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Antagonistic effects of protein kinase C α and δ on both transformation and phospholipase D activity mediated by the epidermal growth factor receptor

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MOLECULAR AND CELLULAR BIOLOGY 1999年第11期19卷 7672-7680页

作者： Hornia, A Lu, ZM Sukezane, T Zhong, MH Joseph, T Frankel, P Foster, DA CUNY Hunter Coll Dept Biol Sci New York NY 10021 USA

Downregulation of protein kinase C delta (PKC delta) by treatment with the tumor-promoting phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) transforms cells that overexpress the non-receptor class tyrosine kinase c-Src (Z. Lu ct al,, Mel. Cell. Biol. 17:3418-3428, 1997). We extended these studies to cells overexpressing a receptor class tyrosine kinase, the epidermal growth factor (EGF) receptor (EGFR cells);like c-Src, the EGF receptor is overexpressed in several human tumors. In contrast with expectations, downregulation of PKC isoforms with TPA did not transform the EGFR cells;however, treatment with EGF did transform these cells. Since TPA downregulates all phorbol ester-responsive PKC isoforms,,ve examined the effects of PKC delta- and PKC alpha-specific inhibitors and the expression of dominant negative mutants for both PKC delta and alpha. Consistent with a tumor-suppressing function for PKC delta, the PKC delta-specific inhibitor rottlerin and a dominant negative PKC delta mutant transformed the EGFR cells in the absence of EGF. In contrast, the PKC alpha-specific inhibitor Go6976 and expression of a dominant negative PKC or mutant blocked the transformed phenotype induced by both EGF and PKC delta inhibition. Interestingly, both rottlerin and EGF induced substantial increases in phospholipase D (PLD) activity, which is commonly elevated in response to mitogenic stimuli, The elevation of PLD activity in response to inhibiting PKC delta, like transformation, was dependent upon PKC alpha and restricted to the EGFR cells. These data demonstrate that PKC isoforms alpha and delta have antagonistic effects on both transformation and PLD activity and further support a tumor suppressor role for PKC delta that may be mediated by suppression of tyrosine kinase-dependent increases in PLD activity.

关键词：苯乙酮类/药理学苯吡喃类/药理学卡唑类/药理学细胞转化肿瘤细胞培养的交叉遗传表皮生长因子/药理学吲哚类/药理学同工酶类/拮抗剂和抑制剂同工酶类/代谢模型遗传学诱变插入磷脂酶D/代谢蛋白激酶C/拮抗剂和抑制剂蛋白激酶C/代谢蛋白激酶Cα 蛋白激酶Cδ 重组蛋白质类/代谢十四酰佛波乙酯/药理学动物大鼠

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Generation of active TGF-β by prostatic cell cocultures using novel basal and luminal prostatic epithelial cell lines

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JOURNAL OF CELLULAR PHYSIOLOGY 2000年第1期184卷 70-79页

作者： Salm, SN Koikawa, Y Ogilvie, V Tsujimura, A Coetzee, S Moscatelli, D Moore, E Lepor, H Shapiro, E Sun, TT Wilson, EL NYU Sch Med Dept Cell Biol New York NY 10016 USA NYU Sch Med Kaplan Canc Ctr New York NY 10016 USA Osaka Univ Sch Med Dept Urol Osaka Japan ZymoGenet Seattle WA USA NYU Sch Med Dept Urol New York NY 10016 USA NYU Sch Med Dept Dermatol New York NY 10016 USA

