14 results on '"Lu, Mu-dan"'
Search Results
2. Sophoricoside attenuates lipopolysaccharide-induced acute lung injury by activating the AMPK/Nrf2 signaling axis.
- Author
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Wu YX, Zeng S, Wan BB, Wang YY, Sun HX, Liu G, Gao ZQ, Chen D, Chen YQ, Lu MD, and Pang QF
- Subjects
- AMP-Activated Protein Kinases metabolism, Acute Lung Injury chemically induced, Acute Lung Injury enzymology, Acute Lung Injury pathology, Animals, Cytokines metabolism, Disease Models, Animal, Inflammation Mediators metabolism, Lipopolysaccharides, Lung enzymology, Lung pathology, Macrophages enzymology, Macrophages pathology, Male, Mice, Mice, Inbred C57BL, Nitric Oxide metabolism, Nitric Oxide Synthase Type II metabolism, Pneumonia chemically induced, Pneumonia enzymology, Pneumonia pathology, RAW 264.7 Cells, Signal Transduction, Acute Lung Injury prevention & control, Anti-Inflammatory Agents pharmacology, Benzopyrans pharmacology, Lung drug effects, Macrophages drug effects, NF-E2-Related Factor 2 metabolism, Pneumonia prevention & control
- Abstract
Sophoricoside (SOP), an isoflavone glycoside isolated from seed of Sophora japonica L., has been reported to have various pharmacological activities, including anti-cancer, anti-allergy and anti-inflammation. However, the effect of SOP on lipopolysaccharides (LPS)-acute lung injury (ALI) is completely unclear. Here, we found that SOP pretreatment significantly ameliorated LPS-induced pathological damage, tissue permeability, neutrophil infiltration and the production of pro-inflammatory cytokines (TNF-α, IL-1β and IL-6) in a murine model of ALI. Besides, SOP reduced the production of pro-inflammatory mediators such as iNOS, NO and inflammatory cytokines including TNF-α, IL-1β and IL-6 in LPS-stimulated RAW264.7 cells and bone marrow derived macrophages. Interestingly, treatment with SOP exhibited no effect on the activation of NF-κB and MAPKs in macrophages but prominently accelerated the expression and nuclear translocation of Nrf2. By using ML385, a specific Nrf2 inhibitor, we found that inhibition of Nrf2 abolished the inhibitory effect of SOP on LPS-induced iNOS expression, NO production as well as pro-inflammatory cytokine generation. SOP also activated AMPK, an upstream protein of Nrf2, under LPS stimuli. Furthermore, we demonstrated that the accelerated expression of Nrf2 induced by SOP was reversed by interference with the AMPK inhibitor Compound C. Taken together, our results suggested that SOP attenuated LPS-induced ALI in AMPK/Nrf2 dependent manner and indicated that SOP might be a potential therapeutic candidate for treating ALI/ARDS., (Copyright © 2020 Elsevier B.V. All rights reserved.)
- Published
- 2021
- Full Text
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3. Nrf2 protects against seawater drowning-induced acute lung injury via inhibiting ferroptosis.
