Publications (17)74.5 Total impact
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Article: Gankyrin gene deletion followed by proteomic analysis: insight into the roles of Gankyrin in Tumorigenesis and Metastasis.
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ABSTRACT: Gankyrin was originally purified and characterized as the p28 component of the 26S proteasome, and later identified as an oncogenic protein in hepatocellular carcinomas (HCC). It has recently been found to be highly expressed in several other malignancies, and compelling evidence show gankyrin plays important roles in tumorigenesis. However, its mechanism of action remains unclear. In order to further clarify the functions of gankyrin and better understand its molecular mechanisms, we generated a gankyrin null cell line, HCT116 gankyrin-/- , by targeted homologous recombination in human colon cancer cells, and then employed two-dimensional electrophoresis (2-DE) based proteomic approaches followed by MS identification to investigate alterations in the proteome due to the gankyrin knockout. Western blot and qRT-PCR assays were also used to examine the protein and mRNA levels of some identified proteins. Compared with wild-type control cells, gankyrin null cells were impaired in terms of their proliferation, migration and anchorage-independent growth. A total of 21 altered proteins were identified, which included 18 proteins that had not previously been reported to be related to gankyrin. Notably, eight metastasis-related proteins were identified. Western blot analyses confirmed that the changes in three examined proteins were consistent with 2-DE gel analysis. In summary, we have generated a useful cell tool to clarify the functions of gankyrin. Our proteomic data provide novel information to better understand the roles and underlying mechanisms by which gankyrin is involved in tumorigenesis and cancer metastasis.BMC Medical Genomics 08/2012; 5:36. · 3.69 Impact Factor -
Article: Comparative autoantibody profiling before and after appearance of malignance: identification of anti-cathepsin D autoantibody as a promising diagnostic marker for lung cancer.
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ABSTRACT: Cancer patients frequently develop autoantibodies. To test the hypothesis that the appearance of autoantibodies precedes the clinical diagnosis of cancer, we applied an immunoproteomic approach to compare autoantibody profiles before and after appearance of malignances. Proteins from A549 cells, a lung adenocarcinoma cell line, were separated by two dimensional electrophoresis and then immunoblotted with serum samples from 8 individuals who were eventually diagnosed with lung cancer. Compared with autoantibody profiles from 3 years prior to the appearance of malignances, 21 immunoreactive spots newly appeared or presented with stronger staining intensity when clinical diagnoses were made. Among them, 10 matched spots on 2-DE gels were identified by mass spectrometry analysis as 5 proteins. With immunoprecipitation analysis, the antigenicity of protein cathepsin D was confirmed, and notably, in lung cancer sera, the occurrences of autoantibodies against the specific forms of cathepsin D differed significantly from the control groups (p<0.05). Our findings suggest that harnessing immunity may have utility for early cancer marker discovery, and that comparing autoantibodies to specific forms of cathepsin D may be a promising early marker of lung cancer.Biochemical and Biophysical Research Communications 01/2012; 420(4):704-9. · 2.48 Impact Factor -
Article: CUEDC2 (CUE domain-containing 2) and SOCS3 (suppressors of cytokine signaling 3) cooperate to negatively regulate Janus kinase 1/signal transducers and activators of transcription 3 signaling.
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ABSTRACT: Janus kinase 1/signal transducers and activators of transcription 3 (JAK1/STAT3) pathway is one of the recognized oncogenic signaling pathways that frequently overactivated in a variety of human tumors. Despite rapid progress in elucidating the molecular mechanisms of activation of JAK/STAT pathway, the processes that regulate JAK/STAT deactivation need to be further clarified. Here we demonstrate that CUE domain-containing 2 (CUEDC2) inhibits cytokine-induced phosphorylation of JAK1 and STAT3 and the subsequent STAT3 transcriptional activity. Further analysis by a yeast two-hybrid assay showed that CUEDC2 could engage in a specific interaction with a key JAK/STAT inhibitor, SOCS3 (suppressors of cytokine signaling 3). The interaction between CUEDC2 and SOCS3 is required for the inhibitory effect of CUEDC2 on JAK1 and STAT3 activity. Additionally, we found CUEDC2 functions collaboratively with SOCS3 to inhibit JAK1/STAT3 signaling by increasing SOCS3 stability via enhancing its association with Elongin C. Therefore, our findings revealed a new biological activity for CUEDC2 as the regulator of JAK1/STAT3 signaling and paved the way to a better understanding of the mechanisms by which SOCS3 has been linked to suppression of the JAK/STAT pathway.Journal of Biological Chemistry 11/2011; 287(1):382-92. · 4.77 Impact Factor -
Article: Detection of D-3-phosphoglycerate dehydrogenase autoantibodies in patients with autoimmune hepatitis: Clinical significance evaluation.
