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1.
XIE Si-ming  SHEN Li-jia 《园艺学报》2004,20(8):1531-1533
The PTEN, having a dual specificity phosphatase activity, is the first tumor suppressor gene that possess phosphatase activity hitherto. Many researches have suggested that PTEN play a major role in the tumorgenesis. In clinical, the head and neck squamous cell carcinoma (HNSCC) is one of the most common malignant tumors. In this review, advances in the research of PTEN and the relationship between the PTEN and HNSCC are discussed.  相似文献   

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AIM: To explore the regulatory effect of microRNA-3666 (miR-3666) on the expression of its target gene phosphatase and tensin homologue deleted on chromosome ten (PTEN) in leukemic cells. METHODS: miR-3666 expression levels in normal peripheral blood mononuclear cells and leukemic cells were determined by quantitative real-time PCR. miR-3666 targeting PTEN 3-untranslated region (3UTR) was predicted by TargetScan software. 3UTR of PTEN was inserted in the dual luciferase reporter vector psiCHECK2. The reporter activity was evaluated by the Dual-Luciferase Reporter Assay System after the luciferase promoter vector and miRNA were co-transfected into HEK293T cell line. K562 cells were transfected with synthetic miR-3666 inhibitor (anti-miR-3666) or a synthetic control miRNA (anti-miR-C). The expression of PTEN protein in the above transfected K562 cells was determined by Western blotting. RESULTS: miR-3666 was up-regulated in the human leukemic cell lines and primary leukemic cells compared to normal peripheral blood mononuclear cells. The results of dual luciferase assays validated PTEN as a specific target gene of miR-3666. Inhibition of miR-3666 resulted in an up-regulation of PTEN protein expression in the K562 cells. CONCLUSION: miR-3666 is over-expressed in leukemic cells. The abnormal over-expression of miR-3666 may play a key role in leukemia due to the down-regulation of PTEN.  相似文献   

4.
AIM: To investigate the effects of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) on the apoptosis, oxidative damage and immune inflammatory factors in myocardial H9c2 cells with anoxia/reoxygenation (A/R). METHODS: The H9c2 cells were used to establish a model of A/R. The H9c2 cells were transfected with PTEN small interfering RNA (siRNA) and negative control. After A/R, the expression of PTEN at mRNA and protein levels was determined by RT-PCR and Western blot, respectively. The cell viability was measured by MTT assay. The apoptosis was analyzed by flow cytometry. Xanthine oxidase method was used to determine superoxide dismutase (SOD) activity. The content of malondialdehyde (MDA) was detected by thiobarbituric acid method. The lactate dehydrogenase (LDH) activity in the supernatant was evaluated by 4-dinitrophenylhydrazine method. The levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and IL-6 in culture supernatant were examined by ELISA. The protein levels of cleaved caspase-3, Bax and FasL in the cells were determined by Western blot. RESULTS: After A/R, the expression of PTEN at mRNA and protein levels was significantly increased in the H9c2 cells (P<0.05). The mRNA and protein levels of PTEN were decreased significantly after transfection with PTEN siRNA (P<0.05). The viability of H9c2 cells was decreased after A/R, while the apoptotic rate was increased. The protein levels of cleaved caspase-3, Bax and FasL were increased in the cells. The MDA level was elevated, the activity of SOD was decreased, and the levels of LDH, TNF-α, IL-1β and IL-6 in the culture supernatant were increased (P<0.05). Down-regulation of PTEN partly antagonized the effects of A/R on the viability, apoptotic rate, MDA content, SOD activity, and the levels of LDH, TNF-α, IL-1β and IL-6 in culture supernatant. CONCLUSION: Down-regulation of PTEN attenuates oxidative damage induced by A/R, reduces apoptosis and secretion levels of TNF-α, IL-1β and IL-6 in the H9c2 cells.  相似文献   

