Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research最新文献_第8页

Polyoma virus middle T and small t antigens cooperate to antagonize p53-induced cell cycle arrest and apoptosis. 多瘤病毒中T和小T抗原协同对抗p53诱导的细胞周期阻滞和凋亡。

Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research Pub Date : 2000-01-01

W Qian, K G Wiman

{"title":"Polyoma virus middle T and small t antigens cooperate to antagonize p53-induced cell cycle arrest and apoptosis.","authors":"W Qian, K G Wiman","doi":"","DOIUrl":"","url":null,"abstract":"Wild-type p53 triggers two distinct biological responses, cell cycle arrest and apoptosis. Several small DNA tumor viruses encode proteins that bind p53 and thus block the function of p53. This probably reflects the need of these viruses to prevent p53-induced cell cycle arrest and apoptosis to allow viral DNA replication. Unlike SV40 large T, polyoma virus large T does not bind p53, and it is still unclear how polyoma virus blocks p53 function. To address this question, we transfected polyoma virus middle T or small t alone or middle T and small t together into J3D mouse T-lymphoma cells carrying temperature-sensitive p53 (ts p53). Induction of wild-type p53 by temperature shift to 32 degrees C triggered both G1 cell cycle arrest and apoptosis in parental J3D-ts p53 cells. In contrast, J3D-ts p53 cells coexpressing middle T and small t showed only a weak G1 cell cycle arrest response after induction of wild-type p53 at 32 degrees C. Fluorescence-activated cell sorter analysis revealed that nearly half of the middle T-expressing cells, 30% of the small t-expressing cells, and a majority of the cells coexpressing middle T and small t were resistant to p53-induced apoptosis. The phosphatidylinositol 3-kinase inhibitor wortmannin partially abrogated the protective effect of middle T but not small t on p53-induced apoptosis, indicating that middle T prevents p53-induced apoptosis through the phosphatidylinositol 3-kinase signal transduction pathway. Our results thus establish a mechanism for polyoma virus-mediated inhibition of p53 function.","PeriodicalId":9753,"journal":{"name":"Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research","volume":"11 1","pages":"31-9"},"PeriodicalIF":0.0,"publicationDate":"2000-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21526514","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Nonapoptotic cell death associated with S-phase arrest of prostate cancer cells via the peroxisome proliferator-activated receptor gamma ligand, 15-deoxy-delta12,14-prostaglandin J2. 通过过氧化物酶体增殖体激活受体γ配体15-脱氧- δ 12,14-前列腺素J2与前列腺癌细胞s期阻滞相关的非凋亡细胞死亡。

Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research Pub Date : 2000-01-01

R Butler, S H Mitchell, D J Tindall, C Y Young

{"title":"Nonapoptotic cell death associated with S-phase arrest of prostate cancer cells via the peroxisome proliferator-activated receptor gamma ligand, 15-deoxy-delta12,14-prostaglandin J2.","authors":"R Butler, S H Mitchell, D J Tindall, C Y Young","doi":"","DOIUrl":"","url":null,"abstract":"15-Deoxy-delta12,14-prostaglandin J2 (15d-PGJ2) is a highly specific activator of the peroxisome proliferator-activated receptor gamma (PPAR-gamma). We investigated the effect of 15d-PGJ2 on three human prostate cancer cell lines, LNCaP, DU145, and PC-3. Western blotting demonstrated that PPAR-gamma1 is expressed predominantly in untreated prostate cancer cells. Treatment with 15d-PGJ2 caused an increase in the expression of PPAR-gamma2, whereas PPAR-gamma1 remained at basal levels. PPARs alpha and beta were not detected in these cells. Lack of lipid accumulation, increase in CCAAT/enhancer binding proteins (C/EBPs), or expression of aP2 mRNA indicated that adipocytic differentiation is not induced in these cells by 15d-PGJ2. 15d-PGJ2 and other PPAR-gamma activators induced cell death in all three cell lines at concentrations as low as 2.5 microM (similar to the Kd of PPAR-gamma for this ligand), coinciding with an accumulation of cells in the S-phase of the cell cycle. Activators for PPAR-alpha and beta did not induce cell death. Staining with trypan blue and propidium iodide suggested that, although the plasma membrane appears intact by electron microscopy, disturbances are evident as early as 2 h after treatment. Mitochondrial transmembrane potentials are significantly reduced by 15d-PGJ2 treatment. In addition, treatment with 15d-PGJ2 resulted in cytoplasmic changes, which are indicative of type 2 (autophagic), nonapoptotic programmed cell death.","PeriodicalId":9753,"journal":{"name":"Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research","volume":"11 1","pages":"49-61"},"PeriodicalIF":0.0,"publicationDate":"2000-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21526516","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Selective loss of the transforming growth factor-beta apoptotic signaling pathway in mutant NRP-154 rat prostatic epithelial cells. 突变型NRP-154大鼠前列腺上皮细胞中转化生长因子- β凋亡信号通路的选择性缺失。

Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research Pub Date : 2000-01-01

S Larisch-Bloch, D Danielpour, N S Roche, R Lotan, A Y Hsing, H Kerner, T Hajouj, R J Lechleider, A B Roberts

{"title":"Selective loss of the transforming growth factor-beta apoptotic signaling pathway in mutant NRP-154 rat prostatic epithelial cells.","authors":"S Larisch-Bloch, D Danielpour, N S Roche, R Lotan, A Y Hsing, H Kerner, T Hajouj, R J Lechleider, A B Roberts","doi":"","DOIUrl":"","url":null,"abstract":"Retroviral insertional mutagenesis was used to select mutant NRP-154 rat prostate carcinoma cells resistant to transforming growth factor (TGF)-beta-induced cell death. Similar to the parental cells, a mutant clone, M-NRP1, expressed TGF-beta receptors and was still responsive to induction both of direct target genes by TGF-beta and of apoptosis by staurosporine or okadaic acid. In contrast, indicators of cell growth, strongly suppressed by TGF-beta in the parental cells, were unaffected in M-NRP1 cells. M-NRP1 cells overexpress the antiapoptotic protein, Bcl-xL, and show dysregulated expression and localization of a protein related to a novel human septin, ARTS (designation of apoptotic response to TGF-beta signals), cloned by homology to an exonic sequence flanked by the viral long terminal repeats in M-NRP1 cells and shown to make cells competent to undergo apoptosis in response to TGF-beta. We propose that ARTS might operate within the same apoptotic pathway as Bcl-xL and that M-NRP1 cells could serve as a useful model for characterization of this pathway.","PeriodicalId":9753,"journal":{"name":"Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research","volume":"11 1","pages":"1-10"},"PeriodicalIF":0.0,"publicationDate":"2000-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21526511","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Inhibition of RNA polymerase I transcription in differentiated myeloid leukemia cells by inactivation of selectivity factor 1. 选择性因子1失活对分化骨髓白血病细胞RNA聚合酶I转录的抑制作用。

Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research Pub Date : 2000-01-01

L Comai, Y Song, C Tan, T Bui

{"title":"Inhibition of RNA polymerase I transcription in differentiated myeloid leukemia cells by inactivation of selectivity factor 1.","authors":"L Comai, Y Song, C Tan, T Bui","doi":"","DOIUrl":"","url":null,"abstract":"Transcription by RNA polymerase I (pol I) regulates the rate of ribosome biogenesis and the biosynthetic potential of the cell; therefore, it plays an important role in the control of cell growth. Differentiation of the human promyelocytic leukemic cell line U937 is accompanied by drastic decreases in pol I transcriptional activity. We have used cell-free extracts prepared from undifferentiated and differentiated U937 cells to investigate the molecular mechanisms responsible for this inhibitory process. Our analysis indicates that the activity of the TATA binding protein (TBP)/TBP-associated factor (TAF) complex selectivity factor 1 (SL1), one of the factors required for accurate and promoter-specific transcription by RNA pol I, is severely repressed in differentiated U937 cells. Moreover, the reduction in SL1 activity is not a consequence of a decrease in SL1, because there is no detectable difference in the abundance of TBP or TAFs before and after U937 cell differentiation. In conclusion, our results indicate that the selectivity factor SL1 is an important target for the regulation of pol I transcription during cell differentiation.","PeriodicalId":9753,"journal":{"name":"Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research","volume":"11 1","pages":"63-70"},"PeriodicalIF":0.0,"publicationDate":"2000-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21526517","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Tumor necrosis factor induces DNA replication in hepatic cells through nuclear factor kappaB activation. 肿瘤坏死因子通过活化核因子κ b诱导肝细胞DNA复制。

Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research Pub Date : 1999-12-01

I Kirillova, M Chaisson, N Fausto

{"title":"Tumor necrosis factor induces DNA replication in hepatic cells through nuclear factor kappaB activation.","authors":"I Kirillova, M Chaisson, N Fausto","doi":"","DOIUrl":"","url":null,"abstract":"Tumor necrosis factor (TNF) signaling through TNF receptor 1 (TNFR1) with downstream participation of nuclear factor kappaB (NFkappaB), interleukin 6 (IL-6), and signal transducers and activators of transcription 3 (STAT3) is required for initiation of liver regeneration. It is not known whether the proliferative effect of TNF on hepatocytes is direct or requires the participation of Kupffer cells, the liver resident macrophages. Moreover, it has not been determined whether NFkappaB activation is an essential step in TNF-induced proliferation. To answer these questions, we conducted studies in LE6 cells, a rat liver epithelial cell line with hepatocyte progenitor capacity. We report that TNF induces DNA replication in growth-arrested LE6 cells and that its effect involves the activation of NFkappaB and STAT3 and an increase in c-myc and IL-6 mRNAs. All of these effects, which mimic the events that initiate liver regeneration in vivo, are blocked if NFKB activation is inhibited by expression of a dominant-inhibitor IkappaBalpha mutant (deltaN-IkappaBalpha). Although NFkappaB blockage by deltaN-IkappaBalpha causes caspase activation and massive death of cells stimulated by TNF, inhibition of NFkappaB and STAT3 binding by the serine protease inhibitor N-tosyl-L-phenylalanine chloromethyl ketone results in G0-G1 cell cycle arrest without death. We conclude that NFkappaB is an essential component of the TNF proliferative pathway and that TNF-induced changes in IL-6 mRNA, STAT3, and c-myc mRNA are dependent on NFkappaB activation. Blockage of NFkappaB inhibits TNF-induced proliferation but does not necessarily cause cell death.","PeriodicalId":9753,"journal":{"name":"Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research","volume":"10 12","pages":"819-28"},"PeriodicalIF":0.0,"publicationDate":"1999-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21473725","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A role for E2F1 in the induction of ARF, p53, and apoptosis during thymic negative selection. 胸腺阴性选择过程中E2F1在诱导ARF、p53和细胞凋亡中的作用。

Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research Pub Date : 1999-12-01

J W Zhu, D DeRyckere, F X Li, Y Y Wan, J DeGregori

引用次数: 0

Establishment of the circumferential actin filament network is a prerequisite for localization of the cadherin-catenin complex in epithelial cells. 环形肌动蛋白丝网络的建立是上皮细胞中钙粘蛋白-连环蛋白复合物定位的先决条件。

Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research Pub Date : 1999-12-01

