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E2F1, a nucleoprotein gene belongs to transcription factor, is closely associated with the development of malignant tumours. Long non-coding RNAs (lncRNAs) are aberrantly expressed in a variety of tumors. In studies of molecular mechanisms associated with lncRNAs and tumours, E2F1 has been identified as a key factor that can play a critical role as an upstream regulator or downstream target of lncRNAs, and even inter-regulate to form a positive feedback loop. This paper reviews the significance of the interaction between E2F1 and lncRNA in malignant tumors in recent years, and aims to provide ideas for the study of tumor mechanisms.
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Objective:To investigate whether SKA1 is a key molecule regulating malignant proliferation of liver cancer, and further explore its mechanism to provide molecular theoretical basis for subsequent targeted therapy.Methods:The data of liver cancer from TCGA database were analyzed by bioinformatics technology. The expression of SKA1 in liver cancer was analyzed. At the same time, we also analyzed the relationship between the expression of SKA1 and the prognosis of patients with liver cancer. The hepatoma cell line overexpressing SKA1 was constructed by liposome-mediated cell transfection technique, and the effect of SKA1 on the proliferation of hepatoma cells was further tested by CCK-8 and plate cloning assay. At the same time, we found that E2F1 is also highly expressed in liver cancer, using bioinformatics technology to analyze the correlation between SKA1 and E2F1 expression, further detecting the binding site of E2F1 in the SKA1 promoter region, and using dual luciferase technology to detect E2F1 against SKA1. Transcriptional activation.Results:KA1 was highly expressed in liver cancer tissues, and the overall survival rate of liver cancer patients with high SKA1 expression was 49.8%, lower than that of patients with low SKA1 expression, showing a negative correlation. E2F1 is also highly expressed in liver cancer tissues, and the survival time of patients with liver cancer with high E2F1 expression is significantly lower than that in the low expression group, which was negatively correlated with poor prognosis. SKA1 overexpression could increase the proliferation ability of liver cancer cells by nearly 50%. SKA1 is regulated by the E2F1 transcription factor, and the E2F1 transcription factor is combined with the SKA1 promoter to transcriptionally activate the expression of SKA1 in liver cancer cells.Conclusion:E2F1 transcriptional activation of SKA1 promotes proliferation of hepatoma cells, leading to poor prognosis in patients with liver cancer
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E2F transcription factor 1 (E2F1) is a major member of the E2F transcription factor family and participates in a wide range of physiological regulatory processes, such as cell cycle, survival, apoptosis, and metabolism. It is proved that the activity of E2F1 is related to the G1/S phase regulation of the cell cycle dependent on tumor suppressor retinoblastoma protein (RB). Recent studies have shown that E2F1 is highly expressed in prostate cancer cells, manifested as an oncogene, and its expression level is closely related to the occurrence, development, and poor clinical prognosis of prostate cancer. Androgen receptor (AR) is the main driving factor for the growth and progression of prostate cancer, and the changes of AR pathway play a key role in the pathological progression of prostate cancer. This article provide a systematic and comprehensive summary on recently published articles to review the role of the E2F1 pathway in prostate cancer.
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Objective:To explore the mechanism of miR-205-5p/E2F1 signal axis in regulating the glioma U251, U87 radiotherapy resistance.Methods:X-ray gradual ascending and intermittent induction method was used to irradiate the glioma U251 cells to establish U251/TR, U87/TR radiation-resistant cell lines. Then, the morphology, migration, invasion and proliferation abilities of cells (U251/TR, U87/TR radiation-resistant cells and U251, U87 radiation-sensitive cells) were analyzed. Luciferase gene detection system and point mutation technique were employed to analyze the mechanism of miR-205-5p and E2F1 gene activity on U251 and U87 radiation-resistant cell lines.Results:Compared with the radiation-sensitive U251 cells, the radiation-resistant cells U251/TR, U87/TR showed increased proliferation activity, enhanced migration and invasion abilities and decreased apoptosis under X-ray irradiation. miR-205-5p mimics transfection could down-regulate the expression of E2F1 factor in U251/TR cells, inhibit cell proliferation, invasion and migration and increase the radiosensitivity of U251/TR cells. miR-205-5p mimics transfection combined with with E2F1 down-regulation exerted anti-tumor effect and decreased cell tolerance by suppressing the Wnt/β-catenin signaling pathway activity.Conclusions:The glioma radiation-resistant cell line U251/TR, U87/TR can be established by X-ray gradual ascending and intermittent induction method. The miR-205-5p/E2F1 signal axis exerts tumor-suppressing effect through the classical Wnt/β-catenin signaling pathway, which can be used as an therapeutic target to increase the radiosensitivity of glioma.