5.
AIM: To explore the effect of microRNA-221 (miR-221) on resistance of lung cancer cells to gefitinib, and to investigate its related mechanism. METHODS: RT-qPCR was used to detect the levels of miR-221 expression between gefitinib-sensitive cell line PC9 and gefitinib-resistant cell line PC9/GR. The PC9/GR cells were transfected with miR-221 inhibitor by Lipofectamine 2000. The drug sensitivity of these cells to gefitinib was determined by CCK-8 assay. The protein expression level of phosphatase and tensin homologue deleted on chromosome ten (PTEN) was determined by Western blot. The 3'-UTR of PTEN was cloned into luciferase reporter vector and its luciferase activity was detected to verify whether miR-221 targets PTEN. RESULTS: The expression level of miR-221 in the PC9/GR cells was significantly higher than that in the PC9 cells (P<0.05). The protein expression level of PTEN in the PC9/GR cells was lower than that in the PC9 cells (P<0.05). The IC50 of gefitinib was significantly reduced in the PC9/GR cells after transfection with miR-221 inhibitor (P<0.05). The protein expression level of PTEN in the cells transfected with miR-221 inhibitor was increased as compared with control group and blank group (P<0.05). Inhibition of miR-221 expression enhanced the enzymatic activity of luciferase reporter vector of PTEN. CONCLUSION: miR-221 enhances the resistance of lung cancer cells to gefitinib by down-regulating the protein expression of PTEN.  相似文献   

6.
PTEN gene, identified in 1997 and named after the separation, was a new candidate tumor suppressor gene. The mutations of PTEN gene, loss of heterozygosity in human tumors are prevalent, such as malignant glioma, endometrial cancer, prostate cancer, breast cancer, etc. The mutation frequency of PTEN is equivalent to p53. As an important functional element and a tumor suppressor gene, most scholars agree that PTEN gene is as important as p53. At present, studies on the PTEN gene mainly concentrated in the tumor area, its functions in the cardiovascular system are few reports. This article reviews the investigation of PTEN gene in the cardiovascular system.  相似文献   

7.
AIM: To investigate the role of extracellular signal-regulated kinase 5 (ERK5) in platelet aggregation in vitro and arterial thrombosis in vivo. METHODS: The expression and phosphorylation levels of ERK5 in human platelet were detected by Western blot. The effects of ERK5 selective inhibitor XMD8-92 on platelet aggregation and dense granule secretion were detected by Chrono-Log aggregometer. The effect of ERK5 on in vivo thrombosis was analyzed using an FeCl3 artery thrombosis model. The effects of XMD8-92 on protein kinase B (PKB/Akt) and phosphatase and tensin homolog deleted on chromosome ten (PTEN) phosphorylation levels were determined by Western blot. RESULTS: ERK5 was stably expressed in human platelets and its phosphorylation level increased significantly after platelet activation (P<0.05). XMD8-92, a selective inhibitor of ERK5, inhibited platelet aggregation and dense granule secretion in response to several platelet stimulators (P<0.05). The results of Western blot showed that XMD8-92 inhibited Akt phosphorylation level by down-regulating PTEN Ser370 phosphorylation and enhancing PTEN activity. The pathway was further confirmed using platelet specific PTEN deficiency mice. The first occlusion time was obviously extended in the mice intravenously given XMD8-92 in the FeCl3-induced carotid artery injury model. CONCLUSION: ERK5 plays a role in platelet activation and arterial thrombosis by influencing PTEN and Akt phosphorylation.  相似文献   

8.
AIM: To investigate the expression and clinical significance of phosphatase and tensin homology deleted on chromosome ten (PTEN) and survivin in laryngeal squamous cell carcinoma (LSCC) and the relationship between the two genes. METHODS: The expression of PTEN and survivin in 57 cases of LSCC, 27 cases of adjacent safety margin (ASM) radomized drawn from the LSCC patient and 22 cases of vocal cord polyp (VCP) were evaluated by SP immunohistochemistry, and the statistics analysis were followed. RESULTS: The positive rates of PTEN in LSCC, ASM and VCP were 89.5% (51/57), 88.9%(24/27) and 95.5% (21/22), respectively. There was no significant difference among them (P>0.05), but the expression degrees were ascending (P<0.01). There was no expression of survivin in VCP. The positive rates of survivin in LSCC and ASM were 50.9% (29/57) and 11.1% (3/24) respectively with the significant difference (P<0.01). However, the difference of the expression degrees between LSCC and ASM was not significant (P>0.05). The expression of neither PTEN nor survivin was related to gender, age, tumor site, differentiation, T classification, clinical stage, nodal metastases, etc (P>0.05). There was no correlation in LSCC between PTEN and survivin expression (r=-0.15, P>0.05). CONCLUSIONS: During the carcinogenesis of LSCC, partial variation maybe occurs in PTEN. Survivin probably plays an important role during the carcinogenesis of LSCC. These changes are the early molecular event of the carcinogenesis. Relationship between PTEN and survivin and the biological behavior of LSCC, such as progression, metastases were not observed.  相似文献   

