Evidence map›Paper›PMID 27588401›Full record

ArticleOncotarget2016

Vitexin suppresses autophagy to induce apoptosis in hepatocellular carcinoma via activation of the JNK signaling pathway.

Jin-Dan He, Zhen Wang, Shi-Peng Li, Yan-Jie Xu, Yao Yu, Yi-Jie Ding, Wen-Li Yu, Rong-Xin Zhang, Hai-Ming Zhang, Hong-Yin Du

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

32 citing papers in PubMed, 68 citations in OpenAlex.

  1. Article
  2. Review
  3. Molecular Mechanisms of Vitexin: An Update on Its Anti-Cancer Functions.International journal of molecular sciences · 2025
    Review
  4. Pharmaceuticals (Basel, Switzerland) · 2025
    Article
  5. The Interplay between Autophagy and Mitochondria in Cancer.International journal of molecular sciences · 2024
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Evidence-based complementary and alternative medicine : eCAM · 2020
    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

10 authors at 2 institutions in 1 country.

Jin-Dan HeFirst Central Clinical College, Tianjin Medical University, Tianjin 300192, P.R. China.
Zhen WangFirst Central Clinical College, Tianjin Medical University, Tianjin 300192, P.R. China.
Shi-Peng LiFirst Central Clinical College, Tianjin Medical University, Tianjin 300192, P.R. China.
Yan-Jie XuFirst Central Clinical College, Tianjin Medical University, Tianjin 300192, P.R. China.
Yao YuFirst Central Clinical College, Tianjin Medical University, Tianjin 300192, P.R. China.
Yi-Jie DingFirst Central Clinical College, Tianjin Medical University, Tianjin 300192, P.R. China.
Wen-Li YuDepartment of Anesthesiology, Tianjin First Central Hospital, Tianjin 300192, P.R. China.
Rong-Xin ZhangLaboratory of Immunology and Inflammation, Department of Immunology, Key Laboratory of Immune Microenvironment and Diseases of Educational Ministry of China, Basic Medical College, Tianjin Medical University, Tianjin 300070, P.R. China.
Hai-Ming ZhangFirst Central Clinical College, Tianjin Medical University, Tianjin 300192, P.R. China.
Hong-Yin DuDepartment of Anesthesiology, Tianjin First Central Hospital, Tianjin 300192, P.R. China.
Tianjin Medical University · CNTianjin First Center Hospital · CN

Funding

NIAAA NIH HHS N01 AA021001
6 · The paper itself

Abstract

Vitexin, a flavonoids compound, is known to exhibit broad anti-oxidative, anti-inflammatory, analgesic, and antitumor activity in many cancer xenograft models and cell lines. The purpose of this study was to investigate the antitumor effects and underlying mechanisms of vitexin on hepatocellular carcinoma. In this study, we found that vitexin suppressed the viability of HCC cell lines (SK-Hep1 and Hepa1-6 cells) significantly. Vitexin showed cytotoxic effects against HCC cell lines in vitro by inducing apoptosis and inhibiting autophagy. Vitexin induced apoptosis in a concentration-dependent manner, and caused up-regulations of Caspase-3, Cleave Caspase-3, and a down-regulation of Bcl-2. The expression of autophagy-related protein LC3 II was significantly decreased after vitexin treatment. Moreover, western blot analysis presented that vitexin markedly up-regulated the levels of p-JNK and down-regulated the levels of p-Erk1/2 in SK-Hep1 cells and Hepa1-6 cells. Cotreatment with JNK inhibitor SP600125, we demonstrated that apoptosis induced by vitexin was suppressed, while the inhibition of autophagy by vitexin was reversed. The results of colony formation assay and mouse model confirmed the growth inhibition role of vitexin on HCC in vitro and in vivo. In conclusion, vitexin inhibits HCC growth by way of apoptosis induction and autophagy suppression, both of which are through JNK MAPK pathway. Therefore, vitexin could be regarded as a potent therapeutic agent for the treatment of HCC.

Indexed as

AnimalsApigeninApoptosisAutophagyAutophagy-Related ProteinsCarcinoma, HepatocellularCaspase 3Cell Line, TumorCell SurvivalHumansLiver NeoplasmsLiver Neoplasms, ExperimentalMaleMAP Kinase Signaling SystemMice, Inbred C57BLXenograft Model Antitumor AssaysApigeninAutophagy-Related ProteinsCaspase 3vitexinapoptosisautophagyhepatocellular carcinomaJNK signalingvitexin

Identifiers

PMID27588401
PMCPMC5356678
OpenAlexW2518640481

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.