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    E2F1 E2F transcription factor 1 [ Homo sapiens (human) ]

    Gene ID: 1869, updated on 21-May-2019

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    inhibition of hsa-mir183 reduced proliferation and impaired colony formation of CML SPCs. Downstream of this, inhibition of E2F1 also reduced proliferation of CML SPCs, leading to p53-mediated apoptosis. In addition, we demonstrate that E2F1 plays a pivotal role in regulating CML SPC proliferation status.

    <i>hsa-mir183/EGR1</i>-mediated regulation of E2F1 is required for CML stem/progenitor cell survival.
    Pellicano F, Park L, Hopcroft LEM, Shah MM, Jackson L, Scott MT, Clarke CJ, Sinclair A, Abraham SA, Hair A, Helgason GV, Aspinall-O'Dea M, Bhatia R, Leone G, Kranc KR, Whetton AD, Holyoake TL., Free PMC Article

    ANP32E is an efficient prognostic marker, and it promotes the G1/S transition and induces tumorigenesis of Triple-negative breast cancer cells by transcriptionally inducing E2F1.

    ANP32E induces tumorigenesis of triple-negative breast cancer cells by upregulating E2F1.
    Xiong Z, Ye L, Zhenyu H, Li F, Xiong Y, Lin C, Wu X, Deng G, Shi W, Song L, Yuan Z, Wang X., Free PMC Article

    identification of protumorigenic transcriptional networks specific to RB loss that were validated in clinical samples demonstrated the ability of RB loss to differentially reprogram E2F1 in human cancers.

    Differential impact of RB status on E2F1 reprogramming in human cancer.
    McNair C, Xu K, Mandigo AC, Benelli M, Leiby B, Rodrigues D, Lindberg J, Gronberg H, Crespo M, De Laere B, Dirix L, Visakorpi T, Li F, Feng FY, de Bono J, Demichelis F, Rubin MA, Brown M, Knudsen KE., Free PMC Article

    E2F1 enhances the invasion and metastasis of prostate cancer through a variety of mechanisms, and its expression level has an important relationship with the adverse prognosis of patients with prostate cancer

    [Effect of transcription factor E2F1 expression on the invasion of prostate cancer].
    Bi XC, Pu XY, Liu JM, Huang S.

    E2F1 requires cIAP1 for chromatin binding.

    E2F1 binds to the peptide-binding groove within the BIR3 domain of cIAP1 and requires cIAP1 for chromatin binding.
    Allègre J, Cartier J, Glorian V, Droin N, Dumetier B, Kayaci C, Berthelet J, Gemble S, Vuillier C, Maillet L, Garrido C, Dubrez L., Free PMC Article

    The authors predict that the induction of expression of RNASEH2A via human papillomavirus 16 E7 and E2F1 may promote DNA replication and cancer cell proliferation.

    Genome-Wide Profiling of Cervical RNA-Binding Proteins Identifies Human Papillomavirus Regulation of RNASEH2A Expression by Viral E7 and E2F1.
    Xu J, Liu H, Yang Y, Wang X, Liu P, Li Y, Meyers C, Banerjee NS, Wang HK, Cam M, Lu W, Chow LT, Xie X, Zhu J, Zheng ZM., Free PMC Article

    KPNA2 mediated nuclear localization of E2F1 and E2F7, where they in turn controlled KPNA2 expression. Taken together, our data provided mechanistic insights into divergently transcriptional regulation of KPNA2, thus pointing to KPNA2 as a potential target for cancer therapy.

    E2F1 and E2F7 differentially regulate KPNA2 to promote the development of gallbladder cancer.
    Xiang S, Wang Z, Ye Y, Zhang F, Li H, Yang Y, Miao H, Liang H, Zhang Y, Jiang L, Hu Y, Zheng L, Liu X, Liu Y.

    Study demonstrated that CDCA3 may target p21 to promote colorectal cancer (CRC) cell proliferation and tumorigenesis, at least partially in an E2F1-mediated manner, and that CDCA3 may serve as a potential prognostic and therapeutic target of CRC.