M P Quinlan, J L Hyatt

{"title":"Establishment of the circumferential actin filament network is a prerequisite for localization of the cadherin-catenin complex in epithelial cells.","authors":"M P Quinlan, J L Hyatt","doi":"","DOIUrl":"","url":null,"abstract":"With the adhesion molecules, the actin cytoskeleton controls cell-cell and cell-substrate interactions and participates in transmembrane signaling. The relationships between actin and adhesion complexes at the sites of adhesion have been well documented. Here we investigate by a series of studies whether a relationship exists between actin organization and the localization and function of the components of the cadherin-catenin complex (CCC) that participates in the cell-cell adherens junction. Reversible actin depolymerization reversibly affects the peripheral distribution of CCCs. Mutations in adenovirus E1A and the small GTPase rac1, but not Ha-ras, disrupt the circumferential, cortical actin filament (CAF) network and the targeting of CCC components to the cell surface. Disruption of actin stress fibers or microtubules does not interfere with CCC localization and function. Constitutive loss of the apical cortical actin ring results in epithelial cells in which components of the CCCs are found only in intracellular vesicles and never at the surface. A kinetic analysis of the de novo appearance of the CAF network and the CCCs at the cell surface was also conducted. When F-actin was dissolved, surface CCC components were internalized. Reestablishment of CAFs required about 4 h, during which time E-cadherin and alpha-catenin were found first in a juxtanuclear location and then in intracellular vesicles or post-Golgi carriers, similar to what was observed in cells expressing mutant E1A or rac1. Thus, disruption of preexisting CCCs resulted in their internalization and recycling to the Golgi. It was only after the regeneration of the filamentous actin ring beneath the cell surface that peripheral localization of CCCs was observed. A similar result was observed with dominant negative rac1. These data suggest that the status of cortical actin is assessed and transduced and thereby regulates the transport and delivery of cadherin and catenins to the cell surface.","PeriodicalId":9753,"journal":{"name":"Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research","volume":"10 12","pages":"839-54"},"PeriodicalIF":0.0,"publicationDate":"1999-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21473727","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Dwarfism and dysregulated proliferation in mice overexpressing the MYC antagonist MAD1. 过表达MYC拮抗剂MAD1的小鼠的侏儒症和增殖失调。

Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research Pub Date : 1999-12-01

C Quéva, G A McArthur, L S Ramos, R N Eisenman

{"title":"Dwarfism and dysregulated proliferation in mice overexpressing the MYC antagonist MAD1.","authors":"C Quéva, G A McArthur, L S Ramos, R N Eisenman","doi":"","DOIUrl":"","url":null,"abstract":"The four members of the MAD family are bHLHZip proteins that heterodimerize with MAX and act as transcriptional repressors. The switch from MYC-MAX complexes to MAD-MAX complexes has been postulated to couple cell-cycle arrest with differentiation. The ectopic expression of Mad1 in transgenic mice led to early postnatal lethality and dwarfism and had a profound inhibitory effect on the proliferation of the hematopoietic cells and embryonic fibroblasts derived from these animals. Compared to wild-type cells, Mad1 transgenic fibroblasts arrested with altered morphology and reduced density at confluence, cycled more slowly, and were delayed in their progression from G0 to the S phase. These changes were accompanied by accumulation of hypophosphorylated retinoblastoma protein and p130. Cyclin D1-associated kinase activity was dramatically reduced in MAD1-overexpressing fibroblasts. However, wild-type cell-cycle distribution and morphology could be rescued in the Mad1 transgenic cells by the introduction of HPV-E7, but not an E7 mutant incapable of binding to pocket proteins. This indicates that the activities of the retinoblastoma family members, via the cyclin D pathway, are likely to be the major targets for MAD1-mediated inhibition of proliferation in primary mouse fibroblasts.","PeriodicalId":9753,"journal":{"name":"Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research","volume":"10 12","pages":"785-96"},"PeriodicalIF":0.0,"publicationDate":"1999-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21473721","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

FADD is required for multiple signaling events downstream of the receptor Fas. FADD是受体Fas下游的多个信号事件所必需的。

Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research Pub Date : 1999-12-01

P Juo, M S Woo, C J Kuo, P Signorelli, H P Biemann, Y A Hannun, J Blenis

引用次数: 0

A random walk in oncogene space: the quest for targets. 癌基因空间中的随机漫步:寻找目标。

Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research Pub Date : 1999-12-01

P K Vogt, M Aoki, I Bottoli, H W Chang, S Fu, A Hecht, J S Iacovoni, B H Jiang, U Kruse

引用次数: 0