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Splicing factor Heterogeneous Nuclear Ribonucleoprotein A2/B1 (HNRNPA2B1 ) is associated with mouse lifespan and human longevity.It also plays a causal role in cancer development.However, whether it participates in cellular senescence, a biological process that contributes to individual aging and inhibits cancer, remains unknown.Here, we report that HNRNPA2B1 showed significantly increased expression in various cancer types while consistently decreased expression in multiple cellular senescence models.Knocking down HNRNPA2B1 in cancer cells leads to a series of senescence- associated phenotvpes.In line with its function as a splicing factor, HNRNPA2B1 downregulation causes alternative splicing changes in over one thousand genes, including those known to have a causal role in senescence.Our results also suggests that the E2F transcription factor 1 (E2F1 ) could regulate the expression of HNRNPA2BI, and E2F1-HNRNPA2B1 may be a new regulatory axis functioning in both cancer and cellular senescence, which might also have potential medical implications for cancer therapies.
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The cell cycle-related transcription factor E2F1 is a member of the cell cycle-related transcription factor E2F family, mainly involved in various cell processes including cell cycle progression, DNA repair, DNA replication, cell differentiation, proliferation, and apoptosis. E2F1 is highly expressed in a variety of tumor tissues and cells, and it plays a role as a cancer-promoting gene. The up-regulation of E2F1 expression is closely related to the occurrence, development, metastasis and prognosis of tumors. Therefore, E2F1 is expected to become a new target for cancer treatment. This article reviews the latest research progress of E2F1 in current common tumors. .
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Background: We assessed the frequency of epigenetic lesions, including lymphoid-specific helicase (LSH), 5-hydroxymethylcytosine (5-hmC) and E2F1, and the possible correlations among molecular findings, phenotype, clinical features, and outcome. Methods: We investigated 181 paraffin-embedded B-cell lymphoma samples using immunohistochemistry and in situ hybridization. Results: The levels of Ki67, LSH, 5-hmC, and E2F1 were all increased in germinal center B-cell lymphomas when compared with those in normal lymph nodes, and LSH was highly expressed in diffuse large B-cell lymphomas (DLBCLs) and Burkitt lymphomas (BLs) that were positive for Epstein-Barr virus (EBV) infection, indicating that LSH is linked to EBV infection in DLBCL and BL. Interestingly, LSH was mainly localized in the germinal centers of lymph nodes whereas 5-hmC staining localized to areas surrounding the germinal centers. Conclusions: These findings indicate a critical role for LSH as a biomarker and therapeutic target in follicular germinal center B-cell lymphoma.