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ABSTRACT: Aim: D-3-phosphoglycerate dehydrogenase (3-PHGDH) was identified as a putative target of autoantibodies in autoimmune hepatitis (AIH). The aims of the present study were to detect anti-3-PHGDH in patients with AIH and other chronic liver diseases and to analyze their clinical relevance. Methods: Human 3-PHGDH gene was cloned and expressed in Escherichia coli and used in enzyme-linked immunosorbent assays and Western blots. Serum from patients with AIH (n = 101), primary biliary cirrhosis (PBC, n = 122), chronic hepatitis C (CHC, n = 117), chronic hepatitis B (CHB, n = 112), and from patients with other autoimmune disease (n = 125) were investigated. Results: The highest incidence and activity of anti-PHGDH was observed in AIH patients. Thirty-two of 40 untreated (80%) and 37 of 61 AIH patients treated with corticosteroid (60.7%) were positive. Antibody titers decreased significantly during corticosteroid treatment. 15.8% of PBC patients, 9.8% of CHB and 12.8% of CHC patients, were anti-PHGDH-positive, with less than 12% of patients positive with other autoimmune diseases via reactions with recombinant 3-PHGDH protein. Conclusion: Anti-PHGDH were detected in chronic liver diseases. They occur predominantly in AIH, and corticosteroid treatment seems to decrease antibody titers. Whether the antibodies are primary or secondary phenomena and whether they are related to the etiology or pathogenesis, at least in a subgroup of patients with chronic liver diseases, has still to be evaluated.Hepatology Research 06/2011; 41(9):867-76. · 2.20 Impact Factor -
Article: Cdk1-phosphorylated CUEDC2 promotes spindle checkpoint inactivation and chromosomal instability.
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ABSTRACT: Aneuploidy and chromosomal instability are major characteristics of human cancer. These abnormalities can result from defects in the spindle assembly checkpoint (SAC), which is a surveillance mechanism for accurate chromosome segregation through restraint of the activity of the anaphase-promoting complex/cyclosome (APC/C). Here, we show that a CUE-domain-containing protein, CUEDC2, is a cell-cycle regulator that promotes spindle checkpoint inactivation and releases APC/C from checkpoint inhibition. CUEDC2 is phosphorylated by Cdk1 during mitosis. Depletion of CUEDC2 causes a checkpoint-dependent delay of the metaphase-anaphase transition. Phosphorylated CUEDC2 binds to Cdc20, an activator of APC/C, and promotes the release of Mad2 from APC/C-Cdc20 and subsequent APC/C activation. CUEDC2 overexpression causes earlier activation of APC/C, leading to chromosome missegregation and aneuploidy. Interestingly, CUEDC2 is highly expressed in many types of tumours. These results suggest that CUEDC2 is a key regulator of mitosis progression, and that CUEDC2 dysregulation might contribute to tumour development by causing chromosomal instability.Nature Cell Biology 01/2011; 13(8):924-33. · 19.49 Impact Factor -
Article: The β2-adrenergic receptor and Her2 comprise a positive feedback loop in human breast cancer cells.
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ABSTRACT: In this study, β2-AR level was found to be up-regulated in MCF-7 cells overexpressing Her2 (MCF-7/Her2). Correlation of β2-AR level with Her2 status was demonstrated in breast cancer tissue samples. Constitutive phosphorylation of ERK, mRNA expression up-regulation of catecholamine-synthesis enzymes, and increased epinephrine release were detected in MCF-7/Her2 cells. β2-AR expression induced by epinephrine and involvement of ERK signaling were validated. The data indicate that Her2 overexpression and excessive phosphorylation of ERK cause epinephrine autocrine release from breast cancer cells, resulting in up-regulation of β2-AR expression. The data also showed that catecholamine prominently stimulated Her2 mRNA expression and promoter activity. The activation and nuclear translocation of STAT3 triggered by isoproterenol were observed. Enhanced binding activities of STAT3 to the Her2 promoter after isoproterenol stimulation were verified. Using STAT3 shRNA and dominant negative STAT3 mutant, the role of STAT3 in isoproterenol-induced Her2 expression was further confirmed. The data support a model where β2-AR and Her2 comprise a positive feedback loop in human breast cancer cells.Breast Cancer Research and Treatment 03/2010; 125(2):351-62. · 4.43 Impact Factor -
Article: [Cloning and expression of 3-phosphoglycerate dehydrogenase gene and its correlative antibodies in diagnosis of autoimmune hepatitis].
