Evidence map›Paper›PMID 27840960›Full record

ArticleOncology reports2017

Hepatitis B virus X protein sensitizes HL-7702 cells to oxidative stress-induced apoptosis through modulation of the mitochondrial permeability transition pore.

Wen-Yu Gao, Dan Li, De-En Cai, Xiao-Yun Huang, Bi-Yun Zheng, Yue-Hong Huang, Zhi-Xin Chen, Xiao-Zhong Wang

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Food science & nutrition · 2025
    Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. The FirstMicroorganisms · 2022
    Article
  8. Mitochondrial Dysfunction and Chronic Liver Disease.Current issues in molecular biology · 2022
    Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Viral Infection Modulates Mitochondrial Function.International journal of molecular sciences · 2021
    Review
  14. Review
  15. Hepatitis B virus X protein promotes liver cell pyroptosis under oxidative stress through NLRP3 inflammasome activation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020
    Article
  16. Review
  17. Review
  18. Article
  19. Review
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 1 country.

Wen-Yu GaoDepartment of Gastroenterology, Fujian Medical University Union Hospital, Fujian 350001, P.R. China.
Dan LiDepartment of Gastroenterology, Fujian Medical University Union Hospital, Fujian 350001, P.R. China.
De-En CaiGraduate School, Fujian Medical University, Fujian 350001, P.R. China.
Xiao-Yun HuangGraduate School, Fujian Medical University, Fujian 350001, P.R. China.
Bi-Yun ZhengDepartment of Gastroenterology, Fujian Medical University Union Hospital, Fujian 350001, P.R. China.
Yue-Hong HuangDepartment of Gastroenterology, Fujian Medical University Union Hospital, Fujian 350001, P.R. China.
Zhi-Xin ChenDepartment of Gastroenterology, Fujian Medical University Union Hospital, Fujian 350001, P.R. China.
Xiao-Zhong WangDepartment of Gastroenterology, Fujian Medical University Union Hospital, Fujian 350001, P.R. China.
Fujian Medical University · CNUnion Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic hepatitis B virus (HBV) infection is a leading cause of liver cirrhosis and cancer. Among the pathogenic factors of HBV, HBV X protein (HBx) is attracting increased attention. Although it is documented that HBx is a multifunctional regulator that modulates cell inflammation and apoptosis, the exact mechanism remains controversial. In the present study, we explored the effect of HBx on oxidative stress-induced apoptosis in normal liver cell line, HL-7702. Our results showed that the existence of HBx affected mitochon-drial biogenesis by modulating the opening of the mitochondrial permeability transition pore (MPTP). Notably, this phenomenon was associated with a pronounced translocation of Bax from the cytosol to the mitochon-dria during the period of exposure to oxidative stress with a release of cytochrome c and activation of cleaved caspase-3 and PARP. Moreover, MPTP blockage with cyclosporin A prevented the translocation of Bax, and inhibited oxidative stress-induced apoptotic killing in the HBx-expressing HL-7702 cells. Our findings suggest that HBx exhibits pro-apoptotic effects upon normal liver cells following exposure to oxidative stress by modulating the MPTP gateway.

Indexed as

Apoptosisbcl-2-Associated X ProteinCell LineHepatocytesHumansHydrogen PeroxideLiverMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreOxidative StressProtein TransportReactive Oxygen SpeciesTrans-ActivatorsViral Regulatory and Accessory ProteinsBAX protein, humanbcl-2-Associated X Proteinhepatitis B virus X proteinHydrogen PeroxideMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreReactive Oxygen SpeciesTrans-ActivatorsViral Regulatory and Accessory Proteins

Identifiers

PMID27840960
PMCPMC5355673
OpenAlexW2556606730

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.