Evidence map›Paper›PMID 31425971›Full record

ArticleVirology2019

HPV16-transformed human keratinocytes depend on SIX1 expression for proliferation and HPV E6/E7 gene expression.

Maria Hosseinipour, Fang Wan, Diego Altomare, Kim E Creek, Lucia Pirisi

Open access · greenAbstract read
In one paragraph

Article in Virology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.8field-weighted citation impact, top 26% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

Maria HosseinipourDepartment of Pathology, Microbiology & Immunology, University of South Carolina School of Medicine at Columbia, Columbia, SC 29208, USA.
Fang WanDepartment of Pathology, Microbiology & Immunology, University of South Carolina School of Medicine at Columbia, Columbia, SC 29208, USA; Inner Mongolia Agricultural University, Hohhot, Inner Mongolia, China.
Diego AltomareDepartment of Drug Discovery and Biomedical Sciences, University of South Carolina College of Pharmacy, Columbia, SC, 29208, USA.
Kim E CreekDepartment of Drug Discovery and Biomedical Sciences, University of South Carolina College of Pharmacy, Columbia, SC, 29208, USA.
Lucia PirisiDepartment of Pathology, Microbiology & Immunology, University of South Carolina School of Medicine at Columbia, Columbia, SC 29208, USA. Electronic address: Lucia.pirisi-creek@uscmed.sc.edu.
University of South Carolina · USInner Mongolia Agricultural University · CN

Funding

South Carolina IDeA Networks of Biomedical Research (SC INBRE V)P20GM103499 · NIGMS · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI EDIE C GOLDSMITH · 2012 to 2026
$61.0M
Targeting NMDA Receptors and Brain Estradiol to Rescue Memory in Aging FemalesP20GM109091 · NIGMS · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI RONINSON, IGOR B · 2014 to 2024
$25.2M
Molecular origin and evolution of HPV inactive head and neck cancersR21CA201853 · NCI · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI PIRISI-CREEK, LUCIA AMELIA · 2016 to 2017
$319k
NCI NIH HHS R21 CA201853NIGMS NIH HHS P20 GM103499NIGMS NIH HHS P20 GM109091
6 · The paper itself

Abstract

The homeodomain transcription factor SIX1 plays a critical role in embryogenesis, is not expressed in normal adult tissue, but is expressed in many malignancies, including cervical cancer. SIX1 drives the progression of HPV16-immortalized human keratinocytes (HKc/HPV16) toward malignancy: HKc/HPV16 express high levels of SIX1 mRNA and protein; overexpression of SIX1 in HKc/HPV16 produces pre-malignant, differentiation-resistant lines (HKc/DR); SIX1 overexpression in HKc/DR induces tumorigenicity. In this paper, we explore the consequences of inhibition of SIX1 expression in premalignant HKc/DR. Only partial inhibition of SIX1 expression could be obtained in HKc/DR by RNA interference. Decreased SIX1 expression (up to 80%) in HKc/DR resulted in slower proliferation, decreased HPV16-E6/E7 mRNA levels, and increased p53 protein levels. Gene expression changes induced in HKc/DR by anti-SIX1 shRNA were indicative of mesenchymal-epithelial transition (MET) and changes in TGF-beta signaling. We conclude that HPV16-transformed cells depend on SIX1 for survival, HPV16 E6/E7 gene expression and epithelial-mesenchymal transition.

Indexed as

Cell Transformation, ViralHost-Pathogen InteractionsCell LineCell ProliferationEpithelial-Mesenchymal TransitionGene SilencingHomeodomain ProteinsHuman papillomavirus 16HumansKeratinocytesOncogene Proteins, ViralPapillomavirus E7 ProteinsRepressor ProteinsSignal TransductionE6 protein, Human papillomavirus type 16Homeodomain Proteinsoncogene protein E7, Human papillomavirus type 16Oncogene Proteins, ViralPapillomavirus E7 ProteinsRepressor ProteinsSIX1 protein, humanHPV16Human keratinocytesHuman papillomavirusSIX1TGF-Beta

Identifiers

PMID31425971
PMCPMC6901751
OpenAlexW2967823861

What OpenQuestion holds

Textmetadata
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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.