- Author
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Qiu YB, Wan BB, Liu G, Wu YX, Chen D, Lu MD, Chen JL, Yu RQ, Chen DZ, and Pang QF
- Subjects
- Acute Lung Injury etiology, Acute Lung Injury prevention & control, Animals, Cell Line, Drowning etiology, Drowning prevention & control, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Respiratory Mucosa metabolism, Acute Lung Injury metabolism, Drowning metabolism, Ferroptosis physiology, NF-E2-Related Factor 2 metabolism, Seawater adverse effects
- Abstract
Background: Ferroptosis is a new type of nonapoptotic cell death model that was closely related to reactive oxygen species (ROS) accumulation. Seawater drowning-induced acute lung injury (ALI) which is caused by severe oxidative stress injury, has been a major cause of accidental death worldwide. The latest evidences indicate nuclear factor (erythroid-derived 2)-like 2 (Nrf2) suppress ferroptosis and maintain cellular redox balance. Here, we test the hypothesis that activation of Nrf2 pathway attenuates seawater drowning-induced ALI via inhibiting ferroptosis., Methods: we performed studies using Nrf2-specific agonist (dimethyl fumarate), Nrf2 inhibitor (ML385), Nrf2-knockout mice and ferroptosis inhibitor (Ferrostatin-1) to investigate the potential roles of Nrf2 on seawater drowning-induced ALI and the underlying mechanisms., Results: Our data shows that Nrf2 activator dimethyl fumarate could increase cell viability, reduced the levels of intracellular ROS and lipid ROS, prevented glutathione depletion and lipid peroxide accumulation, increased FTH1 and GPX4 mRNA expression, and maintained mitochondrial membrane potential in MLE-12 cells. However, ML385 promoted cell death and lipid ROS production in MLE-12 cells. Furthermore, the lung injury became more aggravated in the Nrf2-knockout mice than that in WT mice after seawater drowning., Conclusions: These results suggested that Nrf2 can inhibit ferroptosis and therefore alleviate ALI induced by seawater drowning. The effectiveness of ferroptosis inhibition by Nrf2 provides a novel therapeutic target for seawater drowning-induced ALI.
- Published
- 2020
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4. Hyperoside suppresses hypoxia-induced A549 survival and proliferation through ferrous accumulation via AMPK/HO-1 axis.
- Author
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Chen D, Wu YX, Qiu YB, Wan BB, Liu G, Chen JL, Lu MD, and Pang QF
- Subjects
- A549 Cells, Antineoplastic Agents, Phytogenic pharmacology, Cell Line, Tumor, Cell Proliferation drug effects, Cell Survival drug effects, Dose-Response Relationship, Drug, Heme Oxygenase-1 antagonists & inhibitors, Humans, Iron metabolism, Phosphorylation drug effects, Protoporphyrins pharmacology, Quercetin administration & dosage, Quercetin pharmacology, AMP-Activated Protein Kinases metabolism, Heme Oxygenase-1 metabolism, Quercetin analogs & derivatives, Tumor Hypoxia drug effects
- Abstract
Background: Hypoxia is commonly existed in tumors and lead to cancer cell chemo/radio-resistance. It is well-recognized that tumor hypoxia is a major challenge for the treatment of various solid tumors. Hyperoside (quercetin-3-O-galactoside, Hy) possesses antioxidant effects and has been reported to protect against hypoxia/reoxygenation induced injury in cardiomyocytes. Therefore, Hy may be attractive compound applicable to hypoxia-related diseases., Purpose: This study was designed to determine the role of Hy in hypoxia-induced proliferation of non-small cell lung cancer cells and the underlying mechanism., Study Design and Methods: A549, a human non-small cell lung cancer (NSCLC) cell line, was used in the present study. 1% O
2 was used to mimic the in vivo hypoxic condition of NSCLC. The potential mechanisms of Hy on hypoxia-induced A549 survival and proliferation, as well as the involvement of AMPK/HO-1 pathway were studied via CCK-8 assay, EdU staining, flow cytometry, qRT-PCR and western blot., Results: We showed that pretreatment with Hy suppressed hypoxia-induced A549 survival and proliferation in dose-dependent manner. In terms of mechanism, hypoxia-treated A549 showed the lower AMPK phosphorylation and the reduced HO-1 expression, which were reversed by Hy pretreatment. Both AMPK inhibitor (Compound C) and HO-1 activity inhibitor (Zinc protoporphyrin IX) abolished Hy-evoked A549 cell death under hypoxia stimuli. Of note, Ferrous iron contributed to Hy-induced A549 cell death under hypoxia, while Hy had no effect on lipid peroxidation under hypoxia., Conclusion: Taken together, our results highlighted the beneficial role of Hy against hypoxia-induced A549 survival and proliferation through ferrous accumulation via AMPK/HO-1 axis., Competing Interests: Conflict of Interest The authors have no conflicts of interest to report., (Copyright © 2019 Elsevier GmbH. All rights reserved.)- Published
- 2020
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5. ERK1/2-HNF4α axis is involved in epigallocatechin-3-gallate inhibition of HBV replication.
