MiR-210 regulates cell cycle in nasopharyngealcarcinoma cell line (CNE-1) under hypoxic condition by reducing the expression of cyclin D1

Objective： The aim of our study was to determine the underlying mechanism of miR-210 on regulation of the cell cycle in nasopharyngeal carcinoma cell line CNE-1, particularly through regulation of cyclin D1, under hypoxic conditions. Methods： The CNE-1 cell line was induced with hypoxia, and the expression levels of endogenic miR-210 and cyclin D1 were detected by real-time PCR and Western blotting. Next, the luciferase assay was used to confirm that cyclin D1 is a target gene for miR-210. Cell cycle and cell proliferation were detected in CNE-1 cells that were cultured under hypoxic conditions with either overexpression or knockout of miR-210 using flow cytometry and MTT assay, respectively. Results： Hypoxia induced the expression of miR-210, resulting in reduced mRNA and protein levels of cyclin D1 and repression of cyclin D1 in CNE-1 cells. Further analysis indicated that miR-210 directly binded to the 3＇UTR of the cyclin D1 gene, thus regulated the expression of cyclin DI. The flow cytometry assay showed that, under hypoxic conditions, miR-210 blocked CNE-1 cells in the G1 phase, and miR-210 also inhibited the proliferation of CNE-1 cells. Conclusion： Under hypoxic conditions, miR-210 directly reduced the expression of cyclin D1, leading to CNE-1 cells blocked in G1 phase.

Effect of cis-9,trans-11-conjugated linoleic acid on cell cycle of gastric adenocarcinoma cell line(SGC-7901)

AIM: To determine the effect of cis -9, trans -11-conjugated linoleic acid (c9, t11-CLA) on the cell cycle of gastric cancer cells (SGC-7901) and its possible mechanism in inhibition cancer growth. METHODS: Using cell culture and immunocytochemical techniques, we examined the cell growth, DNA synthesis, expression of PCNA, cyclin A, B(1), D(1), p16(ink4a) and p21(cip/waf1) of SGC-7901 cells which were treated with various c9, t11-CLA concentrations (25, 50, 100 and 200 micromol.L(-1))of c 9, t 11-CLA for 24 and 48h, with a negative control (0.1% ethane). RESULTS: The cell growth and DNA synthesis of SGC-7901 cells were inhibited by c9, t11-CLA.SGC-7901 cells. Eight day after treatment with various concentrations of c9, t11-CLA mentioned above, the inhibition rates were 5.92%, 20.15%, 75.61% and 82.44%, respectively and inhibitory effect of c9, t11-CLA on DNA synthesis (except for 25 micromol.L, 24h) showed significantly less (3)H-TdR incorporation than that in the negative controls (P【0.05 and P【0.01). Immunocytochemical staining demonstrated that SGC-7901 cells preincubated in media supplemented with different c9, t11-CLA concentrations at various times significantly decreased the expressions of PCNA (the expression rates were 7.2-3.0%, 24h and 9.1-0.9% at 48h, respectively), Cyclin A (11.0-2.3%, 24h and 8.5-0.5%,48h), B(1) (4.8-1.8% at 24h and 5.5-0.6% at 48h)and D(1) (3.6-1.4% at 24h and 3.7%-0 at 48h) as compared with those in the negative controls(the expressions of PCNA, Cyclin A, B(1) and D(1) were 6.5% at 24h and 9.0% at 48h, 4.2% at 24h and 5.1% at 48h, 9.5% at 24h and 6.0% at 48h,respectively)(P【0.01), whereas the expressions of P16(ink4a) and P21(cip/waf1), cyclin-dependent kinases inhibitors(CDKI), were increased. CONCLUSION: The cell growth and proliferation of SGC-7901 cell is inhibited by c9, t11-CLA via blocking the cell cycle, with reduced expressions of cyclin A,B(1) and D(1) and enhanced expressions of CDKI(P16(ink4a) and p21(cip/waf1)).

