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1.
AIM: To explore the effect of microRNA (miR)-21 on proliferation, migration and differentiation abilities of c-Kit+ cardiac stem cells (CSCs). METHODS: c-Kit+ CSCs were cultured and selected by the methods of enzyme digestion and magnetic bead separation. miR-21 mimics (50 nmol/L) and mimics negative control (MNC) were transfected into c-Kit+ CSCs with Lipofectamine® 2000. The cells was divided into 3 groups:control group:c-Kit+ CSCs without any pretreatment; MNC group:the cells were transfected with MNC for 48 h; mimics group:the cells were transfected with miR-21 mimics for 48 h. qPCR was used to assess the expression of miR-21 in each group. CCK-8 and EdU assays were used to determine the cell proliferation. qPCR and immunofluorescence were used to detect the differentiation in each group. Scratch assay was adopted to explore the migration ability of the cells. RESULTS: The expression of c-Kit in the c-Kit+ CSCs were 90.8%, with 0.6% of CD45 and 0.5% of CD34. A significant increase in miR-21 expression was observed when the cells were transfected with miR-21 mimics for 48 h (P<0.05). CCK-8 and EdU assays showed that miR-21 significantly increased cell proliferation as compared with MNC group and control group (P<0.05). No difference in the expression of Nkx2.5, CD31 and α-SMA at mRNA and protein levels was observed, and no difference of the migration ability in 3 groups of the c-Kit+ CSCs was found. CONCLUSION: Over-expression of miR-21 significantly promotes the proliferation of c-Kit+ CSCs, without any effect on the cell migration and differentiation.  相似文献   

2.
AIM: To observe the effects of interleukin-32γ (IL-32γ)on the proliferation and cell cycle of rat vascular smooth muscle cells (VSMCs). METHODS: The VSMCs were isolated from the thoracic aorta of SD rats by the method of tissue-piece inoculation. The cells were cultured and treated with different concentrations of IL-32γ. The proliferation of the cells was examined by MTT assay. The cell cycles were analyzed by flow cytometry. The protein levels of NF-κB p65 and cyclin D1 were detected by Western blotting. The expression of proliferating cell nuclear antigen (PCNA)was examined by immunocytochemical staining. RESULTS: Administration of IL-32γ at the concentrations of 10~50 μg/L for 24~48 h significantly promoted the proliferation of VSMCs in a dose- and time-dependent manner. After stimulation with IL-32γ at the concentration of 50 μg/L for 24 h, the cell cycle transition from G1 phase to S/G2 phase was accelerated and the expression levels of NF-κB p65, cyclin D1 and PCNA increased as compared with those in control group. CONCLUSION: IL-32γ promotes the proliferation of rat VSMCs and accelerates the cell cycle transition via upregulating the expression of NF-κB p65 and cyclin D1.  相似文献   

3.
AIM: To clarify the effect of SC58125 on cell proliferation and apoptosis in HepG-2 cells and explore the molecular mechanisms. METHODS: Cell culture, MTT, TUNEL, DNA ladder, flow cytometry and Western blot analysis were employed in the present study. RESULTS: SC58125 inhibited the growth of HepG-2 cells and induced the apoptosis. Furthermore, it arrested G0/G1 phase and inhibited S phase in HepG-2 cells. Depressed expression of P33cdk2, P34cdc2, cyclin B1, cyclin E, Mpm-2, Rb, PCNA proteins were found in HepG-2 cells treated with SC58125. CONCLUSION: SC58125 inhibits cell proliferation and induces apoptosis, which may be related to the altered low protein levels of P33cdk2, P34cdc2, cyclin B1, cyclin E, Mpm-2, Rb, PCNA.  相似文献   

4.
AIM:To investigate the effect of L-arginine (L-Arg) on intimal proliferation and expression of related cell cycle regulatory factors after vascular injury in rats. METHODS:Rats were divided into three groups :sham operation group, balloon injury group(this group included balloon 48 h,7 d and 14 d subgroup) and balloon+L-Arg group. Neointima area were calculated morphologiocally. The expression of cyclin dependent kinase-2(CDK2),cyclin E and proliferation cell nuclear antigen (PCNA) were measured by means of immunohistochemical technique and computer image analyzer. RESULTS:After vascular balloon injury, the level of plasma NO decreased, CDK2、cyclin E and PCNA expressed in the media at 48 h and in the neointima at 7 d and 14 d but with low and undetected expression in the media, the expression of CDK2, cyclin E and PCNA increased with the intima thickening. Compared with balloon 14 d group, the plasma NO level increased (P＜0.01), the neointima area reduced by 59.1%(P＜0.01) and the positive expression indexes of CDK2, cyclin E and PCNA decreased by 36.1%, 46.3% and 76.2% respectively in balloon+L-Arg group (P all＜0.01). CONCLUSION:L-Arg can effectively repress intima proliferation after vascular injury, which may be associated with its inhibiting the proliferation of vascular smooth muscle cell through downregulating the excessive expression of CDK2, cyclin E and PCNA.  相似文献   