- Author
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Wang ZY, Li YQ, Guo ZW, Zhou XH, Lu MD, Xue TC, and Gao B
- Subjects
- Animals, Antiviral Agents administration & dosage, Antiviral Agents pharmacology, Catechin administration & dosage, Catechin pharmacology, Disease Models, Animal, Dose-Response Relationship, Drug, Gene Expression Regulation, Viral drug effects, Hep G2 Cells, Hepatitis B genetics, Hepatitis B virology, Hepatocyte Nuclear Factor 4 genetics, Hepatocyte Nuclear Factor 4 metabolism, Humans, Mice, Mice, Inbred C57BL, Mitogen-Activated Protein Kinase 1 metabolism, Mitogen-Activated Protein Kinase 3 metabolism, Catechin analogs & derivatives, Hepatitis B drug therapy, Hepatitis B virus drug effects, Virus Replication drug effects
- Abstract
Epigallocatechin gallate (EGCG), a major polyphenol in green tea, exhibits diverse biological activities. Previous studies show that EGCG could effectively suppress HBV gene expression and replication, but the role of EGCG in HBV replication and its underlying mechanisms, especially the signaling pathways involved, remain unclear. In this study we investigated the mechanisms underlying EGCG inhibition on HBV replication with a focus on the signaling pathways. We showed that EGCG (12.5-50 μM) dose-dependently inhibited HBV gene expression and replication in HepG2.2.15 cells. Similar results were observed in HBV mice receiving EGCG (25 mg· kg
-1 · d-1 , ip) for 5 days. In HepG2.2.15 cells, we showed that EGCG (12.5-50 μM) significantly activate ERK1/2 MAPK signaling, slightly activate p38 MAPK and JAK2/STAT3 signaling, while had no significant effect on the activation of JNK MAPK, PI3K/AKT/mTOR and NF-κB signaling. By using specific inhibitors of these signaling pathways, we demonstrated that ERK1/2 signaling pathway, but not other signaling pathways, was involved in EGCG-mediated inhibition of HBV transcription and replication. Furthermore, we showed that EGCG treatment dose-dependently decreased the expression of hepatocyte nuclear factor 4α (HNF4α) both at the mRNA and protein levels, which could be reversed by pretreatment with the ERK1/2 inhibitor PD98059 (20 μM). Moreover, we revealed that EGCG treatment dose-dependently inhibited the activity of HBV core promoter and the following HBV replication. In summary, our results demonstrate that EGCG inhibits HBV gene expression and replication, which involves ERK1/2-mediated downregulation of HNF4α.These data reveal a novel mechanism for EGCG to inhibit HBV gene expression and replication.- Published
- 2020
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6. Curcumin ameliorates hepatic chronic inflammation induced by bile duct obstruction in mice through the activation of heme oxygenase-1.
- Author
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Chen D, Wu C, Qiu YB, Chu Q, Sun XQ, Wang X, Chen JL, Lu MD, Chen DZ, and Pang QF
- Subjects
- Animals, Anti-Inflammatory Agents, Non-Steroidal therapeutic use, Bile Ducts surgery, Cholestasis immunology, Curcumin therapeutic use, Disease Models, Animal, Heme Oxygenase-1 antagonists & inhibitors, Heme Oxygenase-1 immunology, Heme Oxygenase-1 metabolism, Hepatitis, Chronic immunology, Hepatitis, Chronic pathology, Humans, Ligation, Lipid Metabolism drug effects, Lipid Metabolism immunology, Liver drug effects, Liver immunology, Liver pathology, Male, Membrane Proteins antagonists & inhibitors, Membrane Proteins immunology, Membrane Proteins metabolism, Mice, Protoporphyrins administration & dosage, Anti-Inflammatory Agents, Non-Steroidal pharmacology, Cholestasis complications, Curcumin pharmacology, Hepatitis, Chronic drug therapy, Membrane Proteins agonists
- Published
- 2020
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7. Explore the dynamic alternation of gene PLAC4 mRNA expression levels in maternal plasma in second trimester for nonivasive detection of trisomy 21.