9.
AIM:To investigate the role of phosphatase and tensin homology deleted on chromosome(PTEN) gene in the cell cycle and invasion ability of human ovarian carcinoma SKOV3 cell line in vitro. METHODS:Human ovarian carcinoma SKOV3 cells were transfected with a eukaryotic expression plasmid vector containing PTEN gene in vitro,and then the positive cell clones were selected and amplified. MTT method was used to observe the inhibitory rate,flow cytometry was used to detect the cycle of transfected PTEN cells and apoptosis level. Western blotting analysis was used to determine PTEN gene expression. The invasiveness of transfected cells were measured quantitatively by Matrigel invasion assays (Transwell chamber). RESULTS:The expression of PTEN mRNA in SKOV3 cells increased after transfection with PTEN gene. Flow cytometry showed that the percentage of cells in S phase increased,but that in G2/M phase decreased. Invasiveness of SKOV3 was significantly decreased. CONCLUSION:The transfection of PTEN gene into SKOV3 cells can inhibit human ovarian carcinoma SKOV3 cell proliferation,invasion and induce SKOV3 cell apoptosis.  相似文献   

10.
AIM: To explore the potential correlation between the expression of phosphatase and tensin homology deleted on chromosome 10(PTEN) and RIF in IgA nephropathy. METHODS: Forty-seven patients diagnosed as primary IgA nephropathy by renal histology were involved. 10 specimens from normal renal tissue of renal carcinoma served as control group. Tubulointerstitial lesion (TIL) was classified by using Katafuchi scale, including no TIL (group I), mild TIL (group II), moderate TIL (group III), severe TIL (group IV). The expressions of PTEN, TGF-β1, α-SMA and ColⅢ in renal tissue were detected by immunohistochemistry. PTEN mRNA was detected by in situ hybridization. RESULTS: Renal tissues from renal biopsy showed abundant expressions of PTEN and PTEN mRNA in endochylema of renal tubular epithelial cells, and negligible expression in glomeruli. With the progress of TIF in IgA nephropathy, the expressions of PTEN and PTEN mRNA decreased gradually (P<0.05). In contrast, the expressions of TGF-β1, α-SMA and ColⅢ increased significantly (P<0.05). The expressions of PTEN and PTEN mRNA in renal tissues were positively with eGFR and urine osmotic pressure (P<0.01), negatively correlated with the expressions of TGF-β1, α-SMA, ColⅢ, urinary protein excretion for 24 h, the rate of sclerosis glomeruli and the scores of vascular lesion (P<0.01). CONCLUSION: These results suggest the loss of PTEN expression in RIF of IgA nephropathy. Moreover, TGF-β signaling induces epithelial to mesenchymal transition and extracellular matrix accumulation possibly through a mechanism dependent on the downregulation of PTEN.  相似文献   

11.
AIM: To investigate the effect of wild-type PTEN transfection on the sensitivity of human leukemia K562 cells to artesunate (ART) and its molecular mechanism. METHODS: The adenovirus containing wild-type PTEN (Ad-WT-PTEN) or empty vectors (Ad) were transfected into K562 cells[with multiplicity of infection (MOI)=200]. The untransfected cells served as normal control. The effect of wild-type PTEN on the inhibition of K562 cell growth by ART was observed. The sensitizing ratio of PTEN combined with ART based on IC50 was calculated. The viability of K562 cells was detected by MTT assay. The apoptosis was analyzed by flow cytometry. The mRNA level of PTEN was assessed by real-time PCR. The protein expression of PTEN, p-Akt and Akt was detected by Western blot. The activity of caspase-3/7 was measured by caspase activity kits. RESULTS: The sensitivity of K562 cells to ART was significantly increased by 2.25 folds after transfected with PTEN based on the IC50. The cell viability in Ad-WT-PTEN+ART group was significantly lower than that in Ad+ART group after transfection for 3 d (P<0.01). The apoptotic rate in Ad-WT-PTEN+ART group was significantly higher than that in Ad+ART group (P<0.01). The expression of PTEN at mRNA and protein levels in the K562 cells after transfection with PTEN was significantly increased, and the protein level of p-Akt and caspase-3/7 activity were down-regulated, particularly in PTEN combined with ART group. CONCLUSION: The wild-type PTEN gene enhances the sensitivity of the K562 cells to ART by down-regulating the level of p-Akt and up-regulating the caspase-3/7 activity.  相似文献   

