Evidence map›Paper›PMID 11244501›Full record

ArticleOncogene2001

Activated ras oncogene collaborates with HBx gene of hepatitis B virus to transform cells by suppressing HBx-mediated apoptosis.

Y C Kim, K S Song, G Yoon, M J Nam, W S Ryu

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

26 citing papers in PubMed, 73 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Structural and biochemical analysis of Bcl-2 interaction with the hepatitis B virus protein HBx.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Dysregulation of apoptosis in hepatocellular carcinoma cells.World journal of gastroenterology · 2009
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Chronic hepatitis B in hepatocarcinogenesis.Postgraduate medical journal · 2006
    Review
  19. Article
  20. 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 1 country.

Y C KimDepartment of Biochemistry, Yonsei University, 134 Shinchondong, Seodaemungu, Seoul, Korea 120-749.
K S Song
G Yoon
M J Nam
W S Ryu
Yonsei University · KRKorea National Institute of Health · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The hepatitis B virus HBx protein is a promiscuous transactivator implicated in the development of hepatocellular carcinoma. The ectopic expression of HBx fails to transform both primary and immortalized rodent cells, but rather induces apoptosis. Furthermore, most transgenic mice harboring HBx do not develop liver tumors. Thus, it remains unclear whether and how HBx contributes to oncogenesis. Here, we show that HBx collaborates with activated H-ras to transform immortalized rodent cells. Indeed, REF52 cells transfected by both HBx and activated H-ras were morphologically transformed and were able to grow in soft agar. Remarkably, nude mice injected with REF52 cells transfected by both HBx and activated H-ras developed tumors, whereas the mice injected with REF52 cells transfected by either gene alone did not. Thus, we concluded that HBx could contribute to neoplastic transformation of cells in collaboration with other oncogenes, such as H-ras, that renders cells to overcome the HBx-mediated apoptosis. Further, we found that HBx mediated apoptosis was suppressed by activated H-ras through activation of the phosphatidylinositol-3 kinase and Akt pathway. Data presented here firmly established the oncogenic potential of HBx during multistage carcinogenesis. Oncogene (2001) 20, 16 - 23.

Indexed as

Gene Expression Regulation, NeoplasticGene Expression Regulation, ViralGenes, rasProtein Serine-Threonine Kinases3T3 CellsAnimalsApoptosisCell LineCell Line, TransformedCell Transformation, NeoplasticCell Transformation, ViralEmbryo, MammalianGenes, SuppressorGenes, ViralHepatitis B virusMiceAkt1 protein, rathepatitis B virus X proteinPhosphatidylinositol 3-KinasesProtein Serine-Threonine KinasesProtein-Tyrosine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktTrans-ActivatorsViral Regulatory and Accessory ProteinsViral Structural Proteins

Identifiers

PMID11244501
OpenAlexW1977638924

What OpenQuestion holds

Textmetadata
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.