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@# Objective: To investigate the correlation between the expression of E2F1 and growth arrest and DNA damage inducible protein 45g (GADD45g) in patients with acute myeloid leukemia (AML), and to explore whether GADD45g exerts its induction of DNA damage, cell apoptosis, senescence, cell cycle arrest and drug sensitivity in AML through inhibition of E2F1. Methods: A total of 32 cases of bone marrow specimens from patients initially diagnosed asAML in Hospital of Blood DiseasesAffiliated to ChineseAcademy of Medical Sciences from January 2013 to December 2016, were selected for this study; In addition, AML cell lines (U937, HL60, THP-1, Molm-13) were also collected for this study. The mRNAexpression of GADD45g and E2F1 in above mentioned specimens and cell lines by qPCR,andtheircorrelationwasalsoanalyzed.Thelentiviral vector over-expressing E2F1 (pLV-E2F1-RFP) was constructed to prepare recombinant lentivirus, which was then transfected Molm-13 and THP-1 cells that over-expressing GADD45g. Whether GADD45g exerts tumor inhibition effect on AML cells through inhibition of E2F1 was determined by comet assay, Annexin V/7AAD flow cytometry, β-galactosidase staining and PI staining flow cytometry etc. Results: The mRNA expression of GADD45g was negatively correlated with E2F1 in bone marrow of AML patients and AML cell lines (r=–0.663, P<0.01). Over-expression of GADD45g significantly inhibited the expression of E2F1 in AML cell lines (all P<0.01). Molm-13 and THP-1 cells that simultaneously over-expressing GADD45g and E2F1 were successfully constructed. Compared with the control group, the protein expressions of GADD45g and E2F1 in over-expression groups were significantly increased (all P<0.01). Compared with cells over-expressing GADD45g alone, simultaneous over-expression of both GADD45g and E2F1 significantly reduced the apoptosis, senescence and DNA damage (all P< 0.01), and rescued cell cycle arrest in Molm-13 and THP-1 cells (all P<0.01), thus further reduced the chemo-sensitivity of AML cells caused by GADD45g over-expression (all P<0.01). Conclusion: GADD45g exerts anti-tumor effect inAMLvia inhibition of E2F1.
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Objective@#To explore the regulatory mechanism of E2F1 transcription factor on M2 macrophages in full-thickness skin defect wounds of mice.@*Methods@#E2F1 gene knockout heterozygotes C57BL/6 mice and wild-type C57BL/6 mice were introduced and self-reproduced. Two weeks after birth, E2F1 gene knockout homozygotes mice and wild-type mice were identified by polymerase chain reaction (PCR). Twelve identified 6-8 weeks old male E2F1 gene knockout homozygotes C57BL/6 mice and wild-type C57BL/6 mice were selected respectively according to the random number table and set as E2F1 gene knockout group and wild-type group. A full-thickness skin defect wound was made on the back of each mouse. On post injury day (PID) 2 and 7, 6 mice in each group were selected according to the random number table and sacrificed, and the wound tissue was excised. The expression of CD68 and CD206 double positive M2 macrophages was observed by immunofluorescence method, and the percentage of CD206 positive cells was calculated. The protein expression of CD206 was detected by Western blotting. The mRNA expression of arginase 1 was detected by real-time fluorescent quantitative reverse transcription PCR (RT-PCR). Wound tissue specimens of the two groups on PID 7 were obtained, and the protein and mRNA expressions of peroxisome proliferator-activated receptor gamma (PPAR-γ) were detected by Western blotting and real-time fluorescent quantitative RT-PCR respectively. The above-mentioned experiments were repeated four times. Three specimens of wound tissue of mice in wild-type group on PID 7 were obtained to detect the relationship between E2F1 and PPAR-γ by co-immunoprecipitation and Western blotting, and this experiment was repeated two times. Data were processed with unpaired t test.@*Results@#The size of PCR products of E2F1 gene knockout homozygotes C57BL/6 mice and wild-type C57BL/6 mice were 227 and 172 bp respectively, which were the same as those of the designed DNA fragments. On PID 2 and 7, the number of CD68 and CD206 double positive M2 macrophages in the wound tissue of mice in E2F1 gene knockout group was more than that of wild-type group, and the percentages of CD206 positive cells in the wound tissue of mice in E2F1 gene knockout group were (0.234±0.032)% and (0.584±0.023)% respectively, which were significantly higher than (0.129±0.017)% and (0.282±0.071)% of wild-type group (t=3.29, 3.54, P<0.05). On PID 2 and 7, the protein expression of CD206 in the wound tissue of mice in E2F1 gene knockout group were 1.00±0.23 and 1.63±0.26 respectively, which were significantly higher than 0.43±0.06 and 0.97±0.08 of wild-type group (t=2.41, 2.45, P<0.05). On PID 2 and 7, the mRNA expressions of arginase 1 in the wound tissue of mice in E2F1 gene knockout group were 0.482±0.105 and 0.195±0.031 respectively, which were significantly higher than 0.163±0.026 and 0.108±0.017 of wild-type group (t=3.04, 2.86, P<0.05). On PID 7, the protein and mRNA expressions of PPAR-γ in the wound tissue of mice in E2F1 gene knockout group were 0.61±0.12 and 0.51±0.13 respectively, which were significantly higher than 0.20±0.04 and 0.20±0.04 of wild-type group (t=3.36, 2.86, P<0.05). On PID 7, detection of the wound tissue of mice in wild-type group showed that PPAR-γ had unidirectional effect on E2F1.@*Conclusions@#E2F1 transcription factor affects the polarization of M2 macrophages by inhibiting the expression of PPAR-γ, thereby inhibiting the healing process of full-thickness skin defect wounds in mice.
