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Proteomic Analysis of the E6 Interactome in Response to Anisomelic Acid Treatment

ABSTRACT: Human papillomavirus (HPV) is a well-known cause of cervical cancer, with the viral oncoprotein E6 playing a key role in carcinogenesis. We previously showed that anisomelic acid treatment reduces E6 protein levels in HPV-positive cancer cells. In this study, we used mass spectrometry-based proteomics to investigate how anisomelic acid affects the HPV16 E6 interactome in normal oral keratinocytes.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture, Keratinocyte

DISEASE(S): Human Papillomavirus Infectious Disease

SUBMITTER: Michael Santos Silva

LAB HEAD: John Eriksson

PROVIDER: PXD065382 | Pride | 2025-09-22

REPOSITORIES: Pride

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			Action	DRS
	20210730_16_1_AA.raw	Raw
	20210730_16_1_AAMG.raw	Raw
	20210730_16_1_control.raw	Raw
	20210730_16_2_AA.raw	Raw
	20210730_16_2_AAMG.raw	Raw

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Publications

Anisomelic acid promotes proteasomal degradation of HPV16 E6 via E3 ligase recruitment: A mass spectrometry-based interactome study.

Santos Silva Michael M Coelho-Rato Leila S LS Delshad Navid N Tarkhova Tatiana T Edman Joakim J Paul Preethy P Meinander Annika A Eriksson John E JE

Journal of proteomics 20250916

Human papillomavirus (HPV) is a major driver of cervical and other epithelial cancers, with the viral oncoprotein E6 playing a central role in tumorigenesis by promoting degradation of the tumor suppressor p53. While prophylactic vaccines prevent infection, there remains a critical need for therapeutic strategies that eliminate established HPV-positive cells. Here, we identify anisomelic acid (AA), a natural diterpenoid, as a novel pharmacological principle that selectively induces the degradati ...[more]

PMID: 40967472

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Expression data from N/Tert-HPV E6 cells in the presence and absence of mitomycin C treatment

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TMEM45A, SERPINB5 and p16INK4A transcript levels are predictive for development of high-grade cervical lesions

Project description:Women persistently infected with human papillomavirus (HPV) type 16 are at high risk for development of cervical intraepithelial neoplasia grade 3 or cervical cancer (CIN3+). We aimed to identify biomarkers for progression to CIN3+ in women with persistent HPV16 infection. In this prospective study, 11,088 women aged 20â29 years were enrolled during 1991-1993, and re-invited for a second visit two years later. Cervical cytology samples obtained at both visits were tested for HPV DNA by Hybrid Capture 2 (HC2), and HC2-positive samples were genotyped by INNO-LiPA. The cohort was followed for up to 19 years via a national pathology register. To identify markers for progression to CIN3+, we performed microarray analysis on RNA extracted from cervical swabs of 30 women with persistent HPV16-infection and 11 HPV-negative women. After further validation, we found that high mRNA expression levels of TMEM45A, SERPINB5 and p16INK4a were associated with increased risk of CIN3+ in persistently HPV16-infected women. We aimed at identifying genes differentially expressed in women with persistent HPV16 infection that either progressed to CIN3+ or not. As a test of principle we first compared HPV16 persistently infected women with HPV-negative women.

2016-07-03 | E-GEOD-75132 | biostudies-arrayexpress

Systematic analysis of IL-1 cytokine signaling by high-risk HPV oncoproteins

Project description:Human papillomavirus (HPV) E6 and E7 oncoproteins are expressed at all stages of HPV-mediated carcinogenesis and are essential drivers of cancers caused by high-risk HPV. Some of the activities of HPV E6 and E7, such as their interactions with host cellular tumor suppressors, have been characterized extensively. There is less information about how high-risk HPV E6 and E7 alter cellular responses to cytokines that are present in HPV-infected tissues and are an important component of the tumor microenvironment. We used several models of HPV oncoprotein activity to assess how E6 and E7 alter the cellular response to the pro-inflammatory cytokine IL-1beta. Models of early-stage HPV infection (human keratinocytes expressing HPV16 E6 and E7) and models of established HPV-positive head and neck cancers (patient-derived xenografts, head and neck cancer cell lines) exhibited similar dysregulation of IL-1 pathway genes and suppressed responses to IL-1beta treatment. Such overlap in cell responses supports that changes induced by HPV E6 and E7 early in infection could persist and contribute to a dysregulated immune environment throughout carcinogenesis. HPV E6 and E7 also drove the upregulation of several suppressors of IL-1 cytokine signaling, including SIGIRR, both in primary keratinocytes and in cancer cells. SIGIRR knockout was insufficient to increase IL-1beta-dependent gene expression in the presence of HPV16 E6 and E7, suggesting that multiple suppressors of IL-1 signaling contribute to dampened IL-1 responses in HPV16-positive cells.

