹膜肥厚を引き起こす。 …
- NAID 110009435918
- TGF-βによる上皮間葉移行の分子機構 東京大・院医・分子病理 齋藤正夫 はじめに Epithelial-Mesenchymal Transition (EMT;上皮間葉移行) は1980年代初めにElizabeth Hayらが提唱した、上皮細胞が間葉系様細胞に形態変化する現象 ...
- EMT (Epithelial-Mesenchymal Transition)制御活性評価 (担当：井本正哉) EMT（上皮間葉転移）は、上皮性のがん細胞が、より運動性の高い間葉系細胞の表現型を獲得し、転移を起こしやすくなった状態をいう。またEMTを起こした細胞 ...
- A mesenchymal-epithelial transition (MET) is a reversible biological process that involves the transition from motile, multipolar or spindle-shaped mesenchymal cells to planar arrays of polarized cells called epithelia. MET is the reverse ...
- epithelial-to-mesenchymal transition、epithelial mesenchymal transformation、epithelial mesenchymal transition、epithelial-to-mesenchymal transitions、EMT
- 上皮間葉転換、上皮間充織変移、epithelial mesenchymal transformation、epithelial mesenchymal transition、epithelial-to-mesenchymal transition、epithelial-to-mesenchymal transitions
- 救急医療技師 emergency medical technicians
- epithelial-to-mesenchymal transition、epithelial mesenchymal transformation、epithelial mesenchymal transition
- dissemination、entry、immigration、metastases、metastasis、metastasize、shift、succession、transfer、transference、transit、transition state、transitional、transitional period、translocation、travel
- dorsal mesoderm、intermediate mesoderm、lateral plate mesoderm、mesenchymal、mesenchyme、mesoderm、paraxial mesoderm