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Objective To study the effect of microRNA-320 (miR-320) targeting E2F1 gene on tumor glycometabolism in colorectal cancer.Methods The miR-320 expression level in colorectal cancer cell lines and cancer tissues was detected using quantitative real-time polymerase chain reaction (qRT-PCR).The binding sites of miR-320 and E2F1 were predicted by bioinformatics.Luciferase assay was used to detect the targeting regulation of miR-320 on E2F1.The relationship between E2F1 and miR-320 was verified in mRNA level and protein level.When the miR-320 in SW480 and LOVO ceils was up-regulated and the E2F1 was down-regulated,the changes of glycometabolism in tumor cells were analyzed using glucose/glucose oxidase kit and lactate test kit.Results The qRT-PCR results showed low expressions of miR-320 in colorectal cancer cell lines and cancer tissues (F =42.327,P ＜ 0.001;t =4.345,P =0.023).Luciferase assay showed that miR-320 could negatively regulate the expression of E2F1 (t =4.716,P =0.042).The expression levels of E2F1 protein and mRNA (t =4.780,P =0.041;t =5.506,P =0.031) confirmed that miR-320 could interact with E2F1 in LOVO and SW480 cells.Overexpression of miR-320 could reduce the contents of glucose (t =5.262,P=0.034;t =21.079,P=0.002) and lactic acid (t =9.609,P=0.011;t =18.582,P=0.003) in the cellular supematant in SW480 and LOVO ceils.Down-regulating the expression of E2F1 at the same time could enhance the inhibitory effect of miR-320 on glucose (t =5.128,P =0.036;t =5.089,P =0.037) and lactic acid (t =8.573,P =0.013;t =13.364,P =0.006).Conclusion E2F1 is the target gene of miR-320,and miR-320 can regulate the glycometabolism of colorectal cancer cells by targeting E2F1 gene.
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Objective To explore the effect of transcription factor E2F1 on the apoptosis of small cell cancer line H446. Methods Plamid vector- mediated E2F1 small hairpin RNA (shRNA) was used to silence E2F1 in H446 cell. RT-PCR and western-blot assay were used to detect the expressions of E2F1 and Bcl-2. The apoptosis rate in H446 cell line was detected by flow cytometry assay. Result E2F1 protein was suppressed in shRNA1-modified H446 cell. Sgnificant difference of the apoptosis was shown between E2F1 shRNA1 group and the other two groups. Additionaly, the expression of Bcl-2 protein increased in E2F1 shRNA1-modified cell line. Conclusions E2F1 is highly expressed in H446 small cell lung cancer cell line. E2F1 promotes apoptosis of H446 through upregulating Bcl-2 expression.
