Evidence map›Paper›PMID 27909336›Full record

ArticleExperimental & molecular medicine2016

C-terminal-truncated HBV X promotes hepato-oncogenesis through inhibition of tumor-suppressive β-catenin/BAMBI signaling.

Seok Lee, Mi-Jin Lee, Jun Zhang, Goung-Ran Yu, Dae-Ghon Kim

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Experimental & molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.5field-weighted citation impact, top 28% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
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  7. Article
  8. TGF-β superfamily co-receptors in cancer.Developmental dynamics : an official publication of the American Association of Anatomists · 2022
    Review
  9. Article
  10. Article
  11. Article
  12. Associations between serum HBX quasispecies and their integration in hepatocellular carcinoma.International journal of clinical and experimental pathology · 2017
    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.

Seok LeeDivision of Gastroenterology and Hepatology, Department of Internal Medicine, The Research Institute of Clinical Medicine of Chonbuk National University, Jeonju, Jeonbuk, Republic of Korea.
Mi-Jin LeeDivision of Gastroenterology and Hepatology, Department of Internal Medicine, The Research Institute of Clinical Medicine of Chonbuk National University, Jeonju, Jeonbuk, Republic of Korea.
Jun ZhangDivision of Gastroenterology and Hepatology, Department of Internal Medicine, The Research Institute of Clinical Medicine of Chonbuk National University, Jeonju, Jeonbuk, Republic of Korea.
Goung-Ran YuDivision of Gastroenterology and Hepatology, Department of Internal Medicine, The Research Institute of Clinical Medicine of Chonbuk National University, Jeonju, Jeonbuk, Republic of Korea.
Dae-Ghon KimDivision of Gastroenterology and Hepatology, Department of Internal Medicine, The Research Institute of Clinical Medicine of Chonbuk National University, Jeonju, Jeonbuk, Republic of Korea.
Jeonbuk National University · KRJeonbuk National University Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

C-terminal-truncated hepatitis B virus (HBV) X (HBx) (ctHBX) is frequently detected in hepatocellular carcinoma (HCC) through HBV integration into the host genome. However, the molecular mechanisms underlying ctHBx-associated oncogenic signaling have not yet been clarified. To elucidate the biological role of ctHBx in hepato-oncogenesis, we functionally analyzed ctHBx-mediated regulation of the activin membrane-bound inhibitor bone morphogenetic protein and activin membrane-bound inhibitor (BAMBI) through transforming growth factor-β (TGF-β) or β-catenin (CTNNB1) in HCC cells and in an animal model, and we compared its role to that of the full-length HBx protein. Ectopic ctHBx expression generated more colonies in anchorage-dependent and -independent growth assays than did HBx expression alone. ctHBx downregulated BAMBI to a greater degree than did HBx in HCC cells. HBx activated the Wnt/β-catenin pathway, which positively regulated the BAMBI expression through T-cell factor 1 signaling, whereas ctHBx negatively regulated the Wnt/β-catenin pathway. BAMBI downregulated the β-catenin and TGF-β1 signaling pathways. TGF-β1 positively regulated BAMBI expression thorough Smad3 signaling. Furthermore, knockdown of BAMBI was more tumorigenic in HCC cells. Therefore, downregulation of both β-catenin and TGF-β1 signaling by BAMBI might contribute to tumor suppression in mice xenotransplanted with HepG2 or SH-J1 cells. Taken together, ctHBx may have a more oncogenic role than HBx through its inhibition of tumor-suppressive β-catenin/BAMBI signaling.

Indexed as

Signal TransductionAnimalsbeta CateninHepatitis BHepatitis B virusHep G2 CellsHumansLiverLiver NeoplasmsMembrane ProteinsMiceTrans-ActivatorsViral Regulatory and Accessory ProteinsWnt Signaling PathwayBAMBI protein, humanbeta Cateninhepatitis B virus X proteinMembrane ProteinsTrans-ActivatorsViral Regulatory and Accessory Proteins

Identifiers

PMID27909336
PMCPMC5192070
OpenAlexW2559728714

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.