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ABSTRACT: To evaluate whether the D-3-phosphoglycerate dehydrogenase (Phgdh) correlative antibodies is crucial for AIH, we cloned Phgdh cDNA and constructed plasmid, then purified and identified the immunoreactivity of the recombinant protein, and established the enzyme linked immunosorbent assay (ELISA) to detect Phgdh autoantigen correlative antibodies in diagnosis of autoimmune hepatitis. The constructed plasmid was transformed into E. coli. BL21(D3). This fusion protein was purified by Ni-NTA chromatography and its immunoreactivity was identified by SDS-PAGE and Western blot. The ELISA with the fusion protein was established first, then, the Phgdh autoantigen correlative antibodies in serum of patients with AIH (65) and patients with PBC (122) as well as chronic hepatitis B (CHB) (56), chronic hepatitis C (CHC) (117), and normal controls (60) were detected. The sequence of Phgdh autoantigen gene was the same as the sequence reported on the genebank. The fusion protein was found about 60kD strip on SDS-PAGE. Western blot analysis showed that the fusion protein had immunoreactivity. When analyzing the serum by ELISA, the immune reactivity to Phgdh was detected in 66.15% of patients with AIH, 21.42% of patients with PBC, 12.50% of patients with CHB, 6.83% of patients with CHC, and 3.30% of normal individuals. The differences of prevalence between AIH patients and healthy controls as well as other diseases were of statistical significance (P less than 0.01). The Phgdh cDNA is successfully cloned into E. coli BL21 (D3). The frequency of antibodies to Phgdh is much higher in patients with AIH than in patients with PBC, CHB, CHC and normal control. The antibodies to Phgdh may have utility in improved diagnosis of AIH.Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology 06/2009; 17(5):378-82. -
Article: Autoantibody profiling of Chinese patients with autoimmune hepatitis using immunoproteomic analysis.
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ABSTRACT: In the present study, immunoproteomic analysis was utilized to systemically characterize global autoantibody profiles in autoimmune hepatitis (AIH). Sera from 21 patients with AIH and 15 healthy controls were analyzed for the antibody reactivity against the protein antigens of HepG2, a human hepatoma cell line. The lysates of HepG2 cells were separated by two-dimensional electrophoresis and then immunoblotted with each serum sample. Matrix-assisted laser desorption/ionization mass spectrometry or/and nanoelectrospray ionization MS/MS were then used to identify antigens, among which a bifunctional enzyme in mitochondrial, fumarate hydratase (FH), was further analyzed by ELISA using recombinant FH as a coating antigen. A total of 18 immunoreactive spots were identified as 13 proteins, 8 of which have not been reported in AIH. Immune reactivity to FH was detected in 66.67% of patients with AIH, 19.35% of patients with primary biliary cirrhosis (PBC), 12.31% of patients with chronic hepatitis B (CHB), 6.35% of patients with chronic hepatitis C (CHC), 11.32% of patients with systemic lupus erythematosus (SLE), and 3.57% of normal individuals. The differences of prevalence between AIH patients and healthy controls as well as other diseases were of statistical significance (P<0.001). These data demonstrate the serological heterogeneity in AIH and suggest the diversity of the mechanisms underlying AIH. FH, recognized mainly in AIH rather than in viral hepatitis and other autoimmune diseases, may have utility in improved diagnosis of AIH.Journal of Proteome Research 05/2008; 7(5):1963-70. · 5.11 Impact Factor -
Article: Serum proteomic-based analysis for the identification of a potential serological marker for autoimmune hepatitis.