5.
AIM: To investigate the effect of calcitonin gene-related peptide (CGRP)transfection into c-kitpos cardiac stem cells (c-kit+CSCs) on the cell viability. METHODS: Under the sterile condition, the auricles of SD rats were taken out,and then c-kit+CSCs were collected through enzyme digestion and immunomagnetic bead separation (MACS). The cells were identified by flow cytometry. c-kit+CSCs were transfected with enhanced green fluorescent protein CGRP lentiviral vector (Lv-EGFP-CGRP) or enhanced green fluorescent protein lentiviral vector (Lv-EGFP). The cells were randomly divided into Lv-EGFP-CGRP-CSCs group, Lv-EGFP-CSCs group and CSCs group. The transfection was observed under the fluorescence microscope. The transfection efficiency was detected by flow cytometry. The CGRP protein secretion in the cell culture supernatants was detected by ELISA. The viability of c-kit+CSCs transfected with Lv-EGFP-CGRP or Lv-EGFP was measured by CCK-8 assay. RESULTS: c-kit+CSCs were isolated and cultured successfully. The expression positive rate of c-kit was 91.0% and the expression positive rates of CD45 and CD34 were 4.5% and 4.0%, respectively. After transfected with lentivirus for 48 h, the stable fluorescence in c-kit+CSCs was observed under fluorescence microscope. The transfection efficiency were 80% when MOI was 20. The level of CGRP was significantly increased in Lv-ECFP-CGRP-CSCs group compared with Lv-EGFP-CSCs group and CSCs group (P<0.05). Meanwhile, transfection with lentiviral vector in each group did not affect the viability of c-kit+CSCs. CONCLUSION: Transfection of Lv-EGFP-CGRP into c-kit+CSCs was successful. The secretion of CGRP was found in the transfected c-kit+CSCs and the viability was not changed after transfection. CGRP-modified c-kit+CSCs may play a role in treating myocardial infarction.  相似文献   

6.
AIM: To determine the effects of catestatin (CST) on calcium handling abnormalities and ventri-cular arrhythmia (VA) after myocardial infarction (MI) in rats. METHODS: The adult male SD rats (n=85) were randomly divided into sham group (n=20) and operation group (n=65). MI was induced by ligation of the left anterior descending coronary artery in operation group. The rats in sham group underwent pericardiotomy but without ligating the artery. The rats survived for 1 week after operation were randomly assigned to MI group and CST group. The rats in CST group was treated with CST (30 mg·kg-1·d-1, intraperitoneal administration) for 4 weeks, while saline was applied to the rats in sham group and MI group. The calcium imaging study was performed by loading isolated ventricular cardiomyocytes with Fura-2 AM. In the whole Langendorff-perfused hearts, the programmed electrical stimulation was used to induce action potential duration (APD) alternans and VA. The protein levels of ryanodine receptor 2 (RyR2), phosphorylated RyR2 (p-RyR2), calcium/calmodulin-dependent protein kinase II (CaMKII) and phosphorylated CaMKII (p-CAMKII) were determined by Western blot. RESULTS: Compared with sham group, the protein levels of p-RyR2 and p-CaMKII, the diastolic intracellular Ca2+ concentrations and the inducibility of VA were significantly increased, whereas the thresholds of Ca2+ transient (CaT) and APD alternans and the CaT amplitude were markedly decreased in MI group (P<0.01). Compared with MI group, the protein levels of p-RyR2 and p-CaMKII, the diastolic intracellular Ca2+ concentration and the inducibility of VA were significantly decreased, while the thresholds of CaT and APD alternans and the CaT amplitude were markedly increased in CST group (P<0.01). No significant difference of the protein expression of RyR2 and CaMKII among the 3 groups was observed (P>0.05). CONCLUSION: CST reduces the susceptibility to VA after MI via preventing calcium handling abnormalities.  相似文献   