- Author
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Yang L, Sun HY, Chen DZ, Lu MD, Tang Y, and Xiao JP
- Abstract
Objective: Noninvasive prenatal detection of trisomy 21 (T21) has been achieved by measuring the ratio of two alleles of a single nucleotide polymorphism in circulating placenta specific 4 (PLAC4) mRNA in maternal plasma with a few assays in recent years. Our research is to explore the variations of PLAC4 mRNA expression level in maternal plasma with normal pregnancies in second trimester, which can provide pregnant women deeper insights with suitable detection period for the non-invasive prenatal detection of T21., Methods: We measured a serial plasma PLAC4 mRNA concentrations weekly from the same 25 singleton normal pregnant women. We recruited maternal plasma samples from 45 singleton pregnant women, comprising of 25 euploid pregnancies (control group; range, 17 to 21 weeks) and 20 T21 pregnancies (T21 group; range, 19 to 24 weeks). With the application of reverse transcription polymerase chain reaction, we achieved an insight of PLAC4 mRNA expression levels in maternal plasma during second trimester with euploid pregnancies., Results: Among the control group, the levels of PLAC4 mRNA expression in the gestation of 17 to 18 weeks were significantly less than those in the gestation of 18 to 21 weeks (P<0.05). The average PLAC4 mRNA concentration of the normal pregnant women was not higher than that of the T21 group (P>0.05)., Conclusion: The PLAC4 mRNA showed a higher level of expression in the gestation of 18 to 21 weeks with an euploid pregnancy of pregnant women. We also found that there was no significant difference in plasma PLAC4 mRNA concentration between the normal and the T21 pregnancies in second trimester.
- Published
- 2015
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8. A multifactorial analysis of the pregnancy outcomes in cytomegalovirus-infected women.
- Author
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Ding ZY, Xu F, Chen DZ, Meng XN, Xu TS, Lu MD, and Zhuge HX
- Subjects
- Adult, Comorbidity, Cytomegalovirus Infections epidemiology, Female, Genotype, Humans, NF-KappaB Inhibitor alpha, Polymorphism, Genetic, Pregnancy, Pregnancy Complications, Infectious epidemiology, Young Adult, Cytomegalovirus genetics, Cytomegalovirus Infections virology, I-kappa B Proteins genetics, NF-kappa B p50 Subunit genetics, Pregnancy Complications, Infectious virology, Pregnancy Outcome epidemiology, Viral Envelope Proteins genetics, Viral Load statistics & numerical data
- Abstract
Aims: To investigate the impacts of cytomegalovirus (CMV) viral load, TORCH (toxoplasmosis, others, rubella, CMV and herpes) coinfections, CMV glycoprotein B (gB) genotypes and maternal genetic polymorphisms on pregnancy outcomes among CMV-infected women., Methods: A total of 731 CMV-infected pregnant women (634 and 97 with normal and adverse pregnancy outcomes, respectively) were recruited. CMV load quantification and screening of TORCH coinfections were performed by using real-time polymerase chain reaction (PCR) and immunodetection techniques, respectively. Genotyping of CMV gB and maternal NFKB1 -94 ins/del, NFKBIA -826C/T and -881A/G polymorphisms was performed by using PCR-restriction fragment length polymorphism., Results: We found that the mean CMV viral load in women with adverse pregnancy outcomes was significantly higher than that in women with normal outcomes at all pregnancy stages (p < 0.01). We also found that TORCH coinfections resulted in a 1.65-fold (95% CI = 1.00-2.73) increase in the risk of adverse pregnancy outcomes (p = 0.05). Additionally, we noticed no significant difference in the distribution of CMV gB genotypes between women with normal and adverse pregnancy outcomes (p = 0.42). We also observed that the ins/ins variant genotype of the NFKB1 polymorphism could reduce the risk of adverse pregnancy outcomes (OR = 0.38, 95% CI = 0.15-0.98; p = 0.04)., Conclusion: CMV viral load, TORCH coinfections and maternal NFKB1 polymorphism could influence pregnancy outcomes among CMV-infected women., (© 2015 S. Karger AG, Basel.)