2022-10-31 | GSE211730 | GEO

RNA expression profile comparison of HFKs expressing E6/E7 from beta-3 HPVs (49, 75, 76, 115) and from HR alpha HPV16 and beta-2 HPV38

Project description:Comparative analysis of RNA expression profiles of keratinocytes expressing E6/E7 from the different beta-3, with the RNA profiles of HPV16 and HPV38 E6/E7 HFKs reveals that HPV115 is the more divergent from the HR-mucosal type. Moreover beta-3 HPV 49, 75 and 76 E6/E7 HFKs show altered expression of genes involved in cell cycle regulation and DNA damage response which are also deregulated by expression of E6/E7 of HPV16.

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Expression data from N/Tert-HPV E6 cells in the presence and absence of mitomycin C treatment

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2013-09-05 | E-GEOD-50568 | biostudies-arrayexpress

Modulation of microRNA-mRNA Target Pairs by Human Papillomavirus 16 Oncoproteins

Project description:The E6 and E7 proteins are the major oncogenic drivers encoded by high-risk human papillomaviruses (HPVs). While many aspects of the transforming activities of these proteins have been extensively studied, there are fewer studies that have investigated how HPV E6/E7 expression affects expression of cellular noncoding RNAs. The goal of our study was to investigate HPV16 E6/E7 modulation of cellular microRNA (miR) levels and to determine the potential consequences on cellular gene expression. We performed deep sequencing of small and large cellular RNAs in primary, undifferentiated cultures of human foreskin keratinocytes (HFKs) with stable expression of HPV16 E6/E7 or a control vector. After integration of the two data sets we identified 51 differentially expressed cellular miRs associated with modulation of 1,456 potential target mRNAs in HPV16 E6/E7 expressing HFKs. We discovered that the degree of differential miR expression in HFKs expressing HPV16 E6/E7 was not necessarily predictive of the number of corresponding mRNA targets or the potential impact on gene expression. Additional analyses of the identified miR-mRNA pairs suggest modulation of specific biological activities and biochemical pathways. Overall, our study supports the model that perturbation of cellular miR expression by HPV16 E6/E7 importantly contributes to the rewiring of cellular regulatory circuits by the high-risk HPV E6 and E7 proteins that contribute to oncogenic transformation.

2017-01-17 | GSE92496 | GEO

Effect of HPV 16 E6, E7 oncoproteins on the expression level of cellular genes

Project description:The life cycle of human papillomaviruses (HPV) is strictly linked to the differentiation of their natural host cells. The HPV E6 and E7 oncoproteins can delay the normal differentiation program of keratinocytes, however, the exact mechanisms responsible for this have not yet been identified. The goal of this study was to investigate the effects of HPV16 oncoproteins on the expression of genes involved in keratinocyte differentiation. Primary human keratinocytes transduced by LXSN (control) retroviruses or virus vectors expressing HPV16 E6, E7 or E6/E7 genes were subjected to gene expression profiling. The results of microarray analysis showed that HPV 16 E6 and E7 have the capacity to down-regulate the expression of several genes involved in keratinocyte differentiation. Quantitative real-time polymerase chain reaction (qRT-PCR) assays were performed to confirm microarray data. To investigate the effects of the HPV oncoproteins on the promoters of selected keratinocyte differentiation genes, luciferase reporter assays were performed. Our results suggest that the HPV 16 E6 and/or E7 oncogenes are able to down-regulate the expression of several genes involved in keratinocyte differentiation, at least partially by down-regulating their promoter activity. This activity of the HPV oncoproteins may have a role in the productive virus life cycle, and also in virus induced carcinogenesis. Primary human foreskin keratinocytes were transduced by retrovirus vectors containing HPV 16 E6, E7, E6/E7 or the control vector LXSN. The global gene expression patterns of transduced keratinocytes were analyzed on Affymetrix microarrays

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Human Papillomavirus (HPV) genomic integration, expression and E6/E7 splicing patterns in cervical cancer associated with HPV16 or HPV18 infection

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