Effects of Cyclin D1 Antisense Oligodeoxyneucleotides on the Growth and Expression of G_1 Phase Regulators in Gastric Carcinoma Cells

To investigate the effects of Cyclin D1 antisense oligodeoxyneucleotides (ASODN) on the growth, cell cycle progression and expression of G 1 phase regulators in human gastric carcinoma cell lines SGC7901 and HS746T, phosphorothioate modified Cyclin D1 ASODN were encapsulated by LipofectAMINE2000 and transfected into gastric carcinoma cells. Dose dependent inhibitory effects were induced by Cyclin D1 ASODN in two gastric carcinoma cell lines. Treatment of gastric carcinoma cells with 0.2 μmol/L Cyclin D1 ASODN for 24 h could significantly inhibit their growth in vitro and in vivo , reduce expression of Cyclin D1mRNA to 26.3 % (SGC7901) and 17.3 % (HS746T) respectively. The percentage of cells in G 0/G 1 phase was increased as revealed by flow cytometry. Immunohistochemical staining showed that the expression of p21 was increased and the expression of Cyclin D1 and pRb was decreased in the two cell lines; the expression of p27 was increased in HS746T, but unchanged in SGC7901. Cyclin D1 ASODN could inhibit the growth and the expression of Cyclin D1 mRNA in gastric carcinoma cells, influence the cell cycle and expression of its regulators.

Differential expression of cell cycle regulators in HCV-infection and related hepatocellular carcinoma

AIM:To investigate cell cycle proteins in chronic hepatitis C virus infection in order to analyze their role in the process of hepatocyte transformation and to characterize their prognostic properties. METHODS:Subjects of the current study included 50 cases of chronic hepatitis C(CHC) without cirrhosis,30 cases of CHC with liver cirrhosis(LC) ,and 30 cases of hepatitis C-related hepatocellular carcinoma(HCC) admitted to the Department of Hepato-Gastroenterology,Theodor Bilharz Research Institute(TBRI) ,Giza,Egypt.Fifteen wedge liver biopsies,taken during laparoscopic cholecystectomy,were also included as normal controls.Laboratory investigations including urine and stool analysis,liver function tests and prothrombin concentration;serologic markers for viral hepatitis and ultrasonography were done for all cases of the study together with immunohistochemical analysis using primary antibodies against Cyclin D1,Cyclin E,p21,p27 and Rb/p105 proteins. RESULTS:Normal wedge liver biopsies didn't express Cyclin E or Rb/p105 immunostaining but show positive staining for Cyclin D1,p21 and p27.Cyclin D1 expressed nuclear staining that was sequentially increased from CHC to LC(P<0.01) to HCC(P<0.001) cases;meanwhile,Cyclin E revealed nuclear positivity only in the case of HCCs patients that was directly correlated to Rb/p105 immuno-reactivity.The expression of p21 and p27 was significantly increased in CHC and LC cases compared to normal controls and HCCs with no significant difference between well-and poorlydifferentiated tumors.p21 showed only a nuclear pattern of staining,while,p27 presented with either cytoplasmic and/or nuclear reactivity in all studied cases.Correlation analysis revealed a direct relation between Cyclin D1 and p21 in CHC cases(P<0.001) ,between Cyclin D1 and Cyclin E in HCCs(P<0.01);however,an inverserelationship was detected between Cyclin D1 and p21 or p27(P<0.001) and between p21 and Rb/p105(P<0.05) in HCCs. CONCLUSION:Upregulation of Cyclin D1 in CHC plays a vital role in the development and differentiation of HCC;while,Cyclin E may be a useful marker for monitoring tumor behavior.p21 and p27 can be used as predictive markers for HCC.Furthermore,higher expression of Rb/p105 as well as inverse relation with p21 and histologic grades suggests its important role in hepatic carcinogenesis.