12.
AIM: To explore the effect of microRNA-221 (miR-221) on the proliferation of lung cancer A549 cells, and to investigate its mechanism. METHODS: The A549 cells were transfected with miR-221 mimics by Lipofectamine 2000. The expression of miR-221 was detected by RT-qPCR. The expression of PTEN at mRNA and protein le-vels was detected by RT-qPCR and Western blot, respectively. The cell proliferation was examined by CCK-8 assay and colony formation assay. The 3'-UTR of PTEN was cloned into luciferase reporter vector and its enzymatic activity was detected to verify whether miR-221 targeted to PTEN. RESULTS: The expression level of miR-221 in the A549 cells was significantly increased after transfection with miR-221 mimics as compared with negative control group and blank group (P<0.01). The mRNA and protein levels of PTEN were significantly down-regulated compared with control group and blank group (P<0.05). In addition, miR-221 over-expression significantly promoted the proliferation of A549 cells (P<0.05). Moreover, miR-221 inhibited the enzymatic activity of luciferase reporter vector of PTEN. CONCLUSION: Over-expression of miR-221 significantly promotes the proliferation ability of human lung cancer A549 cells by down-regulation of PTEN.  相似文献   

13.
AIM: To explore the relationship and molecular mechanism between microRNA-21(miR-21) and Schwann cells (SC) following peripheral nerve injury. METHODS: The mRNA expression of miR-21 and phosphatase and tensin homologue deleted on chromosome ten (PTEN) in animal model were detected by real-time PCR. The over-expression of miR-21 and inhibition of miR-21 expression in the Schwann cells according to transfection of lentiviral vectors were performed, the nonspecific miRNA was used as a negative control (NC). The cell apoptosis was measured by flow cytometry. The mRNA expression of miR-21 and PTEN in the cells was detected by real-time PCR. The protein expression of PTEN and cleaved caspase-3 was determined by Western blot. RESULTS: The level of miR-21 was significantly higher and the mRNA level of PTEN was significantly lower in the model of nerve injury than those in control group. miR-21 over-expression decreased the number of apoptotic Schwann cells compared with NC-SC. The mRNA expression of PTEN was down-regulated by over-expression of miR-21. The protein expression of PTEN and cleaved caspase-3 was down-regulated by over-expression of miR-21(P<0.05). CONCLUSION: miR-21 may play an important role in the peripheral nerve injury through inhibiting apoptosis of Schwann cells by down-regulating the expression of PTEN.  相似文献   

14.
LIU An  HUANG Cheng-gang  XU Jia 《园艺学报》2016,32(7):1227-1234
AIM: To investigate the therapeutic effects of lentivirus-mediated shRNA targeting growth hormone secretagogue receptor 1a(GHSR1a) on colorectal cancer cell line SW480 both in vitro and in vivo. METHODS: Human GHSR1a sequence was used for the design of shRNA targeting GHSR1a, which was introduced to lentivirus, followed by transfection into SW480 cells. CCK-8 assay was performed to detect cell viability. The mRNA expression of GHSR1a and PTEN in colorectal cancer cells was detected by RT-PCR. The protein levels of GHSR1a, ghrelin, PTEN, p-AKT and p53 were determined by Western blot. Stable GHSR1a silencing in SW480 xenografts in nude mice was established. After the mice were sacrificed and weighted, immunohistochemistry was used to detect the positive expression of Ki-67 and PTEN in the tumors. RESULTS: GHSR1a was over-expressed in the malignant cells in comparison with the normal cells in vitro. The tumor specific lentivirus-mediated shRNA targeting GHSR1a gene and GHSR1a knockdown SW480 cells were successfully constructed. After transfection with GHSR1a shRNA, the expression of GHSR1a at mRNA and protein levels was markedly inhibited in the SW480 cells. Furthermore, GHSR1a silencing by specific shRNA showed increased PTEN, inhibition of AKT phosphorylation and promotion of p53 release in the SW480 cells. In vivo results demonstrated that down-re-gulation of GHSR1a in the SW480 cells significantly decreased the expression of Ki-67 and increased the expression of PTEN in the tumor tissues, leading to a marked reduction in tumor weight in comparison to blank control or negative control tumors. CONCLUSION: Down-regulation of GHSR1a by shRNA technique inhibits the growth of colorectal cancer cell line and xenograft tumor through activation of the PTEN/PI3K/AKT signaling pathways.  相似文献   