- Published
- 2015
- Full Text
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9. JAB1 and phospho-Ser10 p27 expression profile determine human hepatocellular carcinoma prognosis.
- Author
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Wang Y, Yu YN, Song S, Li TJ, Xiang JY, Zhang H, Lu MD, Ji F, and Hu LQ
- Subjects
- Adult, Aged, Blotting, Western, COP9 Signalosome Complex, Carcinoma, Hepatocellular diagnosis, Carcinoma, Hepatocellular mortality, Case-Control Studies, Cyclin-Dependent Kinase Inhibitor p27 genetics, Female, Follow-Up Studies, Humans, Immunoenzyme Techniques, Immunoprecipitation, Liver Neoplasms diagnosis, Liver Neoplasms mortality, Lymphatic Metastasis, Male, Middle Aged, Mutagenesis, Site-Directed, Mutation genetics, Neoplasm Grading, Neoplasm Invasiveness, Neoplasm Recurrence, Local metabolism, Neoplasm Recurrence, Local mortality, Neoplasm Recurrence, Local pathology, Neoplasm Staging, Phosphorylation, Prognosis, Survival Rate, Tumor Cells, Cultured, alpha-Fetoproteins metabolism, Carcinoma, Hepatocellular metabolism, Cyclin-Dependent Kinase Inhibitor p27 metabolism, Intracellular Signaling Peptides and Proteins metabolism, Liver Neoplasms metabolism, Peptide Hydrolases metabolism
- Abstract
Purpose: To elucidate the clinicopathological significance and the role of Jun Activation Domain-Binding Protein 1 (JAB1), Ser10-phosphorylated p27 (p27S10), and total p27 in human hepatocellular carcinoma (HCC) prognosis., Methods: We evaluated the expression of JAB1 and p27S10 in tissues by immunohistochemical and immunoblot analyses. p27 Ser10 phosphorylation and Ser10 phosphorylation-dependent p27-JAB1 interaction were demonstrated in proliferating Huh7 cells following transfection of pEGFP-p27WT/p27S10A/p27S10D plasmids and pcDNA3.1-p27WT/p27S10A/p27S10D-Myc plasmids. Univariate and multivariate analysis were used to determine their role in HCC prognosis., Results: JAB1 and p27S10 are overexpressed in HCC samples compared with paired normal tissues. There was a strong correlation between JAB1 and p27S10 expression (P < 0.001), and expression of both inversely correlated with total p27 levels (P < 0.001). High JAB1 and p27S10 expression correlated with histological grade, vascular invasion, and serum α-fetoprotein (AFP) level (all P < 0.01). Total p27 expression also correlated with histological tumor grade (P = 0.048) and AFP level (P = 0.015). The p27S10(high)/JAB1(high)/p27(1ow) profile was the most reliable indication of poor prognostic. Ser10 phosphorylation increased and total p27 levels decreased in a time-dependent manner in serum-starved Huh7 cells following addition of serum. Immunoprecipitation analysis revealed that p27 Ser-to-Asp substitution at position 10 (S10D) markedly enhanced the interaction between JAB1 and p27, but replacement of S10A reduced binding., Conclusions: This study revealed that combined JAB1, p27S10, and total p27 expression may serve as a prognostic marker for HCC.