Vitamin C Inhibits Benzo[a]pyrene-Induced Cell Cycle Changes Partly via Cyclin D1/E2F Pathway in Human Embryo Lung Fibroblasts

Objective To study the molecular mechanism of the inhibitory effects of vitamin C on benzo[a]pyrene （B[a]P）-induced changes of cell cycle in human embryo lung fibroblast （HELF） cells. Methods The stable transfectants, HELF transfected with antisense cyclin D1 and antisense CDK4, were established. Cells were cultured and pretreated with vitamin C before stimulation with B[a]P for 24 h. The expression levels of cyclin DI, CDK4, E2FI, and E2F4 were determined by Western blot. Flow cytometric analysis was employed to detect the distributions of cell cycle. Results B[a]P significantly elevated the expression levels of cyclin D 1, E2F1, and E2F4 in HELF cells. Vitamin C decreased the expression levels of cyclin D 1, E2F1, and E2F4 in B [a]P-stimulated HELF cells. Dose-dependent relationships were not found between the different concentrations of vitamin C （10, 100, 500, 1000, and 5000 lamol/L） and the expression levels of cyclin D 1, E2F1, and E2F4 in HELF cells. The expression levels of cyclin D1, E2FI, and E2F4 in B[a]P-treated transfectants were lower than those in B[a]P-treated HELF cells. The expression levels of cyclin DI and E2F4 treated with vitamin C and antisense cyclin D1 were decreased compared with those treated with antisense cyclin DI alone. The effects of vitamin C combined with antisense CDK4 on the expression levels of cyclin DI and E2FI/E2F4 were similar to those of antisense CDK4 alone. B[a]P progressed HELF cells from GI to S phase. Both vitamin C and antisense cyclin DI suppressed the changes of cell cycle progressed by B[a]P. However, antisense CDK4 did not attenuate the above changes. Vitamin C combined with antisense CDK4 markedly suppressed B[a]P-induced changes of cell cycle as compared with antisense CDK4. But the inhibitory effects of vitamin C combined with antisense cyclin DI on B[a]P-induced changes of cell cycle were similar to those of vitamin C alone or antisense cyclin DI alone. Conclusions B[a]P progressed HELF cells from G1 to S phase via intracellular signaling pathway of cyclin D I/E2F. Vitamin C may modulate this signaling pathway to protect cells from injury caused by B[a]P.

Medicated Serum of Qishen Yiqi Pill Affect Vascular Smooth Muscle Cell Proliferation,Cell Cycle,Cyclin D1 and CDK4 Mechanism Research

Observation of stilbene dropping pill and yiqi drug-containing serum influence mechanism of vascular smooth muscle proliferation， cell cycle and Cyclin D1 and CDK4Choose male SD rats were randomly divided into 2 groups， lavage qishen yiqi pill and the gastric saline group，extract the drug-containing serum and normal serum；To set the two groups of serum respectively different concentrations，concentration in different time by CCK8 detection effects on vascular smooth muscle cell proliferation， select best concentration and action time.Flow cytometry instrument and high-throughput screening detect serum medicated effect on vascular smooth muscle cell cycle；Western blot detect the drug-containing serum of cell cycle protein Cyclin D1 and CDK4 expression.Result is 5%， 10% medicated serum inhibits cell proliferation significantly higher than the normal serum concentrations of same within 24 h， 48 h.G1 phase cells 5% medicated serum group was obviously higher than that of 5% in normal group (P<005)， serum and cell proliferation index significantly less than 5% normal serum group (P<005)，At the same time， Cyclin D1 and CDK4 expression significantly less than 5% normal serum group (P<005).Conclusion serum of qishen yiqi pill can inhibit vascular smooth muscle cell proliferation， may be through inhibiting cell cycle protein Cyclin D1 and CDK4 expression， block the cell cycle G1 process is closely related to the role.

THE OVEREXPRESSION AND SIGNIFICANCE OF CYCLIN D1 AND P53 IN CERVICAL SQUAMOUS CELL CARCINOMAS

Objective To investigate the significance of overexpresson of cyclin D1 and P53 protein in cervical squamous cell carcinomas.Methods Fifty cases of invasive cervical squamous cell carcinomas and 10 cases of normal cervical squamous epithelia were investigated with immunihistochemical technique. Results The overexpression of cyclin D1 and P53 in invasive cervical carcinomas was 70% and 50%, respectively. There was no overexpression of them in the control group. The overexpression of cyclin D1 in grade Ⅱ and Ⅲ was much higher than that in gradeⅠ(P<0.05). The overexpresson of cyclin D1 in stage Ⅲ of cervical carcinoma was significantly higher than that in stage Ⅱ (P<0.05). The overexpression of P53 in grade Ⅱ and grade Ⅲ of cervical carcinoma was remarkably higher than that in grade Ⅰ (P<0.05).Conclusion The action point of both cyclin D1 and P53 may be at G1/S transition. The overexpression of them was associated with development and progression of cervical carcinoma probably in different mechanisms and different pathways.

