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The Y-located testis-specific protein Y-encoded (TSPY) and its X-homologue TSPX originated from the same ancestral gene, but act as a proto-oncogene and a tumor suppressor gene, respectively. TSPY has specialized in male-specific functions, while TSPX has assumed the functions of the ancestral gene. Both TSPY and TSPX harbor a conserved SET/NAP domain, but are divergent at flanking structures. Specifically, TSPX contains a C-terminal acidic domain, absent in TSPY. They possess contrasting properties, in which TSPY and TSPX, respectively, accelerate and arrest cell proliferation, stimulate and inhibit cyclin B-CDK1 phosphorylation activities, have no effect and promote proteosomal degradation of the viral HBx oncoprotein, and exacerbate and repress androgen receptor (AR) and constitutively active AR variant, such as AR-V7, gene transactivation. The inhibitory domain has been mapped to the carboxyl acidic domain in TSPX, truncation of which results in an abbreviated TSPX exerting positive actions as TSPY. Transposition of the acidic domain to the C-terminus of TSPY results in an inhibitory protein as intact TSPX. Hence, genomic mutations/aberrant splicing events could generate TSPX proteins with truncated acidic domain and oncogenic properties as those for TSPY. Further, TSPY is upregulated by AR and AR-V7 in ligand-dependent and ligand-independent manners, respectively, suggesting the existence of a positive feedback loop between a Y-located proto-oncogene and male sex hormone/receptors, thereby amplifying the respective male oncogenic actions in human cancers and diseases. TSPX counteracts such positive feedback loop. Hence, TSPY and TSPX are homologues on the sex chromosomes that function at the two extremes of the human oncogenic spectrum.
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The Y-located testis-specific protein Y-encoded (TSPY) and its X-homologue TSPX originated from the same ancestral gene, but act as a proto-oncogene and a tumor suppressor gene, respectively. TSPY has specialized in male-specific functions, while TSPX has assumed the functions of the ancestral gene. Both TSPY and TSPX harbor a conserved SET/NAP domain, but are divergent at flanking structures. Specifically, TSPX contains a C-terminal acidic domain, absent in TSPY. They possess contrasting properties, in which TSPY and TSPX, respectively, accelerate and arrest cell proliferation, stimulate and inhibit cyclin B-CDK1 phosphorylation activities, have no effect and promote proteosomal degradation of the viral HBx oncoprotein, and exacerbate and repress androgen receptor (AR) and constitutively active AR variant, such as AR-V7, gene transactivation. The inhibitory domain has been mapped to the carboxyl acidic domain in TSPX, truncation of which results in an abbreviated TSPX exerting positive actions as TSPY. Transposition of the acidic domain to the C-terminus of TSPY results in an inhibitory protein as intact TSPX. Hence, genomic mutations/aberrant splicing events could generate TSPX proteins with truncated acidic domain and oncogenic properties as those for TSPY. Further, TSPY is upregulated by AR and AR-V7 in ligand-dependent and ligand-independent manners, respectively, suggesting the existence of a positive feedback loop between a Y-located proto-oncogene and male sex hormone/receptors, thereby amplifying the respective male oncogenic actions in human cancers and diseases. TSPX counteracts such positive feedback loop. Hence, TSPY and TSPX are homologues on the sex chromosomes that function at the two extremes of the human oncogenic spectrum.