Two prostatic epithelial lines, one of basal origin and one of luminal origin, were established from the dorsolateral prostates of p53 null mice. The cell lines are nontumorigenic when inoculated subcutaneously under the renal capsule or intraprostatically in syngeneic mice. The luminal cell line (PE-L-1) expresses cytokeratins 8 and 18 and the basal cell line (PE-B-1) expresses cytokeratins 5 and 14. The basal cells require serum for growth, whereas the luminal cells grow only in serum-free medium. Both cell lines require the presence of growth factors for optimal growth in culture, with EGF and FGF-2 having the greatest effect on the growth rate. Both lines express androgen receptor (AR) mRNA and protein. Androgen stimulates growth of the basal cell line, indicating that the ARs are functional, whereas growth of the luminal cells is unaffected by androgens. The luminal line is significantly inhibited by exogenous TGF-beta and produces low levels of endogenous TGF-beta. In contrast, the basal cell line produces significant amounts of TGF-beta and its growth is not influenced by this cytokine. Coculture of luminal cells with prostatic smooth muscle cells results in the generation of increased levels of biologically active TGF-beta, indicating a paracrine mechanism of TGF-beta activation that may be involved in the maintenance of normal prostatic function. To our knowledge this is the first report describing both basal and luminal prostatic cell lines from a single inbred animal species and the first indication that prostatic epithelial and stromal cells interact to generate the biologically active form of TGF-beta. These lines will provide an important model for determining basal/luminal interactions in both in vitro and in vivo assays. J. Cell. Physiol. 184:70-79, 2000. (C) 2000 Wiley-Liss, Inc.

关键词：生物学鉴定法细胞分裂/药物作用细胞系霍乱毒素/药理学共同培养技术表皮生长因子/药理学上皮细胞/细胞学上皮细胞/药物作用上皮细胞/生理学成纤维细胞生长因子2/药理学基因 p53 生长物质/药理学氢化可的松/药理学胰岛素/药理学角蛋白质类/分析小鼠近交C57BL 小鼠基因敲除肌平滑/细胞学肌平滑/药物作用肌平滑/生理学前列腺/细胞学前列腺/药物作用前列腺/生理学受体雄激素/分析受体雄激素/遗传学受体转化生长因子β/分析受体转化生长因子β/遗传学逆转录聚合酶链反应转化生长因子β/生物合成转化生长因子β/药理学动物男(雄)性小鼠

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Expression and action of kit ligand/stem cell factor in normal human and bovine ovarian surface epithelium and ovarian cancer

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BIOLOGY OF REPRODUCTION 2000年第6期62卷 1600-1609页

作者： Parrott, JA Kim, G Skinner, MK Washington State Univ Dept Genet & Cell Biol Ctr Reprod Biol Pullman WA 99163 USA

Greater than 95% of ovarian cancers originate from the epithelial cells on the surface of the ovary termed ovarian surface epithelium (OSE). A normal aspect of OSE function is repeated proliferation after ovulation, and this is postulated to be involved in part in the onset of ovarian cancer. The hypothesis tested is that locally produced growth factors have an important role in controlling OSE proliferation. The current study investigates the potential role of the growth factor kit ligand (KL)/stem cell growth factor and its receptor c-kif in normal OSE biology and ovarian cancer. Human tumors from borderline, stage I, and stage III cases of ovarian cancer were found to express KL and c-kif protein in the epithelial cell component by ICC analysis. The stromal cell component of human ovarian tumors contained little immunostaining. Bovine ovarian physiology and endocrinology are similar to the human such that cow ovaries were used as a model system to investigate normal OSE functions. KL and c-kit proteins were detected in the OSE from both normal human and bovine ovaries. Adjacent ovarian stromal tissue contained less intense but positive KL and c-kif immunostaining. To extend the ICC results, RNA was collected from normal bovine OSE and ovarian stromal cells to examine KL gene expression. KL transcripts were detected in cultured OSE and stromal cells by Northern blot analysis. KL gene expression was found to be high in freshly isolated OSE but low in freshly isolated stroma using a quantitative polymerase chain reaction procedure. Levels of KL gene expression in cultured OSE and stroma increased to high levels. Observations indicate that normal OSE expresses high levels of KL in vivo and in vitro. The actions of KL on the growth of both normal OSE cells and ovarian cancer cells was investigated. KL was found to stimulate the growth of normal OSE cells in a similar manner to epidermal growth factor. Observations demonstrate the production and action of KL by normal

