Evidence map›Paper›PMID 26934469›Full record

ReviewCancer biology & therapy2016

Targeting blockage of STAT3 inhibits hepatitis B virus-related hepatocellular carcinoma.

Yinli Yang, Bingqing Zheng, Qiuju Han, Cai Zhang, Zhigang Tian, Jian Zhang

Open access · bronzeAbstract readReview
In one paragraph

Review in Cancer biology & therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

27 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. The regulatory roles of STAT3 protein in the pathogenesis of viral infections.Frontiers in cellular and infection microbiology · 2025
    Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Signaling Induced by Chronic Viral Hepatitis: Dependence and Consequences.International journal of molecular sciences · 2022
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. 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

6 authors at 2 institutions in 1 country.

Yinli Yanga Institute of Immunopharmaceutical Sciences, School of Pharmaceutical Sciences, Shandong University , China.
Bingqing Zhenga Institute of Immunopharmaceutical Sciences, School of Pharmaceutical Sciences, Shandong University , China.
Qiuju Hana Institute of Immunopharmaceutical Sciences, School of Pharmaceutical Sciences, Shandong University , China.
Cai Zhanga Institute of Immunopharmaceutical Sciences, School of Pharmaceutical Sciences, Shandong University , China.
Zhigang Tiana Institute of Immunopharmaceutical Sciences, School of Pharmaceutical Sciences, Shandong University , China.
Jian Zhanga Institute of Immunopharmaceutical Sciences, School of Pharmaceutical Sciences, Shandong University , China.
Shandong University · CNUniversity of Science and Technology of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis B virus (HBV) infection is a significant cause of liver disease pathogenesis, which results in the development of hepatic dysfunction, cirrhosis and hepatocellular carcinoma (HCC). Our previous studies showed that oncogene STAT3 might be an ideal target for HCC therapy. Here, we investigated whether targeting blockage of STAT3 signaling is efficient for HBV-related HCC. Based on the refractory of HCC and the persistence of HBV, in this study, we designed shRNAs targeting STAT3. The results showed that blocking STAT3 signaling by shRNAs could promote HBV positive HCC cell apoptosis and induce cell cycle arrest, resulting in HCC cell growth inhibition in vitro. Importantly, STAT3-shRNAs efficiently suppressed HBV replication, which would reduce HBV-derived stimulation to STAT3 signaling and augment STAT3-shRNAs-mediated anti-HCC effect. Finally, STAT3-shRNAs-mediated anti-HBV positive HCC effect was confirmed in xenograft nude mice. This study suggested that targeting STAT3 therapies such as STAT3-shRNAs may be an efficacious strategy for HBV-related HCC.

Indexed as

AnimalsCarcinoma, HepatocellularHumansLiver NeoplasmsMiceMice, NudeSTAT3 Transcription FactorTransfectionSTAT3 Transcription FactorGene targeted therapyHBVHCCSTAT3

Identifiers

PMID26934469
PMCPMC4910934
OpenAlexW2330987887

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.