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The E2F-1 transcription factor is post-translationally modified and stabilized in response to various forms of DNA damage to regulate the expression of cell-cycle and pro-apoptotic genes. The sustained overexpression of E2F-1 is a characteristic feature of gastric cancer. In this study, we investigated the role of short hairpin RNA (shRNA) targeting E2F-1 gene on human gastric cancer MGC-803 cell growth in vivo, and preliminarily revealed the mechanism. Thus, we constructed recombinant pGCSIL-GFP-shRNA-E2F-1 lentiviral vector to knock down E2F-1 expression in human gastric cancer MGC-803 cells in vivo, and studied the effect of E2F-1 shRNA on growth of MGC-803 tumor and evaluated its treatment efficacy. Our data demonstrated that in a mouse model of established gastric cancer, intratumor injection of lentiviral shRNA targeting E2F-1 definitely decreased the endogenous E2F-1 mRNA and protein expression in MGC-803 tumor, and inhibited tumor growth and promoted tumor cells apoptosis. Moreover, we found that E2F-1 shRNA increased the expression of phosphatase and tensin homolog (PTEN), activated caspase-3 and caspase-9, and suppressed nuclear factor (NF)-kappaB expression in tumor tissue as determined by reverse transcription (RT)-PCR and western blotting. In summary, shRNA targeting of E2F-1 can effectively inhibits human gastric cancer MGC-803 cell growth in vivo and may be a potential therapeutic strategy for gastric cancer.
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Animaux , Humains , Mâle , Souris , Apoptose , Technique de Western , Caspase-3/métabolisme , Caspase-9/métabolisme , Cellules cultivées , Facteur de transcription E2F1/antagonistes et inhibiteurs , Vecteurs génétiques/administration et posologie , Lentivirus/génétique , Souris de lignée BALB C , Souris nude , Interférence par ARN , Petit ARN interférent/génétique , Tumeurs de l'estomac/génétiqueRÉSUMÉ
Objective To investigate the effect of morphine on the expression of p53 mRNA and E2F-1 mRNA in human gastric carcinoma cell line MGC-803 .Methods The human gastric cancer cell line MGC-803 was purchased from Cell Biology Research Institute, Chinese Academy of Sciences, and cultured in DMEM liquid culture mediun. The cells were seeded in 6-well plates (1 × 103/ml or 2 × 105/ml, 1 ml/well) and divided into 2 groups (n = 18 wells each):group Ⅰ normal control (group C); group Ⅱ was exposed to 10 μmol/L morphine (group M). The proliferation of the cells was determined by colony formation assay at 7 day of incubation with morphine. The expression of p53 mRNA and E2F-1 mRNA was detected and the ulrastructure of the cells examined with transmission electron microscope after being incubated with morphine for 24 h. Results The proliferation of the cells and E2F-1 mRNA expression were significantly lower and p53 mRNA expression was significantly higher in group M than in group C (P ＜ 0.05). The nuclear evelope was intact and the nucleolus and chromosomes were clearly visible in group C, while in group M fragmentation of nuclear envelope and nucleolus and apoptotic bodies were observed. Conclusion Morphine can inhibit the proliferation of the cells and accelerate the cell apoptosis through up-regulating the expression of p53 gene and down-regulating the expression of E2F-1gene in human gastric carcinoma cell line MGC-803.
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E2F1 plays a key role in cell-cycle regulation in mammals, since its transcription factor activity controls genes required for DNA synthesis and apoptosis. E2F1 deregulation is a common feature among different tumor types and can be a major cause of cell proliferation. Thus, blocking E2F1 expression by RNA interference represents a promising therapeutic approach. In this study, the introduction of specific short hairpin RNAs (shRNAs) reduced E2f1 expression by up to 77 percent, and impaired rat glioma cell proliferation by approximately 70 percent, as compared to control cells. Furthermore, we investigated the expression of E2f1 target genes, Cyclin A and Cyclin E. Cyclin A was found to be down-regulated, whereas Cyclin E had similar expression to control cells, indicating that gene(s) other than E2f1 control its transcription. Other E2f family members, E2f2 and E2f3, which have been classified in the same subgroup of transcriptional activators, were also analyzed. Expression of both E2f2 and E2f3 was similar to control cells, showing no cross-inactivation or up-regulation to compensate for the absence of E2f1. Nevertheless, their expression was insufficient to maintain the initial proliferation potential. Taken together, our results suggest that shE2f1 is a promising therapy to control tumor cell proliferation.