7.
AIM:To investigated the effect of 7-hydroxyisoflavone (7-HIF) on the proliferation, apoptosis and stem-like cell feature of colorectal cancer cells. METHODS:The effect of 7-HIF on the proliferation of HCT116 cells was detected by WST-1 assay and colony formation assay. The effects of 7-HIF on the cell cycle distribution and apoptosis in the HCT116 cells were analyzed by flow cytometry. The expression of cell-cycle related proteins and the stemness related proteins was determined by Western blot. RESULTS:After treated with 7-HIF (200 μmol/L), the viability of HCT116 cells was inhibited, and the size and number of the colony were decreased as compared with control group (P<0.05). The G0/G1 phase of the cell cycle was increased. The proportion of S phase was decreased and the cells were mainly arrested in G0/G1 phase. The apoptotic rate of HCT116 cells was 21.4%, which was significantly higher than that in the control group (1.1%). The results of Western blot revealed that the expression of inhibitor of differentiation 1(Id1) was significantly decreased (P<0.05). The expression of cell cycle markers cyclin D1 and cyclin E, the proliferative markers survivin and PCNA, and stem cell markers CD133, ALCAM and EpCAM were all down-regulated by 7-HIF treatment (P<0.05). CONCLUSION:7-HIF inhibits the proliferation and induces the apoptosis of colorectal cancer cells, and inhibits the stem-like cell feature, which may be related to Id1 inhibition.  相似文献   

8.
AIM: To investigate the effect of Ikaros isoforms on the proliferation of human ovarian cancer SKOV3 cells. METHODS: Three isoforms of Ikaros, IK1, IK2 and IK6, were transfected into ovarian cancer SKOV3 cells. CCK-8 assay and cell counting were used to detect the effects of Ikaros isoforms on the proliferation of SKOV3 cells. The cell cycle was analyzed by flow cytometry. The cell cycle-related proteins were detected by Western blot. RESULTS: IK1 and IK2 expression inhibited SKOV3 cells proliferation. Flow cytometry analysis indicated that IK1 and IK2 induced SKOV3 cell cycle arrest at the G1 phase. IK6 isoform exerted no obvious effect on the proliferation or cell cycle of SKOV3 cells. Compared with control EV group, IK1 group and IK2 group showed a dramatic elevation in the expression of the cell cycle inhibitor p21, along with a substantial decrease in the expression of the cell cycle inducers cyclin D1 and cyclin D2, which did not change in IK6 group. CONCLUSION: IK1 and IK2 significantly inhibit the proliferation of ovarian cancer SKOV3 cells and induce cell cycle arrest at G1 phase by regulation of cell cycle-related proteins cyclin D1, cyclin D2 and p21, while IK6 isoform exerts no obvious effect on the proliferation and cell cycle of SKOV3 cells.  相似文献   

9.
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10.
AIM: To investigate the role of prostaglandin E2 receptor 2 agonist (EP2A) in proliferation and homing of human CD34+ cells. METHODS: Bone marrow fluid and peripheral blood containing stem cells were collected from healthy donors mobilized by granulocyte colony-stimulating factor in our department. Human CD34+ cells were isolated by the method of magnetic-activated cell sorting microbeads. Bone marrow mononuclear cells were isolated by Ficoll-Paque centrifugation, and the bone marrow mesenchymal stem cells (BMMSC) were cultured with L-DMEM. Human CD34+ cells and BMMSC were divided into 4 groups, and treated with PGE2 (as positive control), DMSO (as negative control), EP2A and EP2A+prostaglandin E2 receptor 2 antagonist (EP2AA), respectively. After exposed to the reagents, human CD34+ cell viability was measured by CCK-8 assay, the number of colonies was evaluated by colony-formation assay, the cell cycle distribution was analyzed by flow cytometry, and the protein expression of survivin, β-catenin and CXC chemokine receptor 4 (CXCR4) was detrmined by Western blot. Moreover, the concentration of stromal cell-derived factor-1α (SDF-1α) in the BMMSC was detected by ELISA. RESULTS: The cell viability and the colony number of human CD34+ cells in EP2A group were not higher than those in negative control group. Furthermore, the proportion of human CD34+ cells treated with EP2A in G2/M phase was not elevated compared with negative control group. The protein expression of survivin and β-catenin did not up-regulated in human CD34+ cells exposed to EP2A, but the protein expression of CXCR4 in human CD34+ cells and the concentration of SDF-1α in BMMSC were elevated. CONCLUSION: EP2A promotes human CD34+ cell homing in vitro but not proliferation.  相似文献   

