FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2899339618> ?p ?o ?g. }

• W2899339618 abstract "Abstract Human papillomaviruses (HPV) are causative agents in ano-genital and oropharyngeal cancers. The virus must reprogram host gene expression to promote infection, and E6 and E7 contribute to this via targeting of cellular transcription factors including p53 and pRb, respectively. The HPV16 E2 protein regulates host gene expression in U2OS cells and in this study we extend these observations into TERT immortalized oral keratinocytes (NOKs) that are capable of supporting late stages of the HPV16 life cycle. We observed repression of innate immune genes by E2 that are also repressed by the intact HPV16 genome in NOKs. RNA-seq data identified 167 up and 395 downregulated genes by E2; there was a highly significant overlap of the E2 regulated genes with those regulated by the intact HPV16 genome in the same cell type. siRNA targeting of E2 reversed repression of E2 targeted genes. The ability of E2 to repress innate immune genes was confirmed in an ano-genital immortalized keratinocyte cell line, N/Tert-1. We present analysis of data from The Cancer Genome Atlas (TCGA) for HPV16 positive and negative head and neck cancers (HNC) suggesting that E2 plays a role in regulation of the host genome in cancers. Patients with HPV16 positive HNC with a loss of E2 expression exhibit a worse clinical outcome and we discuss how this could, at least partially, be related to the loss of E2 host gene regulation. Importance HPV16 positive tumors that retain expression of E2 have a better clinical outcome than those that have lost E2 expression. It has been suggested that this is due to a loss of E2 repression of E6 and E7 expression but this is not supported by data from tumors where there is not more E6 and E7 expression in the absence of E2. Here we report that E2 regulates host gene expression and place this regulation in context of the HPV16 life cycle and HPV16 positive head and neck cancers (the majority of which retain E2 expression). We propose that this E2 function may play an important part in the increased response of HPV16 positive cancers to radiation therapy. Therefore, host gene regulation by E2 may be important for promotion of the HPV16 life cycle, and also for the response of HPV16 positive tumors to radiation therapy." @default.
• W2899339618 created "2018-11-09" @default.
• W2899339618 creator A5003165520 @default.
• W2899339618 creator A5009512283 @default.
• W2899339618 creator A5016141749 @default.
• W2899339618 creator A5033883424 @default.
• W2899339618 creator A5056101043 @default.
• W2899339618 creator A5065954539 @default.
• W2899339618 creator A5068523915 @default.
• W2899339618 creator A5079888439 @default.
• W2899339618 creator A5081013459 @default.
• W2899339618 date "2018-11-05" @default.
• W2899339618 modified "2023-10-16" @default.
• W2899339618 title "Human papillomavirus 16 E2 regulates keratinocyte gene expression relevant to cancer and the viral life cycle" @default.
• W2899339618 cites W155823813 @default.
• W2899339618 cites W1843128023 @default.
• W2899339618 cites W1856542380 @default.
• W2899339618 cites W1966676297 @default.
• W2899339618 cites W1972256398 @default.
• W2899339618 cites W1980142476 @default.
• W2899339618 cites W1990657900 @default.
• W2899339618 cites W1991263063 @default.
• W2899339618 cites W1993025278 @default.
• W2899339618 cites W1995750237 @default.
• W2899339618 cites W1996216604 @default.
• W2899339618 cites W2001486015 @default.
• W2899339618 cites W2004907920 @default.
• W2899339618 cites W2005060345 @default.
• W2899339618 cites W2008312219 @default.
• W2899339618 cites W2009506842 @default.
• W2899339618 cites W2009959680 @default.
• W2899339618 cites W2032572462 @default.
• W2899339618 cites W2032780125 @default.
• W2899339618 cites W2033901551 @default.
• W2899339618 cites W2045531948 @default.
• W2899339618 cites W2050115527 @default.
• W2899339618 cites W2051606353 @default.
• W2899339618 cites W2052500339 @default.
• W2899339618 cites W2052632246 @default.
• W2899339618 cites W2053249188 @default.
• W2899339618 cites W2059807343 @default.
• W2899339618 cites W2063475378 @default.
• W2899339618 cites W2075604614 @default.
• W2899339618 cites W2079095145 @default.
• W2899339618 cites W2079162651 @default.
• W2899339618 cites W2091095196 @default.
• W2899339618 cites W2108720228 @default.
• W2899339618 cites W2110664940 @default.
• W2899339618 cites W2113174452 @default.
• W2899339618 cites W2129945630 @default.
• W2899339618 cites W2130277283 @default.
• W2899339618 cites W2138027990 @default.
• W2899339618 cites W2139348853 @default.
• W2899339618 cites W2141929435 @default.
• W2899339618 cites W2146124794 @default.
• W2899339618 cites W2146416184 @default.
• W2899339618 cites W2149166037 @default.
• W2899339618 cites W2151746267 @default.
• W2899339618 cites W2169330919 @default.
• W2899339618 cites W2170640097 @default.
• W2899339618 cites W2170973430 @default.
• W2899339618 cites W2231279381 @default.
• W2899339618 cites W2487963119 @default.
• W2899339618 cites W2551811079 @default.
• W2899339618 cites W2586267950 @default.
• W2899339618 cites W2620624302 @default.
• W2899339618 cites W2750092411 @default.
• W2899339618 cites W2792033579 @default.
• W2899339618 cites W2794971178 @default.
• W2899339618 cites W2804500296 @default.
• W2899339618 doi "https://doi.org/10.1101/461715" @default.
• W2899339618 hasPublicationYear "2018" @default.
• W2899339618 type Work @default.
• W2899339618 sameAs 2899339618 @default.
• W2899339618 citedByCount "3" @default.
• W2899339618 countsByYear W28993396182018 @default.
• W2899339618 countsByYear W28993396182019 @default.
• W2899339618 crossrefType "posted-content" @default.
• W2899339618 hasAuthorship W2899339618A5003165520 @default.
• W2899339618 hasAuthorship W2899339618A5009512283 @default.
• W2899339618 hasAuthorship W2899339618A5016141749 @default.
• W2899339618 hasAuthorship W2899339618A5033883424 @default.
• W2899339618 hasAuthorship W2899339618A5056101043 @default.
• W2899339618 hasAuthorship W2899339618A5065954539 @default.
• W2899339618 hasAuthorship W2899339618A5068523915 @default.
• W2899339618 hasAuthorship W2899339618A5079888439 @default.
• W2899339618 hasAuthorship W2899339618A5081013459 @default.
• W2899339618 hasConcept C104317684 @default.
• W2899339618 hasConcept C136449434 @default.
• W2899339618 hasConcept C141231307 @default.
• W2899339618 hasConcept C150194340 @default.
• W2899339618 hasConcept C165864922 @default.
• W2899339618 hasConcept C186310378 @default.
• W2899339618 hasConcept C2777074287 @default.
• W2899339618 hasConcept C502942594 @default.
• W2899339618 hasConcept C54355233 @default.
• W2899339618 hasConcept C81885089 @default.
• W2899339618 hasConcept C86803240 @default.
• W2899339618 hasConcept C8891405 @default.
• W2899339618 hasConceptScore W2899339618C104317684 @default.

• next