Subject(s)
Humans , Male , Carcinogenesis/genetics , Cell Cycle Proteins/genetics , Chromosomes, Human, Y/genetics , DNA-Binding Proteins/genetics , Proto-Oncogene Mas , Testis/metabolismABSTRACT
AIM:To investigate the mechanism of the radiosensitizing effect of maximum non-cytotoxic doses of tetrandrine (Tet) on nasopharyngeal carcinoma cell lines CNE1 and CNE2.METHODS:The cells were treated with maximum non-cytotoxic doses of Tet (for CNE1 cells at 1.5 μmol/L and for CNE2 cells at 1.8 μmol/L),irradiation at 4 Gy,or combination of irradiation and maximum non-cytotoxic doses of Tet.The cell cycle distribution was analyzed by flow cytometry.The protein levels of γ-H2AX,cleaved caspase-3,p-CDC25C,CDK1,p-CDK1,cyclin B1,ERK and p-ERK were determined by Western blot.RESULTS:The expression of γ-H2AX was increased in CNE1 cells and CNE2 cells after combined treatment with irradiation and maximum non-cytotoxic doses of Tet.The percentages of CNE1 cells and CNE2 cells at G2/M phase in irradiation group were (18.09 ±0.42)％ and (18.48 ± 1.32)％,respectively,which were decreased to (15.88 ± 1.04) ％ and (13.80 ± 0.82) ％ in combined treatment group,respectively (P ＜ 0.05).Combined treatment enhanced the increase in the protein level of cleaved caspase-3 caused by irradiation.The protein levels of pCDC25C and p-CDK1 were increased in a dose-dependent manner by Tet treatment (P ＜ 0.05),while the expression of CDK1 showed no difference among different doses of Tet treatments.The protein levels of p-CDC25C,p-CDK1 and CDK1 showed no difference after the treatment with maximum non-cytotoxic doses of Tet.The combined treatment with irradiation and the maximum non-cytotoxic doses of Tet decreased the protein levels of p-CDC25C and p-CDK1 (P ＜0.05),increased the expression of cyclin B1,and had no influence on the expression of CDK1 （ P ＜0.05).The combined treatment resulted in an increase in the protein level of p-ERK1 (P ＜ 0.05).CONCLUSION:The maximum non-cytotoxic doses of Tet enhance the DNA damage and apoptosis in CNE1 cells and CNE2 cells caused by irradiation,and the mechanism might be associated with ending of G2/M arrest via activation of ERK/CDC25C/CDK1/cyclin B1 pathways.
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AIM:To investigate the mechanism of the radiosensitizing effect of maximum non-cytotoxic doses of tetrandrine (Tet) on nasopharyngeal carcinoma cell lines CNE1 and CNE2.METHODS:The cells were treated with maximum non-cytotoxic doses of Tet (for CNE1 cells at 1.5 μmol/L and for CNE2 cells at 1.8 μmol/L),irradiation at 4 Gy,or combination of irradiation and maximum non-cytotoxic doses of Tet.The cell cycle distribution was analyzed by flow cytometry.The protein levels of γ-H2AX,cleaved caspase-3,p-CDC25C,CDK1,p-CDK1,cyclin B1,ERK and p-ERK were determined by Western blot.RESULTS:The expression of γ-H2AX was increased in CNE1 cells and CNE2 cells after combined treatment with irradiation and maximum non-cytotoxic doses of Tet.The percentages of CNE1 cells and CNE2 cells at G2/M phase in irradiation group were (18.09 ±0.42)％ and (18.48 ± 1.32)％,respectively,which were decreased to (15.88 ± 1.04) ％ and (13.80 ± 0.82) ％ in combined treatment group,respectively (P ＜ 0.05).Combined treatment enhanced the increase in the protein level of cleaved caspase-3 caused by irradiation.The protein levels of pCDC25C and p-CDK1 were increased in a dose-dependent manner by Tet treatment (P ＜ 0.05),while the expression of CDK1 showed no difference among different doses of Tet treatments.The protein levels of p-CDC25C,p-CDK1 and CDK1 showed no difference after the treatment with maximum non-cytotoxic doses of Tet.The combined treatment with irradiation and the maximum non-cytotoxic doses of Tet decreased the protein levels of p-CDC25C and p-CDK1 (P ＜0.05),increased the expression of cyclin B1,and had no influence on the expression of CDK1 （ P ＜0.05).The combined treatment resulted in an increase in the protein level of p-ERK1 (P ＜ 0.05).CONCLUSION:The maximum non-cytotoxic doses of Tet enhance the DNA damage and apoptosis in CNE1 cells and CNE2 cells caused by irradiation,and the mechanism might be associated with ending of G2/M arrest via activation of ERK/CDC25C/CDK1/cyclin B1 pathways.