15.
ATM:To observe the expression change of PTEN and autophagy in the renal tissues of diabetic rats, and to explore the regulatory mechanism of PTEN/AKT/mTOR pathway to autophagy in diabetic nephropathy. METHODS: The Sprague-Dawley rats were randomly divided into normal control group and diabetic group (8 in each group). The diabetic rat model was established by injection of streptozotocin. The biochemical and kidney indexes were measured after the model of diabetic nephropathy was successfully established. The expression location of PTEN in the renal tubular epithelial cells was observed by the method of immunohistochemistry. The protein levels of autophagy-related protein LC3, PTEN and PTEN/AKT/mTOR signalling molecules were determined by Western blotting. The mRNA expression of PTEN was detected by real-time PCR. RESULTS: The blood glucose, 24 h urine protein and kidney index in diabetic group were all obviously higher than those in control group. Compared with control group, the protein levels of LC3I and LC3II in diabetic group were obviously decreased. PTEN was mainly located in the renal tubular epithelial cells. Compared with control group, the protein expression of PTEN was significantly down-regulated in diabetic group. Furthermore, the activity of PTEN/AKT/mTOR pathway increased in diabetic nephropathy rats. CONCLUSION: The level of autophagy in renal tissues of diabetic rats is decreased, whereas the activity of PTEN/AKT/mTOR pathway is increased. The level of autophagy may be mediated by PTEN/AKT/mTOR pathway.  相似文献   

16.
AIM:To investigate the down-regulation of phosphatase and tensin homolog deleted on chromosome 10(PTEN) gene by adenovirus-mediated short hairpin RNA(shRNA) on proliferation and apoptosis of activated hepatic stellate cells(HSCs) in vitro and the related signaling transduction pathways. METHODS:The activated HSCs were cultured in vitro and transfected with recombinant adenovirus expressing shRNA targeting PTEN. The proliferation of HSCs was measured by MTT assay and the apoptosis was assessed by TUNEL and flow cytometry. Western blotting was used to detect the protein levels of PTEN, Bax, Bcl-2, Akt, p-Akt, ERK1/2 and p-ERK1/2 in HSCs, and real-time fluorescent quantitative PCR was applied to detect the mRNA expression of Akt and ERK1. RESULTS:The recombinant adenovirus expressing shRNA targeting PTEN was successfully transfected into activated HSCs in vitro, and significantly promoted the proliferation of HSCs in a time-dependent manner within a certain extent. The apoptotic rate of HSCs was significantly decreased 72 h after transfection(P<0.05). Meanwhile, reduced expression of Bax and elevated expression of Bcl-2 were induced 72 h after transfection(P<0.05). Furthermore, the expression of p-Akt and p-ERK1/2 were increased significantly(P<0.05), while no significant difference in the expression of Akt and ERK1 at mRNA and protein levels was observed(P>0.05). CONCLUSION:Down-regulation of PTEN by adenovirus-mediated shRNA dramatically promotes the proliferation of activated HSCs, and inhibits the apoptosis through Bcl-2/Bax pathway. In addition, the phosphorylation of Akt and ERK1/2 is increased, indicating that PI3K/Akt and ERK1/2 signal transduction pathways may play an important role in the regulation of proliferation and apoptosis of HSCs.  相似文献   

17.
以生物菌肥拮抗细菌、解磷细菌、解钾细菌和黄绿木霉菌为实验材料,通过盆栽番茄试验,研究不同生物菌肥对土壤养分含量及土壤酶活性的影响。结果表明:添加黄绿木霉菌的处理,土壤养分含量均高于清水处理与化肥处理。跟踪测定番茄不同生长时期土壤中的脲酶、磷酸酶活性,结果表明:不同处理土壤中的脲酶与磷酸酶在番茄不同生长时期有相同的变化趋势,即由发芽期至开花期,酶活性逐渐增强,而后下降;而比较不同处理的酶活性,其中以解磷细菌、解钾细菌、拮抗细菌和黄绿木霉菌混合处理效果最为明显。所有使用生物菌肥的处理,脲酶与磷酸酶的活性均高于化肥处理与清水处理,其中混合处理比化肥处理在番茄不同生长时期的土壤脲酶活性均高出30 %,磷酸酶活性均高出27 %;但比较番茄收获后土壤过氧化氢酶与纤维素酶的活性,不同处理间差异不显著。  相似文献   

