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Distinctive and complementary roles of e2f transcription factors during plant replication stress responses

Molecular Plant 2023年第8期16卷 1269-1282页

作者： Maherun Nisa Thomas eekhout Clara Bergis Jose-Antonio Pedroza-Garcia Xiaoning He Christelle Mazubert Ilse Vercauteren Toon Cools Rim Brik-Chaouche Jeannine Drouin-Wahbi Layla Chmaiss David Latrasse Catherine Bergounioux Klaas Vandepoele Moussa Benhamed Lieven De Veylder Cécile Raynaud Universite Paris-Saclay CNRSINRAEUniversite EvryInstitute of Plant Sciences Paris-Saclay(IPS2)91190 Gif-sur-YvetteFrance Universite de Paris Cite CNRSINRAEInstitute of Plant Sciences Paris-Saclay(IPS2)91190 Gif-sur-YvetteFrance Department of Plant Biotechnology and Bioinformatics Ghent University9052 GhentBelgium Center for Plant Systems Biology VIB9052 GhentBelgium Present address:Plant Molecular and Cellular Biology Laboratory Salk Institute for Biological StudiesLa JollaCA 92037USA

Survival of living organisms is fully dependent on their maintenance of genome integrity,being permanently threatened by replication stress in proliferating *** the plant DNA damage response(DDR)regulator SOG1 has been demonstrated to cope with replication defects,accumulating evidence points to other pathways functioning independent of ***,we report the roles of the Arabidopsis e2fA and ef2B transcription factors,two well-characterized regulators of DNA replication,in plant response to replication *** a combination of reverse genetics and chromatin immunoprecipitation approaches,we show that e2fA and e2fB share many target genes with SOG1,providing evidence for their involvement in the *** of double-and triple-mutant combinations revealed that e2fB,rather than e2fA,plays the most prominent role in sustaining plant growth in the presence of replication defects,either operating antagonistically or synergistically with ***,SOG1 aids in overcoming the replication defects of e2fA/e2fB-deficient ***,our data reveal a complex transcriptional network controlling the replication stress response in which e2fs and SOG1 act as key regulatory factors.

关键词： replication stress e2f SOG1 cell cycle Arabidopsis

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e2f transcription factors and digestive system malignancies: How much do we know?

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World Journal of Gastroenterology 2013年第21期19卷 3189-3198页

作者： Athanasios Xanthoulis Dina G Tiniakos Department of Surgery Section of Gastroenterological SurgeryLevanger HospitalNord-Tr ndelag Hospital Trust7600 LevangerNorway Laboratory of Histology-embryology Medical SchoolNational and Kapodistrian University of Athens11527 AthensGreece

e2f family of transcription factors regulates various cellular functions related to cell cycle and apoptosis. Its individual members have traditionally been classified into activators and repressors, based on in vitro studies. However their contribution in human cancer is more complicated and difficult to predict. We review current knowledge on the expression of e2fs in digestive system malignancies and its clinical implications for patient prognosis and treatment. e2f1, the most extensively studied member and the only one with prognostic value, exhibits a tumor-suppressing activity in esophageal, gastric and colorectal adenocarcinoma, and in hepatocellular carcinoma (HCC), whereas in pancreatic ductal adenocarcinoma and esophageal squamous cell carcinoma may function as a tumorpromoter. In the latter malignancies, e2f1 immunohistochemical expression has been correlated with higher tumor grade and worse patient survival, whereas in esophageal, gastric and colorectal adenocarcinomas is a marker of increased patient survival. e2f2 has only been studied in colorectal cancer, where its role is not considered significant. e2f4's role in colorectal, gastric and hepatic carcinogenesis is tumor-promoting. e2f8 is strongly upregulated in human HCC, thus possibly contributing to hepatocarcinogenesis. Adenoviral transfer of e2f as gene therapy to sensitize pancreatic cancer cells for chemotherapeutic agents has been used in experimental studies. Other therapeutic strategies are yet to be developed, but it appears that targeted approaches using e2f-agonists or antagonists should take into account the tissue-dependent function of each e2f member. further understanding of e2fs' contribution in cellular functions in vivo would help clarify their role in carcinogenesis.

关键词： e2f Colorectal cancer Gastric cancer esophageal cancer Pancreatic cancer Hepatocellular carcinoma Digestive system malignancies

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e2f transcription factors and digestive system malignancies:How much do we know?