Cell cycle exit and neuronal differentiation 1-engineered embryonic neural stem cells enhance neuronal differentiation and neurobehavioral recovery after experimental traumatic brain injury

Our previous study showed that cell cycle exit and neuronal differentiation 1(CEND1)may participate in neural stem cell cycle exit and oriented differentiation.However,whether CEND1-transfected neural stem cells can improve the prognosis of traumatic brain injury remained unclear.In this study,we performed quantitative proteomic analysis and found that after traumatic brain injury,CEND1 expression was downregulated in mouse brain tissue.Three days after traumatic brain injury,we transplanted CEND1-transfected neural stem cells into the area surrounding the injury site.We found that at 5 weeks after traumatic brain injury,transplantation of CEND1-transfected neural stem cells markedly alleviated brain atrophy and greatly improved neurological function.In vivo and in vitro results indicate that CEND1 overexpression inhibited the proliferation of neural stem cells,but significantly promoted their neuronal differentiation.Additionally,CEND1 overexpression reduced protein levels of Notch1 and cyclin D1,but increased levels of p21 in CEND1-transfected neural stem cells.Treatment with CEND1-transfected neural stem cells was superior to similar treatment without CEND1 transfection.These findings suggest that transplantation of CEND1-transfected neural stem cells is a promising cell therapy for traumatic brain injury.This study was approved by the Animal Ethics Committee of the School of Biomedical Engineering of Shanghai Jiao Tong University,China(approval No.2016034)on November 25,2016.

Pharmacological evaluation and mechanistic study of compound Xishu Granule in hepatocellular carcinoma

Objective:In this study,we used HepG2 human hepatocellular carcinoma cells to study the effects of Compound Xishu Granule(CXG)on cell proliferation,apoptosis,and the cell cycle in vitro.We also used a xenograft tumor model to study the anti-tumor effects of CXG and related mechanisms in vivo.Methods:The effect of CXG on cell viability was measured using Cell Counting Kit-8 and a colony formation assay.The effect of CXG on apoptosis and the cell cycle was analyzed using flow cytometry.The in vivo anti-tumor effect of CXG was assessed by measuring the volume change in xenograft tumors after drug administration.The CXG anti-tumor mechanism was studied using western blotting assay to detect cell cycle and apoptotic associated proteins.Results:CXG suppressed HepG2 cell proliferation in a time-and dose-dependent manner in vitro.Colony formation experiments showed that CXG administration for 24 h significantly reduced HepG2 cell formations(P<.01).Flow cytometric analysis showed that CXG treatment for 48 h promoted apoptosis and blocked HepG2 cells in the G2/M phase.Western blotting results showed that Bax was significantly upregulated and Bcl-2 was down-regulated in graft tumor tissues and HepG2 cells after CXG administration,which increased the Bax/Bcl-2 ratio.PLK1,CDC25 C,CDK1,and Cyclin B1 expression were upregulated.CXG had a good inhibitory effect on graft tumor growth in vivo.Conclusion:CXG has good anti-tumor effects in vitro and in vivo.In vitro,CXG promoted HepG2 cell apoptosis and induced G2/M phase arrest.In vivo,CXG significantly inhibited graft tumor growth.The CXG mechanism in treating hepatocellular carcinoma may be that CXG can induce abnormal apoptotic and cell cycle associated protein expression,leading to mitotic catastrophe and apoptosis.