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Aim To investigate the effect of hesperidin on human lung cancer cell A549 and the possible mechanism.Methods The cell apoptosis and necrosis of A549 treated with hesperidin were measured by the Hoechst 33342/PI fluorescent dye based on microfluidic chip technology.Cell cycle and apoptosis rate were evaluated by flow cytometry(FCM).The expressions of the related genes were detected through the real-time fluorescent quantitative PCR technology(RT-PCR) including VEGF, PI3K and PTEN.The protein expressions of Bcl-2, Cyclin B1, PI3K, Akt and PTEN were detected by Western blot after hesperidin intervention.Results The proliferation of A549 cells was significantly inhibited by hesperidin in a dose-dependent manner.FCM results showed that hesperidin could not only influence the G0/G1 phase and S phase, but also promote the apoptosis of lung cancer cells.Meanwhile, the apoptosis and necrosis rate was increased from(6.7±0.6)% to(27.9±1.1)% compared with that of control group(P<0.05).From the level of molecular, the gene expressions of VEGF and PI3K were decreased, while the PTEN was increased after hesperidin stimulation.Western blot results showed that the expression of protein Bcl-2, Cyclin B1 and Akt were decreased, which all showed close relationship with cell apoptosis, cell cycle and PI3K-Akt signaling pathway.The expression of PI3K was increased, but the change of PTEN was not statistically significant compared with that of control group.Conclusion Hesperidin induces lung cancer cell apoptosis through PI3K-Akt signaling pathway, which blocks cancer cell division and destroys the balance of related protein expression.
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Objective To explore the mechanism of neuropmtective effects of puerarin for the treatment of acute spinal ischenia-reperfusion injury in a rat model.Methods Acute spinal ischemia-reperfusion injury was induced via aortic occlusion in 28 male Sprague-Dawley rats.The animals were randomly divided into four groups,as follows:group negative contrast (NC sham operation),group positive control group (IR+ S ischemia/reperfusion + saline),group puerarin (IR+P ischemia/reperfusion + puerarin),group mscovitine (IR+R ischemia/reperfusion + roscovitine).The motor function,spinal infarction volume,apoptosis indices,and CDK5 and P25 activities were examined.Results Spinal ischemia-reperfusion caused the injury of the spines and was associated with motor deficit,elevation of CDK5 and P25 activities,and increase in the spinal apoptosis and spinal infarction volume.Puerarin improved motor function and decreased apoptosis,spinal infarction volume,and CDK5 and P25 activities.Conclusion The findings of the present study indicated that puerarin treatment-mediated reduction of spinal injury was associated with the inhibition of CDK5 and P25,and that the inhibition was one among the neuroprotective mechanisms of puerarin against acute ischemia/reperfusioninduced spinal injury in rats.
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Purpose To investigate the expression of polo-like kinase 1 (Plk1) and Cyclin B1, p21WAF1in cervical carcinoma, and to determine the relationship between the expression of the three proteins and tumor clinicopathological features. Methods The expres-sion of Plk1, Cyclin B1 and p21WAF1 was detected in 102 cases of cervical carcinoma, 20 cases of (cervical intraepithelial neoplasia, CIN) , and 20 cases of nomal cervical tissues by the technique of tissue chip and immunohistochemical staining of EliVision. Statistical analyses of the data were performed with SPSS 19. 0 software. Results The positive rates of Plk1 in cervical carcinoma and CIN were 70. 5%, 55. 0%, respectively, which were significantly higher than normal cervical tissues (10%) (P<0. 01);The positive rates of Cyclin B1 in cervical carcinoma and CIN were 52. 9% and 30. 0%, respectively, which were significantly higher than normal cervical tissues (10%)(P <0.01); The positive rates of p21WAF1 in cervical carcinoma and CIN were 23.5% and 10.0%, respectively, which were significantly higher than normal cervical tissues ( 0 ) ( P<0. 01 ) . There were no significant differences between cervical carcinoma and CIN in the positive rates of Plk1, Cyclin B1 and p21WAF1. The expression of Plk1 was associated with the depth of carci-noma invasion (P<0. 05), that of Cyclin B1 was associated with lymph node metastases and the depth of carcinoma invasion (P<0. 05)and that of p21WAF1 in cervical carcinoma was associated with histological grade (P<0. 05). In cervical carcinoma, the expres-sion of Plk1 was positively correlated with Cyclin B1 (rs =0. 297, P=0. 002) and negatively correlated with p21WAF1(rs = -0. 403, P<0. 001). Conclusion The expression of Plk1, Cyclin B1 and p21WAF1 is involved in the occurrence and development of cervical carcinoma, and the former two are also related with prognosis of cervical carcinoma. The combination of the three would provide a new target for clinical treatment.