关键词：细胞分裂表皮生长因子/药理学上皮细胞/代谢上皮细胞/病理学基因表达免疫组织化学卵巢肿瘤/代谢卵巢肿瘤/病理学卵巢/化学卵巢/代谢卵巢/病理学 RNA 信使/分析逆转录聚合酶链反应干细胞因子/遗传学干细胞因子/药理学干细胞因子/生理学动物牛女(雌)性人类

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STIMULATION OF SUGAR UPTAKE IN CULTURED FIBROBLASTS BY EPIDERMAL GROWTH-FACTOR (EGF) AND EGF-BINDING ARGININE ESTERASE

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JOURNAL OF CELLULAR PHYSIOLOGY 1976年第4期89卷 633-639页

作者： BARNES, D COLOWICK, SP VANDERBILT UNIV SCH MED DEPT IRON STEEL & OTHER MET NASHVILLE TN 37232 USA

Mouse epidermal growth factor causes a rapid increase in 2-deoxyglucose uptake in stationary phase mouse (3T3) cells or human fibroblasts. Maximum effect is approximately two fold over control levels for 3T3 cells and about 50% over controls for human fibroblasts. Maximum effect on 3T3 cells is seen about two hours after addition of 10 ng/ml EGF to the culture medium. Stimulation is easily measureable within the first fifteen minutes after addition of the hormone and may be detected at hormone concentrations as low as 0.1 ng/ml. The EGF-binding arginine esterase found associated with EGF in the mouse submaxillary gland causes an enhancement of the EGF effect. In serum-free medium, the EGF effect is still readily observed, but no enhancement by the esterase is seen. SV40 virus-transformed 3T3 cells show no effect on deoxyglucose uptake after addition of 10 ng/ml EGF to the culture medium, but a response may be demonstrated after these cells are incubated for 12 hours or more in serumless medium. EFG stimulates transport of 3-O-methylglucose in stationary phase 3T3 and human fibroblasts but no EGF stimulation of alpha-amino-isobutyrate uptake in 3T3 cells is seen under conditions is reproted to inhibit intracellular degradation of human EGF by human fibroblasts, does not diminish the EGF effect on deoxyglucose uptake in human fibroblasts.

关键词：氨基异丁酸类/代谢碳水化合物代谢细胞系脱氧葡萄糖/代谢表皮生长因子/代谢表皮生长因子/药理学酯酶类/代谢酯酶类/药理学成纤维细胞/药物作用成纤维细胞/代谢甘露醇/代谢甲基葡糖苷类/代谢肽类/药理学蛋白质结合动物人类小鼠

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Opposite effects of Ras or PKC activation on the expression of the SPRR2A keratinocyte terminal differentiation marker

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EXPERIMENTAL CELL RESEARCH 1999年第2期250卷 475-484页

作者： Sark, MWJ Borgstein, AM Medema, JP van de Putte, P Backendorf, C Leiden Univ Leiden Inst Chem Genet Mol Lab NL-2333 CC Leiden Netherlands Univ Utrecht Physiol Chem Lab NL-3584 CG Utrecht Netherlands

Epidermal growth factor (EGF) enhances the expression of the keratinocyte terminal differentiation marker SPRR2A, when added to monolayers of basal keratinocytes, induced to stratify by increasing the extracellular calcium concentration. A similar stimulation is found during suspension-induced differentiation in methylcellulose. This effect, which is observed after several hours of EGF addition, is restricted to terminally differentiating keratinocytes and is dependent on PKC signaling. EGF also transiently activates the Ras signaling pathway, with a maximum induction after 10 min (Medema et at, 1994, Mel. Cell. Biol. 14, 7078-7085). The cellular effects of activated Ras were determined by transient transfection of Ha-ras(Leu-61) into normal human keratinocytes. Activated Ras completely inhibited PHC-mediated expression of SPRR2A This inhibition is mediated via c-Jun as it is reversed by a dominant-negative c-Jun mutant (cJun Delta 6/194) and c-Jun can substitute for activated Ras. The inhibitory effect is targeted to a 150-bp minimal promoter region, which is essential and sufficient for SPRR2A expression during keratinocyte terminal differentiation This indicates that the Ras and PKC pathways, which both can be triggered by EGF, although at different time points, have opposite effects on SPRR2A gene expression. (C) 1999 Academic Press.