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The mechanism and interaction among Rb/p16,Rb/E2F1 and HDAC1 proteins in gallbladder carcinoma were investigated. By using the immunoprecipitation method,the interactions among Rb,pl6,E2F1,HDAC1 proteins in gallbladder carcinoma cell line (Mz-ChA-1) were studied.It was found that there were Rb and E2F1 proteins in the precipitates with anti-HDAC1,and there were HDAC1 and E2F1 proteins in the precipitate with anti-Rb. It was concluded that there are specific interactions among Rb,HDAC1 and E2F1 proteins in gallbladder carcinoma,indicating the existence of the direct Rb/E2F1/HDAC1 signal transduction pathway. There is no direct relationship between p16 proteins with Rb,HDAC1,and E2F1 proteins.
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OBJECTIVE: The aim of this study was to evaluate the correlation of E2F-1 and Ki-67 expression with clinicopathological prognostic factors. METHODS: Retrospectively, endometrial cancer slide samples (n=71) were analyzed. E2F-1 and Ki-67 were evaluated using immunohistochemical staining. And as a control (n=21), endometrial tissues were obtained by hysterectomy with benign gynecologic disease. RESULTS: Of 71 cases, the positive E2F-1 expression was 53.5% (38/71) in endometrial cancer. The expression of E2F-1 showed a remarkable positive correlation with myometrial invasion (P=0.001) and lymphovascular invasion (P=0.000). The Ki-67 labeling index was 30.56+/-25.67 in endometrial cancer and 9.38+/-8.35 in normal endometrial tissues (P=0.001). The Ki-67 labeling index showed positive correlations with increased tumor size (P=0.046, gamma=0.238), positive lymph node metastasis (P=0.001, gamma=0.396), cervical invasion (P=0.000, gamma=0.404) and lymphovascular tumor invasion (P=0.000, gamma=0.597). There was a positive correlation between E2F-1 and Ki-67 expression (P=0.000, gamma=0.734). CONCLUSION: The Ki-67 expression seems to be related with tumor invasiveness and growth in endometrial cancer and shows a remarkable positive correlation with E2F-1. The E2F-1 expression seems to be not related as a direct prognostic factor but related with tumor invasiveness and growth in endometrial cancer.
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Femelle , Tumeurs de l'endomètre , Hystérectomie , Noeuds lymphatiques , Métastase tumorale , Études rétrospectivesRÉSUMÉ
Objective To detect the expression of c-met (hepatocyte growth factor receptor), e2f-1 (transcription factor) and Ki-67 in tissues of gastric cancer, explore the relationship among them, and investigate their correlationship with clinicopathological characteristics and prognosis. Methods The tissue samples of gastric cancer from 86 patients with radical resection were subjected to immunohistochemical staining, and the expression of c-met, e2f-1 and Ki-67 was detected. The relationship between the clinicopathological characteristics and the expression of c-met, e2f-1 and Ki-67, and that among the expression of c-met, e2f-1 and Ki-67 were explored by univariate and multivariate data analysis. And the relationship between prognosis and expression of c-met, e2f-1 and Ki-67 was analysed by Log rank test. Results c-met, e2f-1 and Ki-67 were widely expressed in tissues of gastric cancer. The higher expression of c-met was associated with higher expression of Ki-67, shorter survival time, upper tumor location, higher lymph node metastasis rate, higher N stage and TNM stage (P<0.05), and the lower expression of e2f-1 was associated with larger tumor diameter, higher TNM stage, deeper invasion, higher lymph node metastasis rate and higher N stage (P<0.05). The multivariate analysis revealed that depth of invasion, N stage, TNM stage and expression of Ki-67 were independent factors for positive expression of c-met, and age and survival time were independent factors for positive expression of e2f-1. Log rank test demonstrated that the factors related to survival included expression of c-met, e2f-1 and Ki-67, N stage, tumor diameter, tumor location, lymph node metastasis rate, depth of invasion and TNM stage. Conclusion c-met is an indicator for malignant behavior and poorer prognosis of gastric cancer. There is a higher expression of e2f-1 in early gastric cancer, while advanced gastric cancer may be associated with a lower expression of e2f-1.