THE EXPRESSION OF p16 AND CYCLIN D_1 IN PROLIFERATIVE ENDOMETRIUM AND ENDOMETRIAL CARCINOMA

Objective To study the role of p16 and cyclin D 1 in the genesis and development of endometrial carcinoma.Methods 12 cases of normal endometrium,22 cases of proliferative endometrium and 41 cases of endometrial carcinoma were detected for the expression of p16 and cyclin D 1 by means of immunohistochemical S P. Results In normal endometrium p16 was expressed while cyclin D 1 was almost negative in the proliferative phase,but both of them were negative in the secretory phase.Among the groups of the simple and compound hyperplasia, the atypical hyperplasia and the endometrial carcinoma,the expression of p16 showed a descending tendency, while the expression of cyclin D 1 showed an ascending tendency.In endometrial carcinomas the expression of p16 was significantly lower than that of normal endometrium and proliferative endometrium( P <0.01, P <0.05).However, the expression of cyclin D 1 in proliferate endometrium and endometrial carcinoma was significantly higher than that in normal endometrium ( P<0.05,P<0.01) .The overexpression of cyclin D 1 in the atypical hyperplasia group was obviously different from that in the simple and compound hyperplasia group ( P <0.01).In endometrial carcinoma,the expression of p16 was decreasing with the descending of cell differentiate degree, on the opposite, the expression of cyclin D 1 was increased and there existed a negative correlation between them.It was also observed that the overexpression of cyclin D 1 was significant different between G 1 and G 2,G 3(P<0.01).Conclusion p16 is a negative regulating factor of cell cycle in endometrial carcinoma, while cyclin D 1 is a positive one.Both of them are important in the genesis and development of endometrial carcinoma.The low expression of p16 and the overexpression of cyclin D 1 are related with the malicious biological behaviors of endometrial carcinoma and maybe play an important role in the judgement of prognosis.Overexpression of cyclin D 1 may be an earlier molecular event in the genesis of endometrial carcinoma.

Effect of Exogenous bFGF on the Proliferation of Human Adenoid Cystic Carcinoma ACC-2 Cells

To observe the effects of basic fibroblast growth factor （bFGF） on human adenoid cystic carcinoma ACC-2 cell line proliferation and ERK, cyclin D1/p21^waf/cip1 signaling pathways, human adenoid cystic carcinoma cells （ACC-2） were cultured and the influence of bFGF of different concentrations on cell proliferation was determined by MTT. Protein was detected by immuno-precipitation and ERK activity by using ERK agent kit. p-ERK1/2 and down-stream cyclin D1, p21^waf/cip1 expression were detected by Western blotting and the interfering role of mitogen protein-activated kinase （MEK） suppressor U0126 in the afore-mentioned indicators was examined. MTT demonstrated ACC-2 cell proliferation was substantially enhanced by bFGF, immuo-precipitation displayed ERK activity was up-regulated by bFGF, and immuno-imprinting also showed p-ERK1/2, cyclin D1 expression was greatly enhanced and p21^waf/cip1 expression was inhibited by bFGE U0126 suppressed the effect of bFGF. It is concluded that bFGF can promote the proliferation of human adenoid cystic carcinoma ACC-2 cells, and its pathways are associated with the up-regulated activity and expression of p-ERK1/2, inhibited p21waf/cip1 expression and enhanced cyclin D1 expression.

Alteration of the Cyclin D1／p16-pRB Pathway, Cellular Proliferation and Apoptosis in Glioma

Objective:To study the alteration of cyclin D1,p16 and pRB in glioma,analyze proliferation and apoptosis of tumor cells,and discuss the pathogenesis of glioma. Methods:Thirty-seven glioma specimens were classified as astrocytoma(25 cases,including 7 fibrillary cases;6 protoplasmic cases;12 anaplastic cases),and glioblastoma(12 cases,including 4 GBM cases).Ten normal brain tissues were taken as controls.The expression of cyclin D1,p16 and pRB were detected by immunohistochemical method.Cellular proliferation was assessed by Ki-67 label index(Ki-67 LI).Cellular apoptosis was detected by TUNEL and apoptotic indices(AI)was calculated. Results:The alterations of three proteins were cyclin D1 overexpression(28/37,75.7%),p16 and pRB deletion(20/37,54.1 % and 12/37,32.4%),which were closely related to tumor types,particularly in malignant glioma.Ki-67 LI and AI were higher when pRB pathway was abnormal.Apoptosis was minor in astrocytic tumors(astrocytomas,0.010±0.002;glioblastomas,0.057±0.016). Conclusion:The abnormalities of cyclin D1/p16-pRB pathway correlated closely with pathogenesis of glioma.