关键词：钙/拮抗剂和抑制剂钙/药理学细胞分化/药物作用细胞培养的酶激活表皮生长因子/药理学基因表达调控/药物作用基因 fos/遗传学吲哚类/药理学角蛋白细胞/细胞学角蛋白细胞/药物作用角蛋白细胞/酶学角蛋白细胞/代谢马来酰亚胺类/药理学膜蛋白质类/遗传学膜蛋白质类/代谢突变癌基因蛋白质p21(ras)/遗传学癌基因蛋白质p21(ras)/代谢启动区(遗传学)/遗传学蛋白激酶C/拮抗剂和抑制剂蛋白激酶C/代谢蛋白质前体/遗传学蛋白质前体/代谢原癌基因蛋白质c-jun/遗传学原癌基因蛋白质c-jun/代谢 RNA 信使/遗传学 RNA 信使/代谢信号传导/药物作用十四酰佛波乙酯/药理学转录遗传/药物作用人类

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Expression of the human hepatocyte growth factor cDNA in primary cultures of rat hepatocytes

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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 1999年第1期257卷 199-205页

作者： Runge, DM Bowen, WC Katyal, S Runge, D Suski, V Michalopoulos, GK Univ Pittsburgh Dept Pathol Pittsburgh PA 15261 USA

Hepatocyte growth factor (HGF) and epidermal growth factor (EGF) are primary mitogens for hepatocytes in culture. hepatocytes express the HGF-receptor MET but not HGF itself. To investigate the influence of autocrine HGF expression on the proliferative potential of hepatocytes, primary cultures were submitted to retrovirus-mediated transduction of the human hgf (huHGF) cDNA. Expression of the transduced cDNA revealed a minimum 2-fold increase in HGF-mRNA, whereas expression of the Escherichia coli beta-galactosidase gene remained even. Estimation of huHGF copy numbers showed there was a minimum 4-fold increase, suggesting an increase in the population of transduced cells. Immunoprecipitation of excreted huHGF and growth bioassays proofed that HGF was present and functional. HGF is excreted into the medium and therefore, by diffusion, available to transduced and non-transduced cells. The increase in huHGF-transduced cells suggests that the autocrine pathway as opposed to the paracrine pathway, which are both present at the same time, confers a growth advantage to these cells. (C) 1999 Academic Press.

关键词：自身分泌性细胞间通讯细胞分裂/药物作用细胞培养的培养基条件性/药理学 DNA/生物合成表皮生长因子/代谢表皮生长因子/药理学基因剂量基因报告/遗传学肝细胞生长因子/遗传学肝细胞生长因子/代谢肝细胞生长因子/药理学原位杂交肝/细胞学肝/药物作用肝/代谢旁分泌细胞细胞间通讯/药物作用沉淀素试验 RNA 信使/代谢逆转录病毒科/遗传学转导遗传/遗传学 β半乳糖苷酶类/遗传学 β半乳糖苷酶类/代谢动物人类大鼠

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Mechanisms of cyclosporine A-induced apoptosis in rat hepatocyte primary cultures

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TOXICOLOGY AND APPLIED PHARMACOLOGY 2000年第3期163卷 209-220页

作者： Grub, S Persohn, E Trommer, WE Wolf, A Novartis Pharma AG Expt Toxicol CH-4002 Basel Switzerland Univ Kaiserslautern Dept Chem Kaiserslautern Germany

