Evidence map›Paper›PMID 24577313›Full record

ArticleInternational journal of molecular sciences2014

HBx protein promotes oval cell proliferation by up-regulation of cyclin D1 via activation of the MEK/ERK and PI3K/Akt pathways.

Heng-Yi Wang, Sheng-Li Yang, Hui-Fang Liang, Chang-Hai Li

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

31 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Nanomedicine (London, England) · 2024
    Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Human DNA Virus Exploitation of the MAPK-ERK Cascade.International journal of molecular sciences · 2019
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  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

4 authors at 3 institutions in 1 country.

Heng-Yi WangDepartment of Surgery, the First Affiliated Hospital of Anhui Medical University, Hefei 230022, China. gdh00909@sina.com.
Sheng-Li YangDepartment of General Surgery, Liyuan Hospital, Tongji Medical College, Huazhong Science and Technology University, Wuhan 430077, China. jixufendou2013@gmail.com.
Hui-Fang LiangHepatic Surgery Center, Tongji Hospital, Tongji Medical College, Huazhong Science and Technology University, Wuhan 430030, China. lianghuifang1997@126.com.
Chang-Hai LiHepatic Surgery Center, Tongji Hospital, Tongji Medical College, Huazhong Science and Technology University, Wuhan 430030, China. lichvip@126.com.
Tongji Hospital · CNFirst Affiliated Hospital of Anhui Medical University · CNHuazhong University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Growing evidence has shown that hepatic oval cells, also named liver progenitor cells, play an important role in the process of liver regeneration in various liver diseases. Oval cell proliferation has been reported in hepatitis B virus (HBV)-associated hepatocellular carcinoma (HCC) and chronic liver disease. Studies have found expression of HBV surface and core antigens in oval cells in the livers of patients with HCC, suggesting that HBV infection of oval cells could be a mechanism of human hepatocarcinogenesis. In addition, there is evidence of multiplication of HBV in oval cell culture. However, little research has been performed to explore the role of HBV-encoded proteins in the proliferation of hepatic oval cells. Previously, we successfully transfected the HBV x (HBx) gene, one of the four genes in the HBV genome, into a rat LE/6 oval cell line. In this study, we tested whether or not the transfected HBx gene could affect oval cell proliferation in vitro. Our results show that overexpression of HBx promotes the proliferation of oval cells and increases cyclin D1 expression, assessed at both the mRNA and protein levels. We also found that HBx activated the PI-3K/Akt and MEK/ERK1/2 pathways in HBx-transfected oval cells. Furthermore, the HBx-induced increases in cyclin D1 expression and oval cell proliferation were completely abolished by treatment with either MEK inhibitor PD184352 or PI-3K inhibitor LY294002. These results demonstrated that HBx has the ability to promote oval cell proliferation in vitro, and its stimulatory effects on cell proliferation and expression of cyclin D1 depend on the activation of the MEK/ERK and PI3K/Akt signaling pathways in cultured oval cells.

Indexed as

AnimalsBenzamidesBlotting, WesternCell LineCell ProliferationChromonesCyclin D1Enzyme ActivationEnzyme InhibitorsLiverMAP Kinase Signaling SystemMorpholinesPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktRats2-(2-chloro-4-iodophenylamino)-N-cyclopropylmethoxy-3,4-difluorobenzamide2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneBenzamidesChromonesCyclin D1Enzyme Inhibitorshepatitis B virus X proteinMorpholinesPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktTrans-ActivatorsViral Regulatory and Accessory Proteins

Identifiers

PMID24577313
PMCPMC3975350
OpenAlexW2033283616

What OpenQuestion 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 OpenQuestion graph.