11.
AIM:To investigate the protein expression of cyclin D2 and p16 in proliferation and differentiation of cultured cardiac myocytes.METHODS:One-day-old Sparague-Dawley rats were used. Cardiac myocytes(CM) were collected by a trypsin-dispersal method and cultured. Cell growth line and fluorescence activated cell sorting (FACS) were used to investigate the proliferation of CM. Ultra-thin sections were made to observe the ultrastructure of CM under transmission electron microscope. The expression of cyclin D2 and p16 in CM were measured using immunocytochemistry and image analysis.RESULTS:①Results of cell growth line and FACS analysis showed that cultured CM could proliferate in the first 3 cultured days, but the ability decreased quickly, concomitant with differentiation. CM was obseved quiescent in cell cycle three days later. The ultrastructure of CM showed the large amount of myofilaments and mitochondrion. ②The protein expression of cyclin D2 in 3,4,5 day CM group was 0.89 times(P＜0.05),0.80 times (P＜0.05) and 0.56 times (P＜0.01) of that in 1 day group, respectively. The expression of p16 in CM was increased during the culture process, 2,3,4,5 day group were 1.63 times, 1.72 times, 1.99 times and 2.84 times (P＜0.01) of that in 1 day group, respectively.CONCLUSION:Cultured neonatal rat cardiac myocytes could proliferate during the first 3 days after incubation, but the ability of proliferation decreased, from the fourth day, concomitant with differentiation. Cyclin D2 and p16 play the key roles in CM postnatal development. Downregulation of cyclin D2 and upregulation of p16 may induce CM differentiation.  相似文献   

12.
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13.
AIM: To observe the expression of cyclin D1 following PKC activation and the correlation between PKC-α and cyclin D1 in asthmatic rat airway smooth muscle cells (ASMCs), and to discuss the effects of cyclin D1 on the proliferation of airway smooth muscle cells regulated by PKC in asthmatic rat. METHODS: Twelve SD rats were randomly divided into control group (group N) and asthmatic 2-week group (group A), and then subdivided into 4 groups based on the drug interventions: (1) control group; (2) PMA; (3) PMA+5 μmol/L Ro-31-8220 group; (4) 5 μmol/L Ro-31-8220 group. The proliferations of ASMCss were examined with cell cycle analysis, MTT colorimetric assay and proliferating cell nuclear antigen (PCNA) immunocytochemical staining. The expressions of PKC-α and cyclin D1 were analyzed by RT-PCR and Western blotting. The data were subject to correlation analysis. RESULTS: (1) Compared to group A1, there were significant differences in the percentage of S+G2/M phase, absorbance A value of MTT and the rate of positive expression of PCNA protein in group A2 and A4 (P<0.01). The same tendency in group N was observed according with group A. (2) Compared with A1, the ratios of A values of PKC-α mRNA and protein in group A2 and A4 were significantly changed (P<0.01) as well as the ratios of A values of cyclin D1 mRNA and protein. (3) There were positive correlations between PKC-α and cyclin D1 in mRNA (r=0.476, P<0.05) and protein(r=0.899, P<0.01). CONCLUSION: The activation of PKC-α promotes ASMCs proliferation in asthmatic rats, and there are positive correlations between the PKC-α and cyclin D1 in mRNA and protein, indicating that the PKC-α signal pathway may be involved in the process of airway smooth muscle remodeling by regulating the expression of cyclin D1 in asthmatic rats.  相似文献   

14.
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15.
AIM: To investigate the roles of intermedin1-53 (IMD1-53) and exteracellular signal-regulated kinase (ERK) signal pathway in the proliferation of rat cardiac fibroblasts (CFBs).METHODS: Isolated and cultured CFBs from new born SD rats were randomly divided into control group, aldosterone (ALD) groups (at different concentrations) and ALD+IMD groups (IMD at different concentrations). The viability of CFBs was determined by MTT assay. Western blotting was used to observe the effect of IMD on ALD-induced ERK phosphorylation.RESULTS: IMD1-53 had no significant effect on the proliferation of CFBs in basal state, but inhibited the CFBs growth stimulated by ALD in a concentration (10-9~10-7 mol/L)-dependent manner. IMD1-53 also inhibited ERK phosphorylation stimulated by ALD in a concentration (10-9~10-7 mol/L)-dependent manner.CONCLUSION: IMD1-53 inhibits the proliferation of CFBs by ERK signal pathway.  相似文献   