    CDCA3 mediates p21-dependent proliferation by regulating E2F1 expression in colorectal cancer.
    Qian W, Zhang Z, Peng W, Li J, Gu Q, Ji D, Wang Q, Zhang Y, Ji B, Wang S, Zhang D, Sun Y., Free PMC Article

    The network model simulations and experimental data indicate the ability of enhanced expression of both miR-205-5p and miR-342-3p to decrease tumor chemoresistance by cooperatively repressing E2F1.

    MiR-205-5p and miR-342-3p cooperate in the repression of the E2F1 transcription factor in the context of anticancer chemotherapy resistance.
    Lai X, Gupta SK, Schmitz U, Marquardt S, Knoll S, Spitschak A, Wolkenhauer O, Pützer BM, Vera J., Free PMC Article

    E2F1 interacts with BCL-xL independently from its BH3 binding interface and induces a stabilization of BCL-xL at mitochondrial membranes. This prevents efficient control of BCL-xL over its binding partners, in particular over BAK resulting in the induction of cell death.

    E2F1 interacts with BCL-xL and regulates its subcellular localization dynamics to trigger cell death.
    Vuillier C, Lohard S, Fétiveau A, Allègre J, Kayaci C, King LE, Braun F, Barillé-Nion S, Gautier F, Dubrez L, Gilmore AP, Juin PP, Maillet L., Free PMC Article

    ANKRD22 exhibits oncogene activity that promotes tumor progression in NSCLC through the transcriptional regulation of E2F1.

    ANKRD22 promotes progression of non-small cell lung cancer through transcriptional up-regulation of E2F1.
    Yin J, Fu W, Dai L, Jiang Z, Liao H, Chen W, Pan L, Zhao J., Free PMC Article

    finding supports that DLX6-AS1 accelerates the glioma carcinogenesis by competing endogenous sponging miR-197-5p to relieve E2F1, acting as a novel therapeutic target for glioma.

    Long noncoding RNA DLX6-AS1 accelerates the glioma carcinogenesis by competing endogenous sponging miR-197-5p to relieve E2F1.
    Li X, Zhang H, Wu X.

    XPC is an RNA polymerase II cofactor recruiting ATAC coactivator complex to promoters by interacting with E2F1.

    XPC is an RNA polymerase II cofactor recruiting ATAC to promoters by interacting with E2F1.
    Bidon B, Iltis I, Semer M, Nagy Z, Larnicol A, Cribier A, Benkirane M, Coin F, Egly JM, Le May N., Free PMC Article

    Our findings reveal that the rs3213173 (C/T) and rs3213176 (G/A) polymorphisms of the E2F1 gene are genetic risk factors for susceptibility to lung cancer and Head and Neck cancer in the North Indian Population.

    The Nonsynonymous Polymorphisms Val276Met and Gly393Ser of E2F1 Gene are Strongly Associated with Lung, and Head and Neck Cancers.
    Singh S, Gupta M, Sharma A, Seam RK, Changotra H.

    CacyBP expression is regulated by E2F1, EGR1, and CREB transcription factors in colorectal cancer HCT116 cells.

    Transcriptional regulation of CacyBP/SIP gene and the influence of increased CacyBP/SIP level on gene expression pattern in colorectal cancer HCT116 cells.
    Kądziołka B, Dębski KJ, Bieganowski P, Leśniak W, Filipek A.

    High E2F1 expression is associated with hepatocellular carcinoma progression.

    SET7/9 promotes hepatocellular carcinoma progression through regulation of E2F1.
    Gu Y, Wang X, Liu H, Li G, Yu W, Ma Q., Free PMC Article

    the expression of miR175p inhibited high glucoseinduced endothelial cell injury by targeting E2F1.

    Overexpression of miR‑17‑5p protects against high glucose‑induced endothelial cell injury by targeting E2F1‑mediated suppression of autophagy and promotion of apoptosis.
    Yuan Y, Li X, Li M.