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World Journal of Gastroenterology 2014年第29期20卷 10212-10216页

作者： Konstantinos evangelou Sophia Havaki Athanassios Kotsinas Laboratory Histology-embryology Medical SchoolNational and Kapodistrian University of Athens

The e2f proteins comprise a family of 8 members that function as transcription factors. They are key targets of the retinoblastoma protein (RB) and were initially divided into groups of activators and repressors. Accumulating data suggest that there is no specific role for each individual e2f member. Instead, each e2f can exert a variety of cellular effects, some of which represent opposing ones. for instance, specific e2fs can activate transcription and repression, promote or hamper cell proliferation, augment or inhibit apoptosis, all being dependent on the cellular context. This complexity reflects the importance that these transcription factors have on a cell’s fate. Thus, delineating the specific role for each e2f member in specific malignancies, although not easy, is a challenging and continuously pursued task, especially in view of potential e2f targeted therapies. Therefore, several reviews are continuously trying to evaluate available data on e2f status in various malignancies. Such reviews have attempted to reach a consensus, often in the simplistic form of oncogenes or tumor suppressor genes for the e2fs. However they frequently miss spatial and temporal alterations of these factors during tumor development, which should also be considered in conjunction with the status of the regulatory networks that these factors participate in. In the current ‘‘Letter to the editor’’, we comment on the flaws, misinterpretations and omissions in one such review article published recently in the World Journal of Gastroenterology regarding the role of e2fs in digestive system malignancies.

关键词： e2f Hepatocellular carcinoma Pancreatic ductal adenocarcinoma Gastrointestinal tract Digestive system p53 p73 Cancer Apoptosis Proliferation

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e2f transcription factors and their complementary roles during DNA damage responses

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Molecular Plant 2023年第9期16卷 1373-1375页

作者： Paula Casati Centro de estudios fotosinteticos y Bioquimicos(CefOBl) Universidad Nacional de RosarioSuipacha 5312000 RosarioArgentina

e2f transcription factors(Tf)comprise a family of proteins that regulate the expression of genes required for S-phase progression,among *** genome encodes six e2f Tfs(e2fA–f),which are classified as typical(e2fA–C)and atypical(e2fD–f)depending on their ability to interact with two DP interaction proteins(DPa and DPb)(Sablowski and Gutierrez,2022).While e2fA–C need to heterodimerize with either DPa or DPb to function,e2fD–f act independently of DP ***,the retinoblastoma-related1(RBR1)protein also binds and inhibits the typical e2f/DP Tf complexes when bound to the promoter of genes,repressing their expression in the absence of a signal to enter a new cell *** general,e2fA and e2fB are considered transcriptional activators,while e2fC is generally considered a repressor of cell proliferation(Sablowski and Gutierrez,2022).In addition,it is well documented that e2fB at least,and probably e2fA,can also stimulate the G2/M transition.

关键词： damage e2f complementary

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Non-Canonical functions of the e2f/DP Pathway with emphasis in Plants

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Phyton-International Journal of experimental Botany 2021年第2期90卷 307-330页

作者： Víctor A.Sánchez-Camargo Samantha Romero-Rodríguez Jorge M.Vázquez-Ramos facultad de Química Departamento de BioquímicaUniversidad Nacional Autónoma de MéxicoAvenida Universidad y CopilcoCiudad de México04510México Plant Development and(epi)Genetics Group Swammerdam Institute for Life SciencesUniversiteit van AmsterdamAmsterdam1098XHNetherlands

The e2f/DP pathway is a widely conserved regulatory mechanism in pluricellular *** family of e2f and DP transcription factors was originally described having a role in the transition from the G1 to the S phase of the cell ***,the discovery of hundreds of possible gene targets and their involvement in many other biochemical processes,soon showed that they participated in cell development and differentiation,chromatin remodeling,DNA repair and *** e2f/DP transcription factors can act as either activators or repressors of transcription depending on their association to other regulatory proteins,particularly the retinoblastoma protein,or even depending to their protein structure that can define their *** plants the e2f/DP pathway also regulates endoreduplication,a process present along the life cycle,from organ elongation to root differentiation and *** transcription factors also help plant cells to respond to environmental disturbances such as those caused by different types of radiation,or by *** review focuses on the“so called”non-canonical functions of the e2f/DP family proteins in animal and plant cells,that are in fact essential activities that connect regulatory circuits among multiple metabolic pathways by means of their atypical functions.