18.
AIM: To investigate the dynamic expression of phosphatase and tensin homolog deleted on chromosome ten (PTEN) in liver tissue in the process of hepatic fibrosis in rats. METHODS: The rat model of hepatic fibrosis used in this study was induced by common bile duct ligation (BDL). Hematoxylin and eosin (HE) and Masson’s trichrome staining were used for observing the histological changes in hepatic fibrosis tissue. At 4 time points, the expressions of PTEN protein and mRNA in hepatic tissues of rats were detected by immunohistochemical staining, Western blotting and real-time fluorescent quantitative PCR assay, respectively. RESULTS: The rat model of hepatic fibrosis was established successfully. With each consecutive week after BDL, increased fibrosis, degeneration and necrosis were found in rat liver cells. Not surprisingly, a disruption of normal architecture and a decrease in normal hepatic cells was concomitantly observed. The immunohistochemical staining indicated that there was extensive expression of PTEN in liver tissues of normal rats, it expressed mainly in the cytoplasm, and with the aggravation of hepatic fibrosis, the expression of PTEN in liver tissues decreased gradually (P<0.01). Western blotting and real-time fluorescent quantitative PCR at weekly time points (1, 2, 3, and 4 weeks) after BDL showed that, the expression of PTEN protein and mRNA in fibrotic rat liver tissue decreased gradually with increasing severity of hepatic fibrosis (P<0.01). Furthermore, all values from BDL rats were significantly lower than those from the sham operation group (P<0.01). CONCLUSION: The expressions of PTEN protein and mRNA in fibrotic liver tissue of rat decrease gradually with the progression of hepatic fibrosis, and increasing severity of fibrosis correlated well with decreasing PTEN expression.  相似文献   

19.
AIM:To explore the function of miR-21 in human glioma cells resistant to carmustine and to elucidate its related mechanism. METHODS:SWOZ2 cells were transfected with miR-21 mimics(SWOZ2-miR-21mimics) or miRNA mimics negative control(control group) by the method of jetPRIME. The real-time fluorescence quantitative PCR was used to detect and compare the levels of miR-21 expression between BCNU-resistant cell line SWOZ2-BCNU and BCNU-sensitive cell line SWOZ2, or between SWOZ2-miR-21 mimic group and control group. The drug sensitivity of these cells to BCNU was determined by CCK-8 assay. The protein expression of phosphatase and tensin homology deleted on chromosome 10(PTEN), phosphorylated protein kinase B(p-Akt) and P-glycoprotein(P-gp) in these cells were also detected by Western blotting. RESULTS:The expression level of miR-21 was remarkably higher in SWOZ2-BCNU cells than that in SWOZ2 cells. The expression level of miR-21 was significantly higher in SWOZ2-miR-21 mimics group than that in control group. The half-maximal inhibitory concentration(IC50) of BCNU was obviously higher for SWOZ2-BCNU cells than that for SWOZ2 cells. The IC50 of BCNU was markedly higher in SWOZ2-miR-21 mimics group than that in control group. PTEN protein expression was remarkably lower, but p-Akt and P-gp protein expression levels were markedly higher in SWOZ2-BCNU cells than those in SWOZ2 cells. The protein level of PTEN was significantly lower, but the protein levels of p-Akt or P-gp were distinctly higher in SWOZ2-miR-21 mimics group than those in control group. CONCLUSION:miR-21 enhances the resistance of human glioma cells to BCNU by down-regulating the expression of PTEN protein.  相似文献   

20.
采后低温诱导菠萝PPO活性升高的机理及其抑制途径   总被引:15,自引:0,他引:15  
周玉婵  潘小平 《园艺学报》1997,24(3):235-238
采后菠萝果实内的PPO(多酚氧化酶)活性和Pi(无机磷离子)浓度分布不均,二者密切相关。低温诱导显著提高了酸性磷酸酶的活性,使果实Pi明显升高。低温诱导减缓了磷脂酶D活性下降的速度,ABA处理可显著减缓低温对PPO的诱导,而CHI(环几亚酰胺)和乙醇也不同程度地抑制了PPO的升高,NaCl处理作用不明显  相似文献   

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