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    E6 E6 [ Human papillomavirus type 16 ]

    Gene ID: 1489078, updated on 20-May-2017

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    Collectively, these results indicate that human papillomavirus 16 E6 induces upregulation of APOBEC3B through increased levels of TEADs, highlighting the importance of the TEAD-APOBEC3B axis in carcinogenesis.

    Human Papillomavirus 16 E6 Upregulates APOBEC3B via the TEAD Transcription Factor.
    Mori S, Takeuchi T, Ishii Y, Yugawa T, Kiyono T, Nishina H, Kukimoto I.,

    A transcriptomic landscape of human papillomavirus 16 E6-regulated gene expression and splicing events in cervical cancer patients has been presented.

    A transcriptomic landscape of human papillomavirus 16 E6-regulated gene expression and splicing events.
    Xu J, Fang Y, Qin J, Chen X, Liang X, Xie X, Lu W.

    The ubiquitylation of beta-catenin by E6AP was dependent on its E3 ubiquitin ligase activity, but it was proteasome-independent and did not require HPV16-E6.

    Ubiquitin ligase E6AP mediates nonproteolytic polyubiquitylation of β-catenin independent of the E6 oncoprotein.
    Kuslansky Y, Sominsky S, Jackman A, Gamell C, Monahan BJ, Haupt Y, Rosin-Arbesfeld R, Sherman L.

    nucleotide changes in E6 occur significantly more often in the mixed form of viral DNA and in low-grade squamous intraepithelial lesions; and the variants without additional mutations may promote integration of HPV16 genome.

    HPV16 E6 polymorphism and physical state of viral genome in relation to the risk of cervical cancer in women from the south of Poland.
    Szostek S, Zawilinska B, Klimek M, Kosz-Vnenchak M.

    We also found VPA suppressed oncogene E6 in a Notch-independent manner, and induced significant apoptosis in E6-overexpressing HPV positive CaSki cells.

    Valproic acid exhibits different cell growth arrest effect in three HPV-positive/negative cervical cancer cells and possibly via inducing Notch1 cleavage and E6 downregulation.
    Feng S, Yang Y, Lv J, Sun L, Liu M.

    Data show that alpha-linolenic acid (ALA) decreased the expression of VEGF and COX2 proteins, and reduced the expression of Human papillomavirus type 16/18 onco-proteins E6 and E7, resulting into restoration of expression of tumor suppressor proteins, p53 and Rb in cervical cancer cell lines.

    Alpha-linolenic acid regulates Cox2/VEGF/MAP kinase pathway and decreases the expression of HPV oncoproteins E6/E7 through restoration of p53 and Rb expression in human cervical cancer cell lines.
    Deshpande R, Mansara P, Kaul-Ghanekar R.

    Expression changes of E6 and E7 significantly promoted the protein expression of HIF-1alpha, the expression of both protein and mRNA of GLUT1, but had no effect on the expression of HIF-1alpha mRNA in lung cancer cells.

    Overexpression of HPV16 E6/E7 mediated HIF-1α upregulation of GLUT1 expression in lung cancer cells.
    Fan R, Hou WJ, Zhao YJ, Liu SL, Qiu XS, Wang EH, Wu GP.

    our results suggest that ERK1/2 signaling pathway is involved in HPV-16 E6 but not E7 oncoprotein-induced HIF-1a, VEGF, and IL-8 expression in NSCLC cells, leading to the enhanced angiogenesis in vitro.

    ERK Signaling Pathway Is Involved in HPV-16 E6 but not E7 Oncoprotein-Induced HIF-1α Protein Accumulation in NSCLC Cells.
    Liu F, Lin B, Liu X, Zhang W, Zhang E, Hu L, Ma Y, Li X, Tang X.

    Our data suggest that the use of HPV 16 spliced transcripts may help to predict for poorer outcomes in patients with HPV positive oropharyngeal cancer

    E6 viral protein ratio correlates with outcomes in human papillomavirus related oropharyngeal cancer.
    Hong A, Zhang X, Jones D, Zhang M, Lee CS, Lyons JG, Veillard AS, Rose B., Free PMC Article

    Within the limitations of this study, the immunoexpression of HPV 16/18 E6 and E7 oncoproteins may have prognostic value regarding cervical squamous intraepithelial lesions persistence in HIV-positive women.

    Immunoexpression of HPV 16/18 E6 and E7 oncoproteins in high-grade cervical squamous intraepithelial lesions in HIV-positive women.
    Rodrigues LC, Speck NM, Focchi GR, Schimidt MA, Marques RM, Ribalta JC.

    HPV16 E6/E7 Oncoproteins Alter the In Vitro Growth of CD44+NGFR+ Human Tonsillar Epithelial Cells.

    Characterization of Epithelial Progenitors in Normal Human Palatine Tonsils and Their HPV16 E6/E7-Induced Perturbation.
    Kang SY, Kannan N, Zhang L, Martinez V, Rosin MP, Eaves CJ., Free PMC Article

    Human papillomavirus type 16 E6 protein, a major etiological molecule of cervical cancer, maintains high YAP protein levels in cervical cancer cells by preventing proteasome-dependent YAP degradation to drive cervical cancer cell proliferation.

