Evidence map›Paper›PMID 35168698›Full record

ArticleBMB reports2022

Hepatitis B virus X protein promotes epithelial-mesenchymal transition of hepatocellular carcinoma cells by regulating SOCS1.

Inho Kang, Ji Ae Kim, Jinchul Kim, Ju Hyeon Lee, Mi-Jee Kim, Jeong Keun Ahn

Open access · greenAbstract readNews
In one paragraph

Article in BMB reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. 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

6 authors at 1 institution in 1 country.

Inho KangDepartment of Microbiology & Molecular Biology, College of Bioscience and Biotechnology, Chungnam National University, Daejeon 34134, Korea.
Ji Ae KimDepartment of Microbiology & Molecular Biology, College of Bioscience and Biotechnology, Chungnam National University, Daejeon 34134, Korea.
Jinchul KimDepartment of Microbiology & Molecular Biology, College of Bioscience and Biotechnology, Chungnam National University, Daejeon 34134, Korea.
Ju Hyeon LeeDepartment of Microbiology & Molecular Biology, College of Bioscience and Biotechnology, Chungnam National University, Daejeon 34134, Korea.
Mi-Jee KimDepartment of Microbiology & Molecular Biology, College of Bioscience and Biotechnology, Chungnam National University, Daejeon 34134, Korea.
Jeong Keun AhnDepartment of Microbiology & Molecular Biology, College of Bioscience and Biotechnology, Chungnam National University, Daejeon 34134, Korea.
Chungnam National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC), a primary type of liver cancer, is one of the leading causes of cancer related deaths worldwide. HCC patients have poor prognosis due to intrahepatic and extrahepatic metastasis. Hepatitis B virus (HBV) infection is one of the major causes of various liver diseases including HCC. Among HBV gene products, HBV X protein (HBx) plays an important role in the development and metastasis of HCC. However, the mechanism of HCC metastasis induced by HBx has not been elucidated yet. In this study, for the first time, we report that HBx interacts with the suppressor of cytokine signaling 1 (SOCS1) which negatively controls NF-κB by degrading p65, a subunit of NF-κB. NF-κB activates the transcription of factors associated with epithelial-mesenchymal transition (EMT), a crucial cellular process associated with invasiveness and migration of cancer cells. Here, we report that HBx physically binds to SOCS1, subsequently prevents the ubiquitination of p65, activates the transcription of EMT transcription factors and enhance cell migration and invasiveness, suggesting a new mechanism of HBV-associated HCC metastasis. [BMB Reports 2022; 55(5): 220-225].

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsCell Line, TumorEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHepatitis B virusHumansNF-kappa BSuppressor of Cytokine Signaling 1 ProteinSuppressor of Cytokine Signaling ProteinsTrans-ActivatorsViral Regulatory and Accessory Proteinshepatitis B virus X proteinNF-kappa BSOCS1 protein, humanSuppressor of Cytokine Signaling 1 ProteinSuppressor of Cytokine Signaling ProteinsTrans-ActivatorsViral Regulatory and Accessory Proteins

Identifiers

PMID35168698
PMCPMC9152579
OpenAlexW4213391503

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.