    The nuclear transcription factor Y subunit beta (NFYB)-E2F transcription factor 1 (E2F1) pathway displays a crucial role in the chemoresistance ofoxaliplatin-resistant colorectal cancer (OR-CRC) by inducing the expression and activation of checkpoint kinase 1 (CHK1), suggesting a possible therapeutic target for oxaliplatin resistance in CRC.

    NFYB-induced high expression of E2F1 contributes to oxaliplatin resistance in colorectal cancer via the enhancement of CHK1 signaling.
    Fang Z, Gong C, Yu S, Zhou W, Hassan W, Li H, Wang X, Hu Y, Gu K, Chen X, Hong B, Bao Y, Chen X, Zhang X, Liu H.

    If, as expected, the consequences of the deregulation of the CDKN1C-E2F1-TP53 axis were the same as those experimentally demonstrated in mouse models, the disruption of this axis might be useful to predict tumor aggressiveness, and to provide the basis towards the development of potential therapeutic strategies in human Precursor T-cell lymphoblastic lymphomas

    RNA-Seq reveals the existence of a CDKN1C-E2F1-TP53 axis that is altered in human T-cell lymphoblastic lymphomas.
    López-Nieva P, Fernández-Navarro P, Vaquero-Lorenzo C, Villa-Morales M, Graña-Castro O, Cobos-Fernández MÁ, López-Lorenzo JL, Llamas P, González-Sanchez L, Sastre I, Pollan M, Malumbres M, Santos J, Fernández-Piqueras J., Free PMC Article

    Antitumor effect of lapatinib and cytotoxic agents by suppression of E2F1 in HER2positive breast cancer.

    Antitumor effect of lapatinib and cytotoxic agents by suppression of E2F1 in HER2‑positive breast cancer.
    Matsumoto A, Hayashida T, Takahashi M, Jinno H, Kitagawa Y.

    Data show that mRNA translation stress induces E2F transcription factor 1 (E2F1) via PI3-kinase p110 subunit delta (PI3Kdelta).

    PI3Kδ activates E2F1 synthesis in response to mRNA translation stress.
    Gnanasundram SV, Pyndiah S, Daskalogianni C, Armfield K, Nylander K, Wilson JB, Fåhraeus R., Free PMC Article

    PPM1B plays a negative role in the activation of the p38-RB1-E2F1 pathway and that targeting PPM1B could be useful in certain types of cancer by stimulating chemotherapy-induced cell death.

    PPM1B depletion in U2OS cells supresses cell growth through RB1-E2F1 pathway and stimulates bleomycin-induced cell death.
    Miller RE, Uwamahoro N, Park JH.

    Studied impact of BET proteins and E2F transcription factor 1 (E2F1) in neoplastic genetic transcription in glioblastoma.

    Targetable BET proteins- and E2F1-dependent transcriptional program maintains the malignancy of glioblastoma.
    Xu L, Chen Y, Mayakonda A, Koh L, Chong YK, Buckley DL, Sandanaraj E, Lim SW, Lin RY, Ke XY, Huang ML, Chen J, Sun W, Wang LZ, Goh BC, Dinh HQ, Kappei D, Winter GE, Ding LW, Ang BT, Berman BP, Bradner JE, Tang C, Koeffler HP., Free PMC Article

    E2F1 knockdown decreased the expression of discoidin domain receptor 1 (DDR1) which plays a crucial role in many fundamental processes such as cell differentiation, adhesion, migration and invasion.

    E2F1 silencing inhibits migration and invasion of osteosarcoma cells via regulating DDR1 expression.
    Wang Z, Sun X, Bao Y, Mo J, Du H, Hu J, Zhang X., Free PMC Article

    Our data imply that downregulation of E2F1 may be a key factor in the celastrol-mediated inhibitory effects in HepG2 cells, and celastrol can serve as a leading compound for the development of compounds designed to inactivate E2F1 for hepatocellular carcinoma therapy

    Celastrol downregulates E2F1 to induce growth inhibitory effects in hepatocellular carcinoma HepG2 cells.
    Ma L, Peng L, Fang S, He B, Liu Z.

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