In rat hepatocytes and isolated liver mitochondrial fractions, Cyclosporine A (CsA) is often used as a specific inhibitor of mitochondrial Ca(2+) release and as a specific blocker of mitochondrial membrane potential and permeability transition (MPT), which are all processes involved in the inhibition of apoptosis. However, neither inhibition nor induction of apoptosis by CsA has yet been described in the rat hepatocyte primary culture during incubation for 4 and 20 h. It was the purpose of the present study to examine by means of morphological and biochemical criteria the effects of CsA on apoptosis and to characterize the underlying mechanisms. Rat hepatocytes were cultured for 4 or 20 h with CsA at concentrations of 0, 10, 25, and 50 mu M. Chromatin condensation and fragmentation, DNA fragmentation (TUNEL), membrane phosphatidylserine distribution (Annexin V), caspase-1, -3, and -6 activity, mitochondrial membrane potential (Rhodamine 123), and cytochrome c release into the cytosol were investigated. Four hours after CsA treatment, chromatin condensation and fragmentation and the number of TUNEL- and Annexin V-positive cells increased dose-dependently without any observable enzyme leakage, which indicated the integrity of the outer cell membrane. After 20 h of CsA incubation apoptosis parameters were further increased and were accompanied by the increased activity of the cysteine protease, caspase-3 (CPP 32), and slightly increased caspase-6 (Mch 2), but not caspase-1 (ICE). The caspase-3 inhibitor, Ac-DEVD-CHO, inhibited caspase-3 activation and attenuated CsA-induced apoptosis and LDH leakage. The caspase-6 inhibitor, Ac-VEID-CHO, only marginally inhibited CsA-induced apoptosis. Decreased mitochondrial membrane potential and cytochrome c release went in parallel with ultrastructural mitochondrial changes and might be regarded as early events that trigger the apoptosis cascade. Transmission electron microscopy confirmed an increase in the number of necrotic cells

关键词：细胞凋亡/药物作用生物学标记半胱氨酸天冬氨酸蛋白酶/代谢细胞培养的环孢菌素/毒性细胞色素c组/代谢胞质溶胶/药物作用胞质溶胶/酶学 DNA/分析 DNA碎片裂/药物作用表皮生长因子/药理学免疫抑制剂/毒性肝/细胞学肝/药物作用膜人工显微镜检查电子线粒体肝/药物作用线粒体肝/酶学磷脂酰丝氨酸类/化学蛋白质类/代谢大鼠 Wistar 动物男(雄)性大鼠

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Inhibition of EGF-dependent calcium influx by annexin VI is splice form-specific

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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 1999年第2期260卷 540-546页

作者： Fleet, A Ashworth, R Kubista, H Edwards, H Bolsover, S Mobbs, P Moss, SE Univ London Univ Coll Dept Physiol Physiol Imaging Consortium London WC1E 6BT England

Annexin VI is a widely expressed calcium and phospholipid-binding protein that lacks a clear physiological role. We now report that A431 cells expressing annexin VI are defective in their ability to sustain elevated levels of cytosolic Ca2+ following stimulation with EGF. Other aspects of EGF receptor signaling, such as protein tyrosine phosphorylation and induction of c-fos are normal in these cells. However, EGF-mediated membrane hyperpolarization is attenuated and Ca2+ entry abolished in cells expressing annexin VI. This effect of annexin VI was only observed for the larger of the two annexin VI splice forms, the smaller splice variant had no discernable effect on either cellular phenotype or growth rate. Inhibition of Ca2+ in-flux was specific for the EGF-induced pathway;capacitative Ca2+ influx initiated by emptying of intracellular stores was unaffected. These results provide the first evidence that the two splice forms of annexin VI have different functions. (C) 1999 Academic Press.

关键词：膜联蛋白A6/药理学钙/代谢钙信号/药物作用细胞分裂/药物作用细胞系表皮生长因子/拮抗剂和抑制剂表皮生长因子/药理学离子转运膜电位/药物作用受体表皮生长因子/代谢

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Isolation of a proliferation inhibitor factor from uterine myomatosis fibroblasts

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PREPARATIVE BIOCHEMISTRY & BIOTECHNOLOGY 1999年第1期29卷 23-33页

作者： Sánchez-Sánchez, L Chávez, MA Manjarrez, A López, R Zenteno, E Weiss-Steider, B Natl Autonomous Univ Mexico Fac Estudios Super Zaragoza Lab Biol Celular & Mol Canc Mexico City 04510 DF Mexico Natl Autonomous Univ Mexico Fac Med Dept Salud Publ Mexico City 04510 DF Mexico Natl Autonomous Univ Mexico Fac Med Lab Inmunol Dept Bioquim Mexico City 04510 DF Mexico