- Published
- 2014
- Full Text
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10. [Expression and significance of c-jun-activation-domain binding protein (JAB1) in hepatocellular carcinoma].
- Author
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Qin J, Wang ZW, Ni QC, Wang Y, Chen L, Lu MD, and Shen AG
- Subjects
- Adult, Aged, COP9 Signalosome Complex, Carcinoma, Hepatocellular pathology, Female, Gene Expression, Humans, Immunohistochemistry, Intracellular Signaling Peptides and Proteins, Ki-67 Antigen biosynthesis, Liver Neoplasms pathology, Male, Middle Aged, Carcinoma, Hepatocellular metabolism, Liver Neoplasms metabolism, Peptide Hydrolases biosynthesis
- Abstract
Objective: to investigate the expression of c-jun-activation-domain binding protein (JAB1) in hepatocellular carcinoma (HCC) and the clinicopathologic significance thereof., Methods: Immunohistochemistry was used on 76 specimens of HCC tissues and native liver tissues adjacent to the HCC tissues, and 10 specimens of normal liver tissues near the liver angioma to detect the expression of JAB1 and the cell proliferative factor Ki67., Results: The expression rate of JAB1 in the HHC tissues was 68.85%, significantly higher than that in the adjacent liver tissues and normal liver tissues near liver angioma (38.72% and 34.36% respectively, both P < 0.001). The expression of JAB1 was correlated with the histological differentiation, serum alpha-fetoprotein level, and metastasis (P = 0.000, 0.015, and 0.000), but not with gender, age, tumor size, serum HBsAg, and existence of necrosis and cirrhosis. The expression rate of Ki67 protein in the HCC tissues was 41.45%, significantly higher than that in the adjacent liver tissues and normal liver tissues near liver angioma (2.11% and 2.01% respectively, both P < 0.001). There was a positive correlation between JAB1 and Ki67 (P < 0.001)., Conclusion: JAB1 is highly expressed in HCC and may play an important role in the oncogenesis and development of HCC. JAB1 may be used as a marker for neoplastic change in liver cells and thus has potential clinicopathologic value.
- Published
- 2008
11. [Growth inhibition of human leukemia cell line U937 by all-trans retinoic acid and its mechanism].
- Author
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Zhao YM, Wang YC, Lu MD, Shen AG, Zhang DM, Lu JX, and Cheng C
- Subjects
- Cell Cycle drug effects, Cyclin-Dependent Kinase Inhibitor p27 metabolism, Humans, S-Phase Kinase-Associated Proteins metabolism, U937 Cells, Cell Proliferation drug effects, Tretinoin pharmacology
- Abstract
Objective: To study the effect of all-trans retinoic acid (ATRA) on U937 cell growth and its mechanism., Methods: Cell cycle was detected by flow cytometry (FCM), expressions of cell cycle associated protein and the p27 related protein were detected by Western blot. The binding of P27 and Skp2 was detected by immunoprecipitation., Results: FCM displayed that ATRA could inhibit the proliferation of U937 cells. At 72 h on 1 micromol/L ATRA treatment, 72% of the cells were arrested at G0/G1 phase. Western blot displayed that ATRA could decrease the expression of cyclin A, up-regulate the expression of p21 and p27, and down-regulate the expression of p27 related proteins Skp2. p27 could bind with Skp2 in U937 cells as detected by immunoprecipitation., Conclusion: ATRA may arrest the proliferation of U937 cells through the reduction of Skp2 expression, and finally the induction of the accumulation of p27.
- Published
- 2008
12. [Expressions of Thr187 phosphorylated p27(kip1) and Skp2 proteins in human hepatocellular carcinomas and their significances].