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ABSTRACT: In the present study, by using a serologic proteomic analysis, we identified phosphoglycerate mutase isozyme B (PGAM-B) as a putative target of autoantibodies in autoimmune hepatitis (AIH). To evaluate whether the identified autoantigen is crucial for AIH, we cloned PGAM-B cDNA and expressed the recombinant protein in Escherichia coli. The soluble PGAM-B was purified by affinity chromatography and used as a coating antigen to determine the frequency of the PGAM-B-autoantibodies (PGAM-B-Abs) in patients with AIH and primary biliary cirrhosis (PBC) as well as chronic hepatitis B (CHB), chronic hepatitis C (CHC), and healthy donors by ELISA. Our study showed that the autoantibody to PGAM-B was predominantly present in AIH patients and 70.04% (50/71) of the tested AIH sera reacted to PGAM-B. The frequency of autoantibodies to PGAM-B is much higher in patients with AIH than in patients with PBC, CHB, CHC, and normal control. The data were further confirmed by using 1-DE Western blot analysis. Our study presents the first description of this protein as a candidate of diagnostic marker for AIH.Biochemical and Biophysical Research Communications 04/2008; 367(2):284-90. · 2.48 Impact Factor -
Article: Fra-1 and Stat3 synergistically regulate activation of human MMP-9 gene.
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ABSTRACT: Fra-1 is overexpressed in a variety of human tumors. Whether MMP-9 expression is regulated by Fra-1 has been contradictory. To clarify the capability of Fra-1 in activating transcription of MMP-9 gene, we analyzed the transcriptional activity of the MMP-9 promoter through the measure of luciferase activities in the MCF-7 cells transiently transfected with Fra-1. The positive regulation of Fra-1 on MMP-9 promoter was not detectable. By the analysis of MMP-9 promoter, a potential Stat3 binding site, just juxtaposed AP-1 consensus sequence, was noticed. The reporter assay showed that MMP-9 promoter was activated remarkably by cotransfection with Fra-1 and Stat3C. DNA affinity precipitation assay confirmed the binding of Stat3 and Fra-1 to the elements of MMP-9 promoter and also revealed c-Jun recruited to Stat3-Fra-1 complex. By immunoprecipitation assay, the Stat3/Fra-1, Stat3/c-Jun and Fra-1/c-Jun complexes were identified in vivo. Our study demonstrated that the activation of MMP-9 promoter is dependent upon interactions of Fra-1/c-Jun with Stat3. A juxtaposed Stat3/AP-1 element plays a crucial role in the manner of enhancersome in the activation of MMP-9 gene. The functional cooperation of the Stat3 and AP-1 transcription factors is required for the transcription of MMP-9 gene.Molecular Immunology 02/2008; 45(1):137-43. · 2.90 Impact Factor -
Article: CUE domain containing 2 regulates degradation of progesterone receptor by ubiquitin-proteasome.
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ABSTRACT: Accumulated evidence indicates that progesterone receptors (PR) are involved in proliferation of breast cancer cells and are implicated in the development of breast cancer. In this paper, a yeast two-hybrid screen for PR led to the identification of CUE domain containing 2 (CUEDC2), whose function is unknown. Our results demonstrate that CUEDC2 interacts with PR and promotes progesterone-induced PR degradation by the ubiquitin-proteasome pathway. The inhibition of endogenous CUEDC2 by siRNA nearly abrogated the progesterone-induced degradation of PR, suggesting that CUEDC2 is involved in progesterone-induced PR ubiquitination and degradation. Moreover, we identify the sumoylation site Lys-388 of PR as the target of CUEDC2-promoted ubiquitination. CUEDC2 decreases the sumoylation while promoting ubiquitination on Lys-388 of PRB. We also show that CUEDC2 represses PR transactivation, inhibits the ability of PR to stimulate rapid MAPK activity, and impairs the effect of progesterone on breast cancer cell growth. Therefore, our results identify a key post-translational mechanism that controls PR protein levels and for the first time provide an important insight into the function of CUEDC2 in breast cancer proliferation.The EMBO Journal 05/2007; 26(7):1831-42. · 9.20 Impact Factor -
Article: Expression and distribution of HSP27 in response to G418 in different human breast cancer cell lines.
