Evidence map›Paper›PMID 25886518›Full record

ArticleBMC cancer2015

HPV-16 impairs the subcellular distribution and levels of expression of protein phosphatase 1γ in cervical malignancy.

Takayuki Seiki, Kazunori Nagasaka, Christian Kranjec, Kei Kawana, Daichi Maeda, Hiroe Nakamura, Ayumi Taguchi, Yoko Matsumoto, Takahide Arimoto, Osamu Wada-Hiraike and 7 more

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 40% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
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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

17 authors at 4 institutions in 2 countries.

Takayuki SeikiDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan. thinmu@yahoo.co.jp.
Kazunori NagasakaDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan. nagasakak-tky@umin.ac.jp.
Christian KranjecInternational Centre for Genetic Engineering and Biotechnology, Area Science Park, Padriciano-99, I-34012, Trieste, Italy. Christian.Kranjec@icgeb.org.
Kei KawanaDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan. kkawana-tky@umin.org.
Daichi MaedaDepartment of Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan. daichimaeda@gmail.com.
Hiroe NakamuraDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan. kamotomoka@yahoo.co.jp.
Ayumi TaguchiDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan. ayumikidu246@yahoo.co.jp.
Yoko MatsumotoDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan. yokomatsumoto@mac.com.
Takahide ArimotoDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan. tarimoto-tky@umin.ac.jp.
Osamu Wada-HiraikeDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan. osamuwh-tky@umin.ac.jp.
Katsutoshi OdaDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan. katsutoshi-tky@umin.ac.jp.
Shunsuke NakagawaDepartment of Obstetrics and Gynecology, Graduate School of Medicine, Teikyo University, Tokyo, 173-8605, Japan. nakagawas-tky@umin.ac.jp.
Tetsu YanoDepartment of Obstetrics and Gynecology, National Center for Global Health and Medicine, Tokyo, 162-8655, Japan. tetu-tky@umin.ac.jp.
Masashi FukayamaDepartment of Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan. mfukayama-tky@umin.org.
Lawrence BanksInternational Centre for Genetic Engineering and Biotechnology, Area Science Park, Padriciano-99, I-34012, Trieste, Italy. banks@icgeb.org.
Yutaka OsugaDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan. yutakaos-tky@umin.ac.jp.
Tomoyuki FujiiDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan. fujiit-tky@umin.ac.jp.
The University of Tokyo · JPInternational Centre for Genetic Engineering and Biotechnology · ITNational Center for Global Health and Medicine · JPTeikyo University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe high risk Human Papillomavirus (HPV) E6 oncoproteins play an essential role in the development of cervical malignancy. Important cellular targets of E6 include p53 and the PDZ domain containing substrates such as hScrib and Dlg. We recently showed that hScrib activity was mediated in part through recruitment of protein phosphatase 1γ (PP1γ).

methodsExpression patterns of hScrib and PP1γ were assessed by immunohistochemistry of HPV-16 positive cervical intraepithelial neoplasm (CIN), classified as CIN1 (n = 4), CIN2 (n = 8), CIN3 (n = 8), cervical carcinoma tissues (n = 11), and HPV-negative cervical tissues (n = 8), as well as by subfractionation assay of the HPV-16 positive cervical cancer cell lines, CaSki and SiHa. To explore the effects of the HPV-16 oncoproteins, we have performed siRNA knockdown of E6/E7 expression, and monitored the effects on the expression patterns of hScrib and PP1γ.

resultsWe show that PP1γ levels in HPV-16 positive tumour cells are reduced in an E6/E7 dependent manner. Residual PP1γ in these cells is found mostly in the cytoplasm as opposed to the nucleus where it is predominantly found in normal cells. We have found a striking concordance with redistribution in the pattern of expression (9/11; 81.8%) and loss of PP1γ expression in HPV-16 positive cervical tumours (2/11; 18.2%). Furthermore, this loss of PP1γ expression and redistribution in the pattern of expression occurs progressively as the lesions develop (8/8; 100%).

conclusionTogether, these results suggest that PP1γ may be a novel target of the HPV-16 oncoproteins and indicate that it might be a potential novel biomarker for HPV-16 induced malignancy.

Indexed as

Human papillomavirus 16Biomarkers, TumorCell Line, TumorFemaleGene ExpressionHumansImmunohistochemistryIntracellular SpaceMembrane ProteinsPapillomavirus InfectionsProtein Phosphatase 1Protein TransportProteolysisTumor Suppressor ProteinsUterine Cervical DysplasiaUterine Cervical NeoplasmsBiomarkers, TumorMembrane ProteinsProtein Phosphatase 1SCRIB protein, humanTumor Suppressor Proteins

Identifiers

PMID25886518
PMCPMC4399203
OpenAlexW1967124331

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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.