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Objective: To observe the effect of monocrotaline (MCT) extract from Crotalaria sessiliflora on inducing human pancreatic cancer cell BxPC-3 into polyploid giant cells in vitro. Methods: BxPC-3 cells (1 × 104/mL) were inoculated with MCT (0, 5, 10, and 20 μg/mL) in RPMI-1640 for 72 h, respectively, then the cell morphology was observed by Giemsa staining, and the DNA content was measured by flow cytometry; BxPC-3 cells-induced apoptosis was checked by AnnexinV-FITC/PI double staining using flowcytometry, BxPC-3 polyploid giant cell genome was checked by chromosome spreading assay, and Cyclin B1 expression also was analysed by Western blotting. Results: Giemsa staining and DNA content by flow cytometry showed that MCT induced BxPC-3 cell into polyploid giant cells in vitro. MCT treatment for 72 h appeared 4N, and 8N polyploid giant of BxPC-3 cells, induction of apoptosis, decreased the expression of cyclin B1 in a dose dependent manner. Chromosome analysis demonstrated once again that polyploid giant cell was mainly in 8N. Conclusion: Monocrotaline might exert its antitumor effect by blocking the cell cycle, inducing apoptosis, and down-regulating Cyclin B1 protein.
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Objective To investigate the effect of artesunate on the cell cycle of human multiple myeloma RPMI8226 cells and explore the related molecularmechanisms. Methods RPMI8226 cellswere treated with 0, 25, and 50 pg/mL artesunate. The morphology change of cells was observed under transmission electron microscope, the cell cycle distribution was detected by flow cytometry, and the expression of cyclin B1 and p34cdc2 protein was examined by Western blotting analysis. Results After treated with 50 pg/mL artesunate for 48 h, most RPMI8226 cells showed characteristic morphology of apoptosis. With the increase of artesuate concentration, the proportion of RPMI8226 cells in G0/G1 phase was significantly decreased (P<0. 05) and that of cells in G2/M phase was significantly increased (P<0.05), suggesting that artesunate induced noticeable G2/M arrest. Cyclin B1 level was increased and the p34cdc2 level was decreased with the increase of artesuate concentration. Conclusion Artesunate can induce G2/M arrests in RPMI8226 cells, which may be related to the increasedcyclin B1 expression and decreased p34cdc2 expression.
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Objective To observe the differences of the radio-biological characteristics between the human malignant glioma cell line SHG-44 and its progeny cells SHG-4410 Gy and to probe the underlying mechanism.Methods The SHG-4410 Gy cells were the progeny of SHG cells that had been irradiated with 10 Gy X-rays and then passaged for 15 generations.The radiosensitivity of SHG-44 and SHG-4410 Gy wre measured by clonogenic assay and the multi-target single-hit model was used to fit the survival curve.The cell cycle redistribution and apoptosis were analyzed by flow cytometry assay.Quantitative Real Time-PCR (qRT-PCR) was used to determine the relative levels of cyclin B1 mRNA and miR-21.Stat3 protein levels were detected by Western blot.Results The values of D0,Dq and SF2 of SHG-4410 Gy cells were significantly higher than those of SHG-44 cells.Flow cytometric analysis showed that there was less G2/M phase arrest in SHG-4410 Gy (F =22.21,P ＜ 0.05).Radiation-induced early apoptotic population was increased from (17.60 ± 0.26) ％ to (28.00 ± 0.36) ％ for SHG-44 cells,but increased from only (4.20 ± 0.30)％ to (5.17 ± 0.65)％ for SHG-4410 Gy.miR-21 in SHG-4410 Gy cells were increased by 1.44 fold of SHG-44 cells,which was associated with the increase of Stat3 protein expression.Conclusions Radioresistance is observed in the progeny of human malignant glioma cell line SHG-44 which had been irradiated with 10 Gy X-rays.The underlying mechanisms may be relative to the upregulation of cyclin B1 that acts as a key downstream gene in the signaling pathway of G2/M phase transition.In addition,the upregulation of miR-21 may be involved in the apoptosis of SHG-4410 Gy cells.
