Evidence map›Paper›PMID 25650660›Full record

ArticleOncotarget2015

Cancerous inhibitor of protein phosphatase 2A contributes to human papillomavirus oncoprotein E7-induced cell proliferation via E2F1.

Weifang Zhang, Hanxiang Chen, Yan Chen, Juan Liu, Xiao Wang, Xiuping Yu, Jason J Chen, Weiming Zhao

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Do or Die: HPV E5, E6 and E7 in Cell Death Evasion.Pathogens (Basel, Switzerland) · 2022
    Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. CIP2A is associated with multidrug resistance in cervical adenocarcinoma by a P-glycoprotein pathway.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    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

8 authors at 2 institutions in 2 countries.

Weifang ZhangInstitute of Pathogenic Biology, Shandong University School of Medicine, Jinan, Shandong, China.
Hanxiang ChenInstitute of Pathogenic Biology, Shandong University School of Medicine, Jinan, Shandong, China.
Yan ChenInstitute of Pathogenic Biology, Shandong University School of Medicine, Jinan, Shandong, China.
Juan LiuInstitute of Pathogenic Biology, Shandong University School of Medicine, Jinan, Shandong, China.
Xiao WangInstitute of Pathophysiology, Shandong University School of Medicine, Jinan, Shandong, China.
Xiuping YuInstitute of Pathogenic Biology, Shandong University School of Medicine, Jinan, Shandong, China.
Jason J ChenDepartment of Medicine, University of Massachusetts Medical School, Worcester, MA, USA.
Weiming ZhaoInstitute of Pathogenic Biology, Shandong University School of Medicine, Jinan, Shandong, China.
Shandong University · CNUniversity of Massachusetts Chan Medical School · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancerous inhibitor of protein phosphatase 2A (CIP2A) is a recently identified oncoprotein that is overexpressed in many human malignant tumors including cervical cancer. Human papillomavirus (HPV) oncoprotein E7 is the key transformation factor in cervical cancer. Our previous data showed a positive association of CIP2A and HPV-16E7 protein levels; however, how CIP2A is regulated by HPV-E7 and the roles of CIP2A in HPV-E7-mediated cell proliferation are unknown. In this study, we demonstrated that HPV-16E7 protein significantly upregulating CIP2A mRNA and protein expression depended on retinoblastoma protein pRb rather than p130. CIP2A siRNA knockdown in HPV-E7-expressing cells inhibited cell proliferation, DNA synthesis and G1/S cell cycle progression. CIP2A siRNA decreased the protein levels of cyclin-dependent kinase 1 (Cdk1), Cdk2 and their partner cyclin A2, with no change in levels of Cdk4, Cdk6 and their partner cyclin D1. The downregulation of Cdk1 and Cdk2 was independent of c-Myc; instead, E2F1 was the main target of CIP2A in this process, as overexpression of E2F1 rescued the inhibitory effects of CIP2A siRNA knockdown on cell proliferation and G1 arrest of HPV-E7-expressing cells. Our studies reveal a novel function of CIP2A in HPV-16E7-mediated cell proliferation.

Indexed as

Cell ProliferationApoptosisAutoantigensBlotting, WesternCell CycleCells, CulturedE2F1 Transcription FactorFlow CytometryHumansIntracellular Signaling Peptides and ProteinsKeratinocytesMembrane ProteinsPapillomaviridaePapillomavirus E7 ProteinsPhosphorylationRetinal Pigment EpitheliumAutoantigensCIP2A protein, humanE2F1 protein, humanE2F1 Transcription FactorIntracellular Signaling Peptides and ProteinsMembrane ProteinsPapillomavirus E7 ProteinsRetinoblastoma ProteinCIP2AE2F1E7G1 arrestHPV

Identifiers

PMID25650660
PMCPMC4467146
OpenAlexW1573142142

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.