16.
AIM: To investigate the effect of down-regulation of X-box binding protein 1 (XBP1) expression on the viability and apoptosis of glioma cells. METHODS: The mRNA expression of XBP1 in the glioma tissues was detected by qPCR. Small interfering RNA (siRNA) interfering with XBP1 expression (XBP1-siRNA) was transfected into human brain glioma U251 cells. At the same time, control group (the cells without special treatment) and negative control (NC-siRNA) group (transfected with siRNA without any interference) were set up. The mRNA expression of XBP1 in the 3 groups 48 h after transfection was detected by qPCR. The protein levels of XBP1, proliferating cell nuclear antigen (PCNA), B-cell lymphoma/leukemia-2 (Bcl-2), Bcl-2-associated X protein (Bax), cyclin D1 (cyclin D1), phosphatidylinositol 3-kinase (PI3K) and phosphorylated Akt (p-Akt) were determined by Western blot. The cell viability was measured by CCK-8 assay. The cell cycle distribution and apoptosis were analyzed by flow cytometry. RESULTS: The expression level of XBP1 in the glioma tissues was significantly higher than that in the tumor adjacent tissues (P<0.05). The XBP1 expression at mRNA and protein levels was significantly decreased in the cells transfected with XBP1-siRNA (P<0.05). No statistically significant difference of the cell viability, cell cycle, apoptotic rate and the protein levels of PCNA, Bcl-2, Bax, cyclin D1, PI3K and p-Akt between NC-siRNA group and control group was observed. Compared with control group, the cell viability, S-phase cells and the protein levels of PCNA, Bcl-2, cyclin D1, PI3K, and p-Akt in XBP1-siRNA group were decreased significantly, and the apoptotic rate, G0/G1-phase cells and Bax protein expression were significantly increased (P<0.05). CONCLUSION: Down-regulation of XBP1 gene expression in brain glioma cells reduces the viability of cancer cells, blocks the cells in G1 phase and promote apoptosis. The mechanism is related to the inhibition of PI3K/Akt signaling pathway.  相似文献   

17.
AIM: To explore the relationship between 3-nitrotyrosine (3-NT) level in hearts or blood and myocardial cell apoptosis in rat diabetic cardiomyopathy (DCM). METHODS: Sixty Sprague-Dawley (SD) rats (male, 8-week-old) were randomly divided into 4 groups: normal group, diabetic cardiomyopathy group (DCM group), diabetic rats treated with valsartan (40 mg·kg-1·d-1, D+V group) and DCM rats treated with valsartan (40 mg·kg-1·d-1, DCM+V group). Apoptotic index (AI) of rat cardiac myocytes was examined by TUNEL. The expression index (EI) of 3-NT in rat cardiac myocytes was examined by immunohistochemistry. The 3-NT concentration in rat serum was examined by ELISA. RESULTS: (1) Significant differences of the heart weight indexes among the 4 groups were observed (P<0.01). The heart weight indexes in DCM group and DCM+V group were higher than those in normal group and D+V group (P<0.01). (2) The EI of 3-NT in the cardiac myocytes was positively correlated with the AI of the cardiac myocytes in the same group (P<0.01), but the concentration of 3-NT in blood had no correlation with the AI of cardiac myocytes (P>0.05). (3) The difference of AI of cardiac myocytes among the 4 groups had statistical significance (P<0.01). The arrangement from high to low of AI was DCM group > D+V group and DCM+V group > N group (P<0.05). (4) The EI of 3-NT in DCM group was the highest as compared to other groups (P<0.05). (5) No statistical difference of 3-NT concentration in blood among the 4 groups was observed (P>0.05). CONCLUSION: (1) The expression of 3-NT in DCM myocardial tissues in SD rats is significantly increased and closely correlated with the apoptosis in myocardial cells. Valsartan inhibits 3-NT expression in DCM myocardial cells, thus inhibits the DCM myocardium apoptosis. (2) The 3-NT level in blood can not be true for reflection of 3-NT expression in DCM myocardial tissues and its effect on myocardial cell apoptosis.  相似文献   