In this work, we report the isolation of a factor from the culture supernatant of confluent fibroblasts from human cervix with the diagnosis of uterine myomatosis. This factor possesses the capacity to inhibit the proliferation of normal fibroblasts. The proliferation inhibitor factor (PIF) was purified from the culture supernatant by precipitation with 80% ammonium sulfate, and by molecular sieve chromatography. Our results indicate that PIF is a protein of 23 kDa, which is highly sensitive to trypsin treatment, and is thermolabile, since temperatures equal to, or above, 60 degrees C eliminate the protein activity in 15 to 20 min. Western blot analyses identified no cross reactions of the purified PIF with TGF-alpha, TNF alpha, IFN gamma, or IL-1 beta, suggesting that PIF is a new protein belonging to the group of factors secreted by fibroblasts able to inhibit cellular proliferation.

关键词：印迹法蛋白质细胞计数色谱法凝胶剂量效应关系药物表皮生长因子/药理学成纤维细胞/化学龙胆紫/分析生长抑制物/分离和提纯干扰素Ⅱ型/药理学白细胞介素1/药理学平滑肌瘤/化学肿瘤蛋白质类/分离和提纯转化生长因子β/药理学肿瘤细胞培养的肿瘤坏死因子α/药理学子宫肿瘤/化学女(雌)性人类

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P70 S6 kinase is regulated by protein kinase Cζ and participates in a phosphoinositide 3-kinase-regulated signalling complex

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MOLECULAR AND CELLULAR BIOLOGY 1999年第4期19卷 2921-2928页

作者： Romanelli, A Martin, KA Toker, A Blenis, J Harvard Univ Sch Med Dept Cell Biol Boston MA 02115 USA Boston Biomed Res Inst Signal Transduct Grp Boston MA 02114 USA

p70 S6 kinase (p70S6K) is an important regulator of cell proliferation. Its activation by growth factor requires phosphorylation by various inputs on multiple sites, Data accumulated thus far support a model whereby p70S6K activation requires sequential phosphorylations at proline-directed residues in the putative autoinhibitory pseudosubstrate domain, as well as threonine 389. Threonine 229, a site in the catalytic loop is phosphorylated by phosphoinositide-dependent kinase 1 (PDK-1), Experimental evidence suggests that p70S6K activation requires a phosphoinositide 3-kinase (PI3-K)-dependent signal(s), However, the intermediates between PI3-K and p70S6K remain unclear. Here,we have identified PI3-K-regulated atypical protein kinase C (PKC) isoform PKC zeta as an upstream regulator of p70S6K. In coexpression experiments, we found that a kinase-inactive PKC zeta mutant antagonized activation of p70S6K by epidermal growth factor, PDK-1, and activated Cdc42 and PI3-K. While overexpression of a constitutively active PKC zeta mutant (myristoylated PKC zeta [myr-PKC zeta]) only modestly activated p70S6K, this mutant cooperated with PDK-1 activation of p70S6K, PDK-1-induced activation of a C-terminal truncation mutant of p70S6K was also enhanced by myr-PKC zeta. Moreover, we have found that p70S6K can associate with both PDK-1 and PKC zeta in vivo in a growth factor-independent manner, while PDK-1 and PKC zeta can also associate with each other, suggesting the existence of a multimeric PI3-K signalling complex. This work provides evidence for a link between a phorbol ester-insensitive PKC isoform and p70S6K. The existence of a PI3-K-dependent signalling complex may enable efficient activation of p70S6K in cells.

关键词：酶激活表皮生长因子/药理学同工酶类/代谢磷酸肌醇3-激酶类/代谢蛋白质结合蛋白激酶C/代谢蛋白质丝氨酸苏氨酸激酶/代谢核糖体蛋白质S6激酶类/遗传学核糖体蛋白质S6激酶类/代谢序列缺失信号传导

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