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ABSTRACT: Heat shock proteins (HSPs) play an important role in folding, intracellular localization and degradation of cellular proteins. However, the cellular role of HSP27 is not completely understood. The conflicting results have been reported regarding stress-induced nuclear translocation of HSP27. In this study, human breast cancer cells transiently and stably expressing HSP27-EGFP chimera were utilized to observe the intracellular localization of HSP27. The data show that the transient and stable expression of HSP27-EGFP displayed distinguishingly cellular localization. The nuclear translocalization of HSP27-EGFP was correlated with the presence of G418. Experiments carried out with different human breast cancer cell lines revealed clearly different distribution patterns of endogenous HSP27. The subcellular distribution of endogenous HSP27 appeared diffuse throughout the cytoplasm in MDA435 cells. In MCF-7 and SKBR3 cells, the accumulation of the protein was distinctly seen along the cell membrane and around nucleus. Moreover, the nuclear translocation of endogenous HSP27 was stimulated by G418 only in MDA435 cells, but not in MCF-7 and SKBR3 cells. Overexpression of HSP27 has been associated with resistance to cisplatin and doxorubicin. The correlation of the expression pattern of HSP27 with the drug resistance may need to be investigated. Further studies on the intracellular function of HSP27 may take into account its interaction proteins in the cells. It may provide useful information for the identification of sensitivity of carcinoma cells to the chemotherapeutic drugs and development of more specific agents to circumvent HSP27.Histochemie 12/2006; 126(5):593-601. · 2.59 Impact Factor -
Article: A novel cis-acting element in Her2 promoter regulated by Stat3 in mammary cancer cells.
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ABSTRACT: Stat3 plays important roles in the development of breast malignancies and oncogenesis. In the present study, a palindromic cis-acting element displaying repression activity in breast cancer cells expressing low level of Her2 was found in Her2 promoter. Deletion analysis showed that the novel element was located within Pal2 region spanning nucleotides -529 to -505. The sequence analysis of Pal2 region revealed a DNA sequence (TTAAGATAA) homologous to the binding site of Stat3, starting from position -529 to -521bp. By reporter assay, Pal2 was found to be regulated by constitutive activated Stat3C. A stimulatory effect both on Her2 mRNA and protein expressions was observed in MCF-7 cells stably expressing Stat3C, suggesting that Stat3 regulated Her2 expression. Using ChIP assays the binding of Stat3 to Her2 promoter was confirmed. The data obtained in this study indicate constitutive activated Stat3 regulates Her2 expression. Further investigation of differential effects of Stat3 exerting on breast cancer cells expressing Her2 at different levels will provide more insights into the roles of Stat3 in Her2 expression as well as the regulation of diverse biological activities.Biochemical and Biophysical Research Communications 07/2006; 345(2):660-8. · 2.48 Impact Factor -
Article: PIAS3 induction of PRB sumoylation represses PRB transactivation by destabilizing its retention in the nucleus.
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ABSTRACT: Progesterone receptor (PR) plays a critical role in cell proliferation and differentiation, and its transcriptional activity is known to be modulated by cofactor proteins. In the present study, we demonstrated that in the presence of progesterone, protein inhibitor of activated STAT-3 (PIAS3) significantly inhibited the PR transcriptional activity and the expression of progesterone-responsive genes. Reduction of endogenous PIAS3 by PIAS3 small-interfering RNA enhanced PR transactivation in a ligand-dependent manner. PIAS3 interacted with PR both in vitro and in vivo and the interaction was enhanced by progesterone. Furthermore, our findings suggested that PIAS3 strongly induced PRB sumoylation at three sites, Lys-7, Lys-388 and Lys-531. In addition, novel roles in PRB nuclear retention and transactivation were identified for these sites. Our data also suggested that PIAS3 was recruited in a largely hormone-dependent manner in response to a progesterone-responsive promoter. Finally, we demonstrated that PIAS3 inhibited the DNA-binding activity of PR and influenced its nuclear export as well as PR transactivation. Taken together, these data strongly suggested that PIAS3 played an important physiological role in PR function.Nucleic Acids Research 02/2006; 34(19):5552-66. · 8.03 Impact Factor -
Article: Proteomic analysis of interleukin 6-induced differentiation in mouse myeloid leukemia cells.