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PURPOSE: The molecular mechanisms that are responsible for the initiation and progression of breast cancers are largely unknown. This study was to analyze the cyclin B1, cdc2, p53 and p16 tumor suppressor genes in human breast cancer. MATERIALS AND METHODS: To investigate the role of cyclin B1, cdc2, p53 and p16 in the pathogenesis and progression of breast carcinomas, 98 cases of breast cancers were examined by immunohistochemical method. The correlations of cyclin B1, cdc2, p53 and p16 expression with various clinico-pathologic findings were analysed. RESULTS: In the normal breast tissues, cyclin B1, cdc2 and p16 were weakly expressed, while p53 was not expressed. On the other hand, cyclin B1, cdc2, p53 and p16 were overexpressed in breast cancer, showing correlation between the expression of cyclin B1 and cdc2 and breast cancers (p=0.00). The overexpressions of cdc2 and p16 were correlated with an infiltrative tumor border pattern and this was statistically significant (p<0.05). In addition, the overexpression of cdc2 was correlated with histologic high grade carcinomas (p=0.00). CONCLUSION: Cyclin B1 and cdc2 appeared to be involved in the genesis or progression of breast cancers. In addition, the overexpressions of p16 and p53 may play important roles in more aggressive tumor and the overexpression of cdc2 is associated with progression of tumor to a higher grade of breast carcinomas. The deranged overexpressions of cyclin B1, cdc2, p16 and p53 may play an important role in human breast carcinogenesis.
Subject(s)
Adult , Aged , Female , Humans , Middle Aged , Breast Neoplasms/genetics , Cyclin B/genetics , Cyclin B1/genetics , Cyclin-Dependent Kinase Inhibitor p16/genetics , Gene Expression Regulation, Neoplastic , Immunohistochemistry , Tumor Suppressor Protein p53/geneticsABSTRACT
Objective To explore the role of Cyclin B1 and Cyclin D1 on Barrett esophagus,Barrett's esophagus mixed with atypical dysplasia and esophageal adenocarcinoma.Methods Cyclin B1 and Cyclin D1 were examined with immunohistochemistry.76 esophageal tissues of patients werB collected,including severe reflux esophagitis(RE,25 cases),Barrett esophagus(BE,35 cases),Barrett esophagus mixed with atypical dysplasia(DY,8 cases),esophageal carcinoma(CA,8 cases).Ten cases with normal esophageal mucosa were examined as the control. Results Cyclin B1 and Cyclin D1 were high expression in the specimens of the BE,DY and CA groups and very low expression in the control and RE group.Statistieal difference Was showed(P<0.01).Expression of Cyclin D1 was increasing gradually from the tissues of intestinal metaplasia,atypical dysplasia to adenocarcinoma(50.04 vs 67.94 vs 74.31).There Was significant difference among these three groups(P<0.01).Conclusion Cyclin B1 and Cyclin D1 as markers of tumour development could evaluate the risk from Barrett esophagus to adenocarcinoma.Perhaps it is the earlv event in the development of esophageal carcinoma.
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BACKGROUND: Hypoxia inducible factor-1alpha(HIF-1alpha) is a transcription factor for various target genes that are involved in adapting cells to hypoxia. It promotes cell proliferation and survival via modulation of such cell cycle regulators such as cyclin A1 and cyclin B1 in response to hypoxia. This is associated with local failure of radiotherapy, which renders a poor prognosis for cervical carcinoma. METHODS: Using the tissue histologic sections and a tissue microarray of the archived biopsy and surgical specimens of uterine cervical carcinoma from 57 patients who were treated with radiation therapy alone, we performed immunohistochemical staining for HIF-1alpha and cyclin A1 and B1 to evaluate the correlations between the expressions of these proteins in tumors and the clinicopathologic parameters associated with the prognosis. RESULTS: The large tumor cell nests and invasive front margins of the tumors showed comparatively intense immunoreactivity of HIF-1alpha. There was no significant correlation between the HIF-1alpha, cyclin A1 and cyclin B1 expressions and the clinicopathologic factors. CONCLUSIONS: The HIF-1alpha expression showed marked intra-tumoral heterogeneity. The HIF-1alpha expression is neither a powerful predictor of resistance to radiotherapy nor is it a poor prognostic marker in cervical carcinoma patients who are treated with radiotherapy. The expressions of cyclin A1 and cyclin B1 are neither independently associated with the response of radiation therapy nor are they associated with the prognostic parameters of uterine cervical carcinoma.