    The Hippo/YAP pathway interacts with EGFR signaling and HPV oncoproteins to regulate cervical cancer progression.
    He C, Mao D, Hua G, Lv X, Chen X, Angeletti PC, Dong J, Remmenga SW, Rodabaugh KJ, Zhou J, Lambert PF, Yang P, Davis JS, Wang C., Free PMC Article

    E6 and E7 have roles in methylation of tumor suppressor genes and inducing phenotype transformation of human cervical carcinoma cells

    E6 and E7 gene silencing results in decreased methylation of tumor suppressor genes and induces phenotype transformation of human cervical carcinoma cell lines.
    Li L, Xu C, Long J, Shen D, Zhou W, Zhou Q, Yang J, Jiang M., Free PMC Article

    Here we demonstrate that E7, and to a lesser extend E6, strongly reduce NFkappaB activation in response to the inflammatory mediator imiquimod. Moreover, we establish that undifferentiated keratinocytes do not express the putative receptor for imiquimod, TLR7

    The human papillomavirus (HPV) E7 protein antagonises an Imiquimod-induced inflammatory pathway in primary human keratinocytes.
    Richards KH, Wasson CW, Watherston O, Doble R, Blair GE, Wittmann M, Macdonald A., Free PMC Article

    The data indicate for the first time that increased cytoplasmic human papillomavirus type 16 E6 levels associated with malignant progression alter Cx43 trafficking and recycling to the membrane and the E6/human Dlg interaction may be involved.

    HPV16 E6 Controls the Gap Junction Protein Cx43 in Cervical Tumour Cells.
    Sun P, Dong L, MacDonald AI, Akbari S, Edward M, Hodgins MB, Johnstone SR, Graham SV., Free PMC Article

    High-risk HPV-type lesions might inhibit the chemokine CCL20 on Langerhans cells through E6 and E7 to escape the immune response.

    Correlation of E6 and E7 levels in high-risk HPV16 type cervical lesions with CCL20 and Langerhans cells.
    Jiang B, Xue M.

    E6 protein functioning as a host miRna modulator and play a role of HPV induced carcinogenesis in patient diagnosed with cervical cancer.

    Human papillomavirus 16 E6 modulates the expression of host microRNAs in cervical cancer.
    Ben W, Yang Y, Yuan J, Sun J, Huang M, Zhang D, Zheng J.

    Data show that ectopic co-expression of HPV16 E6 with human papillomavirus type 16 (HPV 16) E6-binding peptide pep11 variants leads to increased E6 protein levels.

    Intracellular Analysis of the Interaction between the Human Papillomavirus Type 16 E6 Oncoprotein and Inhibitory Peptides.
    Stutz C, Reinz E, Honegger A, Bulkescher J, Schweizer J, Zanier K, Travé G, Lohrey C, Hoppe-Seyler K, Hoppe-Seyler F., Free PMC Article

    E6-HPV16/E7-HPV16 promoted the activity of MT1-MMP and MMP-2/9, contributing to the migration of cervical cells and neoplasm invasiveness.

    E6/E7 oncoproteins of high risk HPV-16 upregulate MT1-MMP, MMP-2 and MMP-9 and promote the migration of cervical cancer cells.
    Zhu D, Ye M, Zhang W., Free PMC Article

    Data show that the site targeted by two microRNAs, miR-875 and miR-3144 is located in HPV16 E6 oncogene open reading frame (ORF).

    Two less common human microRNAs miR-875 and miR-3144 target a conserved site of E6 oncogene in most high-risk human papillomavirus subtypes.
    Lin L, Cai Q, Zhang X, Zhang H, Zhong Y, Xu C, Li Y., Free PMC Article

    The association of HPV infection and E6 expression increases the risk of cervical cancer.

    Expression of HPV-16 E6 protein and p53 inactivation increases the uterine cervical cancer invasion.
    Yang X, Lu L.

    Our results unraveled the possibility that HPV-16 E6/E7 could promote cell invasive potential via regulating cadherin switching, and consequently contribute to progression and metastasis of cervical cancer.

    HPV-16 E6/E7 promotes cell migration and invasion in cervical cancer via regulating cadherin switch in vitro and in vivo.
    Hu D, Zhou J, Wang F, Shi H, Li Y, Li B.

    UBE3A dampens ERK pathway signalling in HPV E6 transformed HeLa cells

    The ubiquitin ligase UBE3A dampens ERK pathway signalling in HPV E6 transformed HeLa cells.
    Aguilar-Martinez E, Morrisroe C, Sharrocks AD., Free PMC Article

    crystal structure of a ternary complex comprising full-length human papilloma virus type 16 (HPV-16) E6, the LxxLL motif of E6AP and the core domain of p53

    Structure of the E6/E6AP/p53 complex required for HPV-mediated degradation of p53.
    Martinez-Zapien D, Ruiz FX, Poirson J, Mitschler A, Ramirez J, Forster A, Cousido-Siah A, Masson M, Vande Pol S, Podjarny A, Travé G, Zanier K., Free PMC Article

    The E6;E7 splice-variant protein, in addition to self-binding, interacts with human papillomavirus 16 E6 and E7 in the presence of GRP78 and HSP90, leading to the stabilization of E6 and E7 by prolonging the half-life of each protein.

    E6^E7, a novel splice isoform protein of human papillomavirus 16, stabilizes viral E6 and E7 oncoproteins via HSP90 and GRP78.
    Ajiro M, Zheng ZM., Free PMC Article

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