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ABSTRACT: Cytokine-induced differentiation of myeloid leukemia cells has important therapeutic implications, but the mechanism remains to be clarified. M1 cell, a mouse acute myeloid leukemia cell line, which underwent growth inhibition, terminal differentiation and apoptosis in response to IL-6, was selected as an experimental model to study on the molecular mechanisms of myeloid cell differentiation on a proteome-wide scale. Cell differentiation was evaluated by cell morphology and CD11b expression. With two-dimensional (2D) gel analyses, 17 protein spots showed obvious changes in quantity during the process of differentiation were found. With matrix-assisted laser desorption/ionization mass spectrometry (MALDI-TOF-MS) or/and nano-electrospray ionization MS/MS (ESI-MS/MS) analysis, 15 protein spots were identified. The mRNA levels of these 15 proteins during differentiation were also examined using a semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) analysis. Except two proteins, the mRNA levels demonstrated similar expression patterns to what the proteomic analysis revealed. The identified proteins were known to be involved in different cellular functions, including protein synthesis, transcription, signal transduction, cell cycle control, cell rescue and defense, cellular organization, and metabolism. Notably, seven proteins were not described before to be involved in differentiation. Our data provide novel information for a better understanding of the mechanisms by which terminal differentiation of acute myeloid leukemia cells induced by IL-6.The International Journal of Biochemistry & Cell Biology 07/2005; 37(6):1197-207. · 4.63 Impact Factor -
Article: [Nano-ESI-MS/MS identification on differentiation-associated proteins in M1 mouse myeloid leukemia cells induced by IL-6].
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ABSTRACT: To identify two differentiation-associated proteins induced by rhIL-6 in M1 mouse myeloid leukemia cells. Protein spots were excised from 2-D gels and digested in-gel with trypsin. The trypsin lysis products were first analyzed by matrix-assisted laser desorption/ionization-time of flight-mass spectrometry (MALDI-TOF-MS) through peptide mass fingerprinting and then performed peptide sequencing by nano-electrospray ionization mass spectrometry/mass spectrometry (nano-ESI-MS/MS). The database search was finished with the Mascot search engine (http://www.matrixscience.co.uk) using the data processed through MaxEnt3 and MasSeq. The two proteins were not revealed by peptide mass fingerprint using MALDI-TOF-MS, while they were respectively identified as Destrin and Putative protein after the sequence of their trypic peptides were obtained by the nano-ESI-MS/MS techniques. Nano-ESI-MS/MS technique can successfully identify the two differentiation-associated proteins induced by rhIL-6 and has great advantage in protein analysis.Zhongguo yi xue ke xue yuan xue bao. Acta Academiae Medicinae Sinicae 11/2004; 26(5):483-7. -
Article: The β2-adrenergic receptor and Her2 comprise a positive feedback loop in human breast cancer cells
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ABSTRACT: In this study, b2-AR level was found to be up-regulated in MCF-7 cells overexpressing Her2 (MCF-7/ Her2). Correlation of b2-AR level with Her2 status was demonstrated in breast cancer tissue samples. Constitutive phosphorylation of ERK, mRNA expression up-regulation of catecholamine-synthesis enzymes, and increased epi-nephrine release were detected in MCF-7/Her2 cells. b2-AR expression induced by epinephrine and involvement of ERK signaling were validated. The data indicate that Her2 overexpression and excessive phosphorylation of ERK cause epinephrine autocrine release from breast cancer cells, resulting in up-regulation of b2-AR expres-sion. The data also showed that catecholamine prominently stimulated Her2 mRNA expression and promoter activity. The activation and nuclear translocation of STAT3 triggered by isoproterenol were observed. Enhanced bind-ing activities of STAT3 to the Her2 promoter after iso-proterenol stimulation were verified. Using STAT3 shRNA and dominant negative STAT3 mutant, the role of STAT3 in isoproterenol-induced Her2 expression was further confirmed. The data support a model where b2-AR and Her2 comprise a positive feedback loop in human breast cancer cells.
Top co-authors
Top Journals
Institutions
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2012
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Beijing Institute of Microbiology and Epidemiology
Beijing, Beijing Shi, China
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2008
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West China University of Medical Sciences
Chengdu, Sichuan Sheng, China
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2006–2007
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National ESCA and Surface Analysis Center For Biomedical Problems
Seattle, WA, USA
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2004
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Academy of Military Medical Sciences
Tianjin, Tianjin Shi, China
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