Subject(s)
Humans , Hypoxia , Biopsy , Cell Cycle , Cell Proliferation , Cyclin A , Cyclin A1 , Cyclin B , Cyclin B1 , Cyclins , Hypoxia-Inducible Factor 1, alpha Subunit , Population Characteristics , Prognosis , Proteins , Transcription Factors , Uterine Cervical NeoplasmsABSTRACT
Objective: To study the expression of p34cdc2 and cyclin B1 in human cervical carcinoma, and the relationship between their expression and clinicopathologyical features of cervical cancer. Methods: A quantitative real-time reverse transcription polymerase chain reaction and Western blotting assay were used to analyze the expression levels of p34cdc2 and cyclin B1 mRNA and protein, respectively, in fresh invasive cervical cancer (n = 62) and control cervical tissues (n = 15). Results: The expression levels of p34cdc2 and cyclin B1 mRNA and protein were significantly higher in cancer tissues than those in control cervical tissues (P = 0.004, P = 0.013; P = 0.016, P = 0.029), and mainly displayed overexpression. Significant positive correlation was found between the expression of p34cdc2 and cyclin B1 mRNA (r = 0.527, P = 0.001) and protein (r = 0.432, P = 0.022) in cervical cancer tissues. A statistical significance was found between the expressions of p34cdc2/cyclin B1 mRNA and lymphatic metastasis in cervical cancer (P = 0.038, P = 0.001). No statistically significant association was found between the age, histological types, the differentiation degree, clinical stages and expression of p34cdc2/cyclin B1 (P > 0.05). Conclusion: p34cdc2 and cyclin B1 are important molecules in regulation of cervical carcinogenesis. Over-expression of p34cdc2/cyclin B1 stimulates cervical cancer cells to overcome G2/ M checkpoint and enter M phase in cell cycle. The high-expression of p34cdc2/ cyclin B1 might become a novel biomarker for studying the mechanism underlying the tumorigenesis and lymphatic metastasis of cervical cancer.
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Objective To describe the spatial and temporal characteristics of neurofibrillary tangles (NFT) in brains of patients with Niemann-Pick disease type C (NPC). Methods In order to analyze formation of NFT in NPC, the brains collected from 17 patients with NPC aged from 7 months to 55 years old were investigated using antibodies against the protein tau and the specific proteins in mitotic phase. Results Typical NFT could be detected in the parahippocampns of a NPC patient as early as at 4 years old. The number of NFT were increasing along with the time. Gradually, the hippocampus and other regions of the temporal lobes and the frontal lobes would be affected with the time. Immunohistochemically, the NFT formed the shape similar to NFT seen in AD brains, without the presence of senile plagues. Interestingly,mitosis-phase markers appeared in the degenerating NPC neurons prior to hyperphesphorylation of tau and formation of NFT. Conclusions The formation of NFT does not result from aging, for there is no close relation between the presence of senile plagues and the formation of NFT. Ectopic activation of cdc2/cyclinB1 kinase complex might be an early event leading to NFT formation. Antagonist of the kinase complex may potentially slow down the formation of NFT.
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PURPOSE: Cell cycle progression is regulated by interactions of specific cyclins and cyclin dependent kinases (CDKs) at the G1-S and G2-M checkpoints and cell cycle deregulation plays a major role in carcinogenesis of human cancers. PATIENTS AND METHODS: To investigate the role of cell cycle regulators in the pathogenesis and progression of human gastric cancers, 23 cases of gastric carcinomas were examined for the expression of cyclin B1, p34cdc2, p27(Kip1) and p53 by immunohistochemical methods, and gene expression was correlated with various clinicopathologic findings. RESULTS: Out of 23 cases studied, cyclin B1 was diffusely expressed in 20 cases (87.0%), p34cdc2 in 14 cases (60.9%) and p53 in 12 cases (52.2%), whereas in normal gastric tissues, cyclin B1 and p34cdc2 were weakly expressed and p53 was not expressed. In contrast, p27(Kip1) was expressed in only 8.7% of gastric carcinomas compared with 78.3% of normal gastric tissues. There was correlation between the expression of cyclin B1 and expression of p34cdc2 (p=0.002), between the expression of cyclin B1 and loss of p27(Kip1) (p=0.025), and between the expression of p34cdc2 and loss of p27(Kip1) (p=0.065). In addition, expression of cyclin B1 was correlated with regional lymph node metastasis (p=0.032). CONCLUSION: Our results indicate that cyclin B1 and p34cdc2 are involved in the genesis or progression of gastric cancers. Furthermore, overexpression of cyclin B1 may play an important role in lymph node metastatic potential of gastric cancer. Thus, abnormal expression of cyclin B1 and CDKs, overexpression of p53 and loss of p27(Kip1) expression may play important roles in human gastric carcinogenesis.
Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , CDC2 Protein Kinase/metabolism , Cyclin B/metabolism , Intracellular Signaling Peptides and Proteins/metabolism , Prognosis , Stomach Neoplasms/diagnosis , Tumor Suppressor Protein p53/metabolismABSTRACT
0.05).Conclusion Cyclin B1 levels in liver cancer tissues were stronger than in adjacent cancer tissues and normal liver tissues.
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0.05).The mRNA expression of Cyclin B1 of IMRT group was significantly higher than that of ART group at each dose point(P
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OBJECTIVE: Cyclin is a family of regulatory proteins that play a key role in controlling the cell cycle. Abnormalities of cell cycle regulators, including cyclins and cyclin dependent kinases (CDKs), have been reported in malignant tumors. This study was undertaken to quantitatively detect cyclin B1 and D1 in cervical cancer. METHODS: A quantitative real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blot analysis were used to analyze the expression of cyclin B1, D1 mRNA and proteins, respectively, in fresh invasive cervical cancer (n=41) and normal cervix tissue (n=10). RESULTS: There was significantly greater cyclin B1 expression in invasive cervical cancer than in normal cervix tissue (p=0.019). However, cyclin D1 expression was not significantly different (p=0.967). A Western blot analysis yielded similar results. CONCLUSION: Our results were consistent with the concept that up-regulation of cyclin B1 expression occurred in cervical cancer and an aberrant expression of cyclin B1 might play an important role in cervical carcinogenesis.
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Female , Humans , Blotting, Western , Carcinogenesis , Cell Cycle , Cervix Uteri , Cyclin B1 , Cyclin D1 , Cyclin I , Cyclin-Dependent Kinases , Cyclins , RNA, Messenger , Up-Regulation , Uterine Cervical NeoplasmsABSTRACT
OBJECTIVE: The objective of this study was to evaluate the relationship between the expression of cyclin B1, D1 and the various prognostic factors in ovarian carcinoma. METHODS: In this study, fresh ovarian tissue samples were obtained from 41 patients treated surgically at our institute from March of 2002 to February of 2005. These included 36 ovarian carcinomas and 5 normal ovarian tissues that were served as the control. Quantitative real-time RT-PCR and Western blot analysis were used in detecting the expression of mRNA and protein of cyclin B1, D1, respectively. RESULTS: The mean 2(-delta delta CT) values of cyclin B1 and D1 mRNA in ovarian carcinoma tissues obtained through quantitative real-time RT-PCR were 5.83+/-12.03, 17.60+/-22.20, respectively, and the mean values in the control were 0.55+/-0.35, 0.50+/-0.26, respectively. The results showed difference in the expression, but were not statistically significant (p=0.67, 0.07, respectively). If the mean densitometer value of cyclin B1 and D1 protein in the control obtained by Western blot analysis was 1, the mean values in ovarian carcinoma tissues were higher, but were not statistically significant (1.30+/-0.73, 1.81+/-1.28, respectively) (p=0.76, 0.06, respectively). The expression of cyclin B1, D1 and various prognostic factors was not statistically related. CONCLUSION: Our results showed that the expression of cyclin B1 and D1 in ovarian carcinoma tissues was higher than in the normal control. This suggested that cyclin B1, D1 and the tumorigenesis and the degree of malignancy was closely related. But the expression of cyclin B1, D1 and various prognostic factors was not statistically related. Further studies based on the correlation between cyclin and response to treatment or survival rate are needed to support cyclin as a prognostic factor of ovarian carcinoma.