细胞周期调控因子p27、Cyclin D1和DNA含量在食管癌中联合检测的意义

目的探讨食管癌中CyclinD1、p27的表达及与DNA含量联合测定的意义及相互关系。方法收集食管癌组织及癌周正常组织标本,应用免疫组织化学检测CyclinD1、p27蛋白表达,应用流式细胞术检测DNA含量。结果食管癌组织中CyclinD1和p27蛋白表达阳性率分别为45.8%和33.3%,CyclinD1表达阳性组的DNA含量显著高于CyclinD1表达阴性组分别为(1.54±0.21)和(1.08±0.43),(P<0.05),而p27表达阳性组的DNA含量和SPF值低于p27蛋白表达阴性组分别为(1.10±0.19),(5.56±5.18)%和(1.66±0.28),(19.78±6.12)%,(P<0.05)。结论CyclinD1、p27蛋白与食管癌的发生、发展有关,检测CyclinD1、p27及DNA含量可作为诊断和评估食管癌恶性程度的重要指标.

Cyclin B1、CDK1在肺癌中过表达及其意义

采用免疫组化ABC法检测 12例肺癌组织、11例癌旁组织及 3例正常肺组织中cyclinB1、CDK1蛋白的表达情况 ,以探讨细胞周期蛋白cyclinB1及细胞周期蛋白依赖性激酶CDK1在不同肺癌组织中的异常表达及其临床意义 .结果显示cyclinB1在正常肺组织、癌旁组织、癌组织中阳性率分别为 0 %、9.1%和 5 0 .0 % ,CDK1的阳性率则为0 %、18.2 %和 75 .0 % ,cyclinB1、CDK1在小细胞肺癌和鳞癌中存在广泛的过表达 ,而在大细胞肺癌中没有表达 。

Pin1和Cyclin D1在人类5种常见肿瘤中的表达及其意义

目的研究人类的肽基脯氨酰异构酶(Pin1)在人类几种重要的肿瘤(肺癌、前列腺癌、乳腺癌、宫颈癌和胃癌)中的表达及与细胞周期蛋白CyclinD1的关系,并探讨它们在肿瘤的发病机制、诊断和治疗中的意义。方法随机收集33例正常组织和171例癌组织(包括37例肺癌、35例前列腺癌、31例乳腺癌、36例宫颈癌和32例胃癌)。采取免疫组织化学Envision法显示Pin1和CyclinD1的表达。结果Pin1和CyclinD1在正常组织中不表达或者低表达,而在各种癌组织中有普遍性的高表达,在肺癌组织、前列腺癌组织、乳腺癌组织、胃癌组织和宫颈癌组织中,Pin1的表达率分别为48·7%、65·7%、48·4%、15·6%和69·4%,CyclinD1的表达率分别为56·8%、60·0%、54·8%、40·6%和58·3%。Pin1和CyclinD1在癌组织中的表达明显高于正常组织中的表达(P<0·05)。Pin1和CyclinD1蛋白在肺癌、前列腺癌、乳腺癌和宫颈癌中表达呈显著正相关(P<0·05)。而Pin1和CyclinD1蛋白在胃癌中的表达相关性不显著(P>0·05)。结论Pin1和CyclinD1在多种肿瘤的发生、发展过程中具有重要作用,如肺癌、前列腺癌、乳腺癌、宫颈癌和胃癌,Pin1与细胞周期代谢或调控有关。Pin1在某些肿瘤(如肺癌、前列腺癌等)中可作为肿瘤标记的参考指标。