- Author
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Wang Y, Chen L, Lu MD, Li P, Cui XP, Qin J, and Shen AG
- Subjects
- Carcinoma, Hepatocellular pathology, Humans, Liver Neoplasms pathology, Neoplasm Staging, Phosphorylation, Carcinoma, Hepatocellular metabolism, Cyclin-Dependent Kinase Inhibitor p27 metabolism, Liver Neoplasms metabolism, S-Phase Kinase-Associated Proteins metabolism
- Published
- 2007
13. [Inhibitory effect of arsenic trioxide on proliferation of human hepatocellular carcinoma cell line SMMC-7721 and the mechanism].
- Author
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Cui XP, Wang Y, Lu MD, Li P, and Shen AG
- Subjects
- Antineoplastic Agents pharmacology, Arsenic Trioxide, COP9 Signalosome Complex, Carcinoma, Hepatocellular metabolism, Carcinoma, Hepatocellular pathology, Cell Line, Tumor, Cell Nucleus metabolism, Cytoplasm metabolism, Humans, Liver Neoplasms metabolism, Arsenicals pharmacology, Cell Proliferation drug effects, Cyclin-Dependent Kinase Inhibitor p27 metabolism, Intracellular Signaling Peptides and Proteins metabolism, Liver Neoplasms pathology, Oxides pharmacology, Peptide Hydrolases metabolism
- Abstract
Background & Objective: Arsenic trioxide (As(2)O(3)) is a new drug used to treat solid tumors. However, the mechanism is still unclear. This study was to investigate the effects of As(2)O(3) on the proliferation of human hepatocellular carcinoma (HCC) cell line SMMC-7721, and to explore the mechanisms., Methods: When treated with 0-8 micromol/L As(2)O(3) for 96 h, the survival rate of SMMC-7721 cells was determined by WST-8 assay. When treated with 2 micromol/L As(2)O(3) for 72 h, the expression of P27(kip1) and c-Jun activation domain-binding protein 1 (JAB1) in SMMC-7721 cells were detected at different time points by Western blot, the subcellular localization of P27(kip1) and JAB1 was detected by subcellular fractionation and immunofluorescent staining., Results: As(2)O(3) significantly inhibited the proliferation of SMMC-7721 cells. The 50% inhibition concentration (IC50) of As(2)O(3) to SMMC-7721 cells was (1.81+/-0.41) micromol/L at 96 h. When SMMC-7721 cells were treated with 2 mumol/L As(2)O(3) for 12 h, the expression of JAB1 was down-regulated and that of P27kip1 was up-regulated. Furthermore, P27(kip1) and JAB1 proteins were translocated from the cytoplasm into nuclei when cells were exposed to 2 micromol/L As(2)O(3) for 12 h and 24 h, respectively. The nuclear accumulation of both proteins was also observed under fluorescence microscope after treatment of 2 micromol/L As(2)O(3)., Conclusion: As(2)O(3) attenuates JAB1 expression, thereby disturbs the location and expression of P27(kip1), and may participate in regulating the proliferation of SMMC-7721 cells through interfering with the function of P27(kip1).
- Published
- 2007
14. [Expression and significance of Ser10 phosphorylated p27(kip1) and JAB1 protein in human hepatocellular carcinoma].
- Author
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Lu MD, Wang Y, Chen L, Qin J, Li P, Cui XP, and Shen AG
- Subjects
- COP9 Signalosome Complex, Carcinoma, Hepatocellular metabolism, Cyclin-Dependent Kinase Inhibitor p27 chemistry, Electrophoresis, Polyacrylamide Gel, Humans, Intracellular Signaling Peptides and Proteins chemistry, Peptide Hydrolases chemistry, Phosphorylation, Carcinoma, Hepatocellular genetics, Cyclin-Dependent Kinase Inhibitor p27 genetics, Cyclin-Dependent Kinase Inhibitor p27 metabolism, Gene Expression Regulation, Neoplastic, Intracellular Signaling Peptides and Proteins genetics, Intracellular Signaling Peptides and Proteins metabolism, Peptide Hydrolases genetics, Peptide Hydrolases metabolism, Phosphoserine metabolism
- Published
- 2007
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