Evidence map›Paper›PMID 23677989›Full record

ArticleThe Journal of biological chemistry2013

Nilotinib induces autophagy in hepatocellular carcinoma through AMPK activation.

Hui-Chuan Yu, Chen-Si Lin, Wei-Tien Tai, Chun-Yu Liu, Chung-Wai Shiau, Kuen-Feng Chen

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

56 citing papers in PubMed, 98 citations in OpenAlex.

  1. The ATG14: multi-layer autophagy control and an emerging therapeutic target in cancer.Apoptosis : an international journal on programmed cell death · 2026
    Review
  2. Regulation of autophagy-mediated pathways by diet, physical activity, and sleep in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Review
  3. Targeting Lysosomes for Enhanced Anti-Cancer Therapeutics and Immune Response.International journal of biological sciences · 2026
    Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Nilotinib: Disrupting the MYC-MAX Heterocomplex.Bioinformatics and biology insights · 2024
    Article
  10. Review
  11. Article
  12. Article
  13. Emerging Role of NLRP3 Inflammasome/Pyroptosis in Huntington's Disease.International journal of molecular sciences · 2022
    Review
  14. Article
  15. Protein clearance strategies for disease intervention.Journal of neural transmission (Vienna, Austria : 1996) · 2022
    Review
  16. Article
  17. Article
  18. Article
  19. New Avenues for the Treatment of Huntington's Disease.International journal of molecular sciences · 2021
    Review
  20. 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

6 authors at 4 institutions in 2 countries.

Hui-Chuan YuDepartment of Medical Research, National Taiwan University Hospital and College of Medicine, Taipei 100, Taiwan.
Chen-Si Lin
Wei-Tien Tai
Chun-Yu Liu
Chung-Wai Shiau
Kuen-Feng Chen
National Clinical Research · USNational Taiwan University Hospital · TWNational Yang Ming Chiao Tung University · TWTaipei Veterans General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is the most common liver cancer and the third-leading cause of cancer death worldwide. Nilotinib is an orally available receptor tyrosine kinase