关键词： e2f DP transcription factors atypical functions plant cells

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SeNeX gene promotes cell proliferation by activating RB/e2f pathway in diffuse large B-cell lymphoma cells

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BIOCeLL 2021年第4期45卷 933-942页

作者： JIYU WANG YING PAN YANG WAN ZHIXIANG WANYAN ZHITAO WANG QIANSHAN TAO ZHIMIN ZHAI Department of Hematology The Second Hospital of Anhui Medical UniversityHefei230601China

The present study aimed to clarify the role of SeNeX in malignant cell proliferation in diffuse large B-cell lymphoma(DLBCL).22 DLBCL patients(6 newly diagnosed cases,7 cases at complete remission,and 9 relapsed cases)were included in the *** results indicated that both SeNeX gene and protein were significantly increased in peripheral blood mononuclear cells(PBMCs)and tumor cells of relapsed DLBCL patients,accompanied by overexpression of p21,p16,and phosphorylated retinoblastoma(Rb).Silencing the SeNeX gene in a DLBCL cell line caused a significant decrease in cell proliferation and inhibited cell cycle progression in the G1 *** Rb and e2f1 were also decreased,and activation of the Rb/e2f1 pathway was obviously *** conclude,the SeNeX gene promotes proliferation in PBMC and tumor cells of DLBCL patients by activating the Rb/e2f1 pathway,in a manner suggesting that increased SeNeX expression affects the relapse of DLBCL and may serve as an important target for DLBCL therapy.

关键词： SeNeX DLBCL Cell proliferation Rb e2f

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Different Patterns of Cyclin D1/CDK4-e2f-1/4 Pathways in Human embryo Lung fibroblasts Treated by Benzo[a]pyrene at Different Doses

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Biomedical and environmental Sciences 2008年第1期21卷 30-36页

作者： MeNG Ye BING-CI LIU XIANG-LIN SHI BAO-RONG YOU HONG-JU DU XIAO-WeI JIA fU-HAI SHeN National Institute of Occupational Health and Poison Control Chinese Center for Disease Control and Prevention 29 Nanwei Road Beijing 100050 China Shanghai Institute for Nutritional Sciences Chinese Academy of Sciences 249 Taiyuan Road Shanghai 200031 China

Objective To investigate the roles of the cyclin D1/CDK4 and e2f-1/4 pathways and compare their work patterns in cell cycle changes induced by different doses of B[a]e Methods Human embryo lung fibroblasts （HeLfs） were treated with 2 μmol/L or 100 μmol/L B[a]P which were provided with some characteristics of transformed cells （T-HeLfs）. Cyclin D l, CDK4 and e2f-1/4 expressions were determined by Western blotting. flow cytometry was used to detect the distribution of cell cycle. Results After B[a]P treatment, the proportion of the first gap （G 1） phase cells decreased. CDK4 and e2f-4 expression did not change significantly. In 2 μmol/L treated cells, a marked overexpression of cyclin D1 and e2f-1 was observed. However, in T-HeLfs overexpression was limited to cyclin D1 only, and no overexpression of e2f-1 was observed. The decreases of G1 phase in response to B[a]P treatment were blocked in antisense cyclin D1 and antisense CDK4 transfected HeLfs （A-D1 and A-K4） and T-HeLfs （T-A-D1 and T-A-K4）. After 2 μmol/L B[a]P treatment, overexpression of e2f-1 was attenuated in A-D1, and e2f-4 expression was decreased significantly in A-K4. In T-A-D1 and T-A-K4, e2f-4 expression was increased significantly, compared with T-HeLfs. The e2f-1 expression remained unchanged in T-A-D1 and T-A-K4. Condusions Cyclin DI/CDK4-e2f-1/4 pathways work in different patterns in response to low dose and high dose B[a]P treatment. In HeLfs treated with 2 μmol/L B[a]P, cyclin D1 positively regulates the e2f-1 expression while CDK4 negatively regulates the e2f-4 expression; however, in HeLfs treated with 100 μmol/L B[a]P, both cyclin D1 and CDK4 negatively regulate the e2f-4 expression.