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Objective:To explore the relationship between the expressions of MCM5 and E2F-1 with the genesis,clinicopathological parameters of gastric carcinoma.Methods:Immunohistochemistry SP method was used to detect the expressions of MCM5 and E2F-1 in gastric car- cinoma tissues of 57 cases and in normal gastric mucosa of 20 cases.The correlation between expressions of MCM5 and E2F-1 and clinicopathological parameters of gastric carcinoma was analysed. Results:The positive expression rate of MCM5 in cancer tissues was 71.9%(41/57),while in normal mucosa it was 0(0/20).The difference between the two groups was statistically significant (P0.05).The correlation between MCM5 and E2F-1 expressions in gastric carcinoma was highly significant positive(r=0.635,P=0.000).Conclusion: Overexpression of MCM5 and E2F-1 corelates with occurence and development of gastric carcinoma.MCM5 and E2F-1 may work in the early phase in carcinogenesis of gastric carcinoma.
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BACKGROUND: E2F1 plays a critical role in the G1-to-S phase transition by inducing various genes that encode S phase-activating proteins and that modulate such diverse cellular functions as DNA synthesis, mitosis and apoptosis. The purpose of this study was to assess the E2F1 expression in relation to the clinicopathologic parameters and other tumor markers in gastrointestinal stromal tumors. METHODS: Immunohistochemical stainings for obtaining the E2F1, p53, and Ki-67 labeling indices were performed on a tissue microarray of 72 gastrointestinal stromal tumor specimens. The clinicopathologic parameters that were analyzed including the risk grade system by Miettinen et al. and the disease-free survival (DFS) rate. RESULTS: 1) An E2F1 expression was correlated with a larger tumor size, a p53 expression and a shorter period of DFS (p=0.014, p=0.007, and p=0.039). 2) A p53 expression was significantly associated with a high risk grade, a larger tumor size, high mitotic counts and a shorter period of DFS (p=0.003, p=0.044, p<0.001, and p<0.0001). 3) A high-risk grade and the epithelioid type were significantly associated with a shorter period of DFS (p=0.0006 and p=0.0008). CONCLUSIONS: E2F1, as well as p53, may be a potentially novel independent prognostic factor for predicting a worse outcome for those patients suffering with Gastrointestinal stromal tumors.
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Humains , Apoptose , Survie sans rechute , ADN , Facteur de transcription E2F1 , Tumeurs stromales gastro-intestinales , Immunohistochimie , Antigène KI-67 , Mitose , Transition de phase , Protéines , Stress psychologique , Marqueurs biologiques tumoraux , Protéine p53 suppresseur de tumeurRÉSUMÉ
OBJECTIVE: To evaluate the clinicopathological implications of Rb pathway alteration and E2F-1 expression in Epithelial ovarian cancer using immunohistochemical staining. METHODS: Tissue samples (n=72) were collected after staging operation between 1998 and 2004. RESULTS: In 72 cases, the overall expression of pRb, and E2F-1 were 59.7% (43/72), and 58.3% (42/72), respectively. pRb expression was inversely correlated with stage, histologic grade and mitotic index. E2F-1 expression was correlated with advanced stages, high grade, mitotic index, Ki-67 labeling index (LI). CONCLUSION: We suggest that Rb pathway alteration and E2F-1 expression could play roles as a new prognostic factors in Epithelial ovarian cancer.