18.
AIM: To investigate the potential role of Src homology 2 domain-containing protein tyrosine phosphatase 2 (SHP-2) in the proliferation of cardiac fibroblasts induced by angiotensin Ⅱ (Ang Ⅱ). METHODS: The neonatal rat cardiac fibroblasts were separated by trypsin digestion. The cardiac fibroblasts were identified by vimentin of immunochemical staining. The proliferation of the cardiac fibroblasts with or without Ang Ⅱ stimulation was measured by MTT assay. Adenoviruses containing SHP-2 gene were transfected into cardiac fibroblasts to overexpress SHP-2. SHP-2 was inhibited by its inhibitor NSC-87877. RESULTS: The proliferation of the cardiac fibroblasts was increased in a dose-dependent manner by the stimulation of Ang Ⅱ and the maximum concentration of Ang II for cell proliferation was 10-7 mol/L. SHP-2 promoted the proliferation of cardiac fibroblasts under the stimulation of Ang Ⅱ. The proliferation rate in mutant group was higher than that in wild-type group (P<0.01). Inhibition of SHP-2 by NSC-87877 attenuated the proliferation. CONCLUSION: The growth promoting effect of Ang Ⅱ on cardiac fibroblasts is regulated by SHP-2.  相似文献   

19.
AIM:To investigate the influences of bradykinin(BK)on left ventricular hypertrophy and cardiac function in angiotensin-converting enzyme inhibitor(ACEI) therapy in rats after myocardial infarction.METHODS:The effects of enalapril (500 μg·kg-1·d-1), enalapril (500 μg·kg-1·d-1)with BKB2 receptor antagonist (Hoe-140 500 μg·kg-1·d-1), losartan(3 mg·kg-1·d-1) on left ventricular end-diastolic pressure (LVEDP), maximum positive left ventricular pressure change (+dp/dtmax) and LVW/BW as well as V(m)n of noinfarcted area were examined after 4 weeks treatment in rats after myocardial infarction.RESULTS:The values of LVEDP, LVW/BW and V(m)n of three treatment groups were higher than that of untreated MI group (P＜0.05),but the +dp/dtmax of three treatment groups were not significantly different compared with the untreated MI group. In addition, no significant difference in MAP was observed among the three treatment groups, but the LVW/BW and V(m)n of enalapril+Hoe-140-treated group were higher than that of enalapril-treated group (P＜0.05) .CONCLUSION:Enalapril can prevent left ventricular hypertrophy and improve cardiac function independent of blood pressure after myocardial infarction, which is partly due to the inhibition of BK degradation.  相似文献   

20.
AIM: To investigate the mechanism that insulin-like growth factor binding protein 7 (IGFBP7) inhibits proliferation of human breast cancer cell line MCF-7. METHODS: Plasmid pCMV6-IGFBP7 or empty plasmid was transfected into MCF-7 cells. The expression of IGFBP7 in MCF-7 cells after transfection was detected by Western blotting. The effects of IGFBP7 on the colony-forming efficiency and the cell cycle were studied by soft agar colony formation assay and flow cytometry,respectively. The effects of IGFBP7 on the expression of ERK1/2, p-ERK1/2, cyclin D1, CDK4, cyclin E, CDK2, p21CIP1/WAF1, p27KIP1, p53, Rb and p-Rb in MCF-7 cells were detected by Western blotting. RESULTS: Only the transfectant of pCMV6-IGFBP7 expressed IGFBP7. IGFBP7 remarkably reduced colony-forming efficiency (P<0.01) and G0/G1 arrest (P<0.01), inhibited phosphorylation of ERK1/2 (P<0.01), down-regulated cyclin D1 and cyclin E (P<0.01), up-regulated p27KIP1, p21CIP1/WAF1 and p53 (P<0.01), and inhibited phosphorylation of Rb (P<0.01) in MCF-7 cells. PD98059, an inhibitor of MEK1 and MEK2, imitated part of the tumor-suppressing activity of IGFBP7. CONCLUSION: IGFBP7 inhibits the proliferation of human breast cancer cell line MCF-7 by down-regulating cyclin D1 and cyclin E, up-regulating p27KIP1, p21CIP1/WAF1 and p53 and inhibiting phosphorylation of Rb. ERK1/2 signaling pathway might be involved in the regulation of cyclin D1 and p27KIP1 by IGFBP7.  相似文献   

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