关键词： Benzo[a]pyrene Cyclin D1 CDK4 e2f Cell cycle

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MicroRNA-let-7a promotes e2f-mediated cell proliferation and NfKB activation in vitro

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Cellular & Molecular Immunology 2014年第1期11卷 79-93页

作者： Cristen B Chafin Nicole L Regna David L Caudell Christopher M Reilly Department of Biomedical Sciences & Pathobiology Virginia-Maryland Regional College of Veterinary Medicine Virginia Polytechnic Institute and StateUniversity Blacksburg VA USA Department of Pathology/Comparative Medicine Wake Forest University Primate Center Wake Forest School ofMedicine Winston-Salem NC USA edward Via College of Osteopathic Medicine Blacksburg VA USA

epigenetic factors, including altered microRNA （miRNA） expression, may contribute to aberrant immune cell function in systemic lupus erythematosus （SLe）. MiRNA-let-7a （let-7a） has been shown to directly alter cell cycle progression and proinflammatory cytokine production. Due to the crucial role of let-7a in cell division and inflammation, we investigated let-7a-mediated proliferation and NfKB translocation in J774A. 1 macrophages and MeS 13 mesangial cells in vitro. In immune-stimulated cells transfected with let-7a, cell proliferation was significantly increased over time. There was a significant increase in the number of immune-stimulated cells in S and G2 phases. Immune-stimulated cells overexpressing let-7a had increased nuclear translocation of NfKB. Bioinformatical analysis revealed that the e2f family, critical regulators of the G1-S transition, has potential binding sites for let-7a in their mRNA transcripts. Let-7a overexpression significantly increased the expression of the cell cycle activator e2f2 and increased retinoblastoma protein （Rb） phosphorylation in immune-stimulated cells. The cell cycle inhibitor e2f5 was significantly decreased in let-7a-transfected cells that were immune-stimulated. Bioinformatical analysis revealed e2f2 and NfKB are transcription factors predicted to regulate the let-7a promoter. We analyzed transcriptional regulation of let-7a by real-time RT-PCR using chromatin immunoprecipitation with e2f2 and NfKB antibodies. There was an increase in e2f2 and NfKB binding in DNA enriched for the let-7a promoter in immune-stimulated cells. Silencing e2f2 or NfKB significantly decreased let-7a expression and IL-6 production in immune-stimulated cells. Taken together, our results suggest that overexpression of let-7a may contribute to hyperplasia and the proinflammatory response in SLe.

关键词： cell proliferation e2f microRNA-let-7a Nf~:B systemic lupus erythematosus

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Vitamin C Inhibits Benzo[a]pyrene-Induced Cell Cycle Changes Partly via Cyclin D1/e2f Pathway in Human embryo Lung fibroblasts

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Biomedical and environmental Sciences 2006年第3期19卷 239-244页

作者： AI GAO BING-CI LIU XIANG-LIN SHI CHUAN-SHU HUANG XIAO-WeI JIA BAO-RONG YOU MeNG Ye fU-HAI SHeN HONG-JU DU National Institute of Occupation Health and Poison Control Chinese Center for Disease Control and Prevention Beijing 100050 China National Institute for Occupational Safety and Health 1095 Willowdale RoadMorgantown WV26506 USA Nelson Institute of environmental Medicine New York University School of Medicine 57 Old Forge Road Tuxedo NY 10987

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

关键词： B[a]P Ascorbic acid Cyclin D1 e2f Cell cycle Antisense

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Dialogue between estrogen receptor and e2f signaling pathways: The transcriptional coregulator RIP140 at the crossroads

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Advances in Bioscience and Biotechnology 2013年第10期4卷 45-54页

作者： Marion Lapierre Aurélie Docquier Audrey Castet-Nicolas Stéphan Jalaguier Catherine Teyssier Patrick Augereau Vincent Cavaillès IRCM—Institut de Recherche en Cancérologie de Montpellier Montpellier France

estrogen receptors and e2f transcription factors are the key players of two nuclear signaling pathways which exert a major role in oncogenesis, particularly in the mammary gland. Different levels of dialogue between these two pathways have been deciphered and deregulation of the e2f pathway has been shown to impact the response of breast cancer cells to endocrine therapies. The present review focuses on the transcriptional coregulator RIP140/NRIP1 which is involved in several regulatory feed-back loops and inhibitory cross-talks between different nuclear signaling pathways. RIP140 regulates the transactivation potential of estrogen receptors and e2fs and is also a direct transcriptional target of these transcription factors. Published data highlight the complex regulation of RIP140 expression at the transcriptional level and its potential role in transcription cross-talks. Indeed, a subtle regulation of RIP140 expression levels has important consequences on other transcription networks targeted by this coregulator. Another level of regulation implies titration mechanisms by which activation of a pathway leads to sequestration of the RIP140 protein and thus impinges other gene regulatory circuitries. Altogether, RIP140 occupies a place of choice in the dialogue between nuclear receptors and e2fs, which could be highly relevant in various human pathologies such as cancer or metabolic diseases.

关键词： RIP140 e2f Transcription factors estrogen Receptors Gene expression Cell Proliferation Breast Cancer endocrine Therapies

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