二烯丙基二硫下调cyclin D1和CDK4的表达诱导人鼻咽癌CNE2细胞G_1期阻滞

目的研究二烯丙基二硫(DADS)对人鼻咽癌CNE2细胞的影响及其分子机制。方法采用MTT法检测DADS对CNE2细胞增殖抑制作用;流式细胞术分析DADS对CNE2细胞周期分布的影响;运用RT-PCR和Western blot方法分析DADS作用CNE2细胞后,cyclin D1和CDK4的表达变化。结果 MTT结果显示,不同浓度DADS(90、140、240、400μmol·L-1)处理CNE2细胞48h后,生长抑制率分别为4.0%、13.8%、25.8%、51.2%;流式细胞术分析显示,DADS阻滞CNE2细胞于G1期,并呈浓度依赖性;RT-PCR和Western blot结果表明,细胞周期调控基因cyclinD1、CDK4表达下调。结论 DADS对CNE2细胞的增殖抑制作用与其阻滞细胞G1期有关,并且可能是通过抑制cyclin D1、CDK4的表达使CNE2细胞阻滞于G1期。

口腔鳞癌中Cyclin D1和Bcl-2蛋白表达相关性的研究

目的研究Cyc lin D1和Bc l-2在口腔鳞癌组织和正常口腔粘膜中的表达及意义。方法用免疫组织化学S-P法对62例口腔鳞癌手术切除标本和10例正常口腔粘膜标本中Cyc lin D1和Bc l-2基因蛋白的表达情况进行检测。结果口腔鳞癌组织中Cyc lin D1表达率67.7%(42/62),正常口腔粘膜组织中未见表达,两组间差异有显著性(P<0.05);Bc l-2在正常口腔粘膜组织中也未见表达,在癌组织中Bc l-2蛋白阳性表达率58.1%(36/62),两组间差异也有显著性(P<0.05)。结论Cyc lin D1和Bc l-2两种蛋白在癌组织中存在过表达,口腔鳞癌组织中Cyc lin D1与Bc l-2的表达呈正相关。过表达的Cyc lin D1与Bc l-2可作为评价口腔鳞癌组织分级的参考指标之一。

金雀异黄素抑制人胃癌细胞增殖作用的研究—抑制细胞DNA合成与cyclin D_1表达的研究

采用细胞增殖、DNA合成实验观察了金雀异黄素 (Gen)对体外培养的人胃癌SGC 790 1细胞的生长抑制作用 ,并观察了Gen对人胃癌细胞细胞周期素D1 (cyclinD1 )蛋白的表达情况。结果显示 ,Gen对胃癌细胞生长及其DNA合成有抑制作用 ,并降低cyclinD1 蛋白的表达 ,且呈剂量 效应关系。结果证实 ,Gen抑制胃癌细胞增殖作用的机制之一可能是通过抑制DNA合成及抑制cyclinD1 的表达。

CyclinE和cdk2在膀胱癌中表达及其临床意义

探讨细胞周期蛋白E(cyclinE)和细胞周期蛋白依赖性激酶 2 (cdk2 )与膀胱癌发病的关系及其临床意义。方法 :应用免疫组化方法检测 16例正常膀胱组织和 88例膀胱移行细胞癌中cyclinE、cdk2和PCNA的表达。结果 :膀胱癌中cyclinE和cdk2表达均显著高于正常膀胱组织。cyclinE表达与膀胱癌病理分级、分期、复发和大小之间密切相关 ;cdk2表达则仅与肿瘤大小和PCNA指数密切相关。cyclinE和cdk2共同阳性表达者的肿瘤复发率明显增高。结论 :cyclinE和cdk2的异常表达在膀胱癌发生发展过程中起重要作用 ,两者共同表达对于术后病人监测及治疗方案的制定具有指导意义。

大鼠肝再生中CyclinD_1、PCNA的动态变化

采用蛋白质印迹技术分析了肝切除不同恢复时期cyclin D1 和PCNA的含量变化,结果显示两者表达趋势基本一致,呈显著正相关(r=0.619**,P<0.01),提示cyclin D1 和PCNA在肝再生中细胞周期的 G1/S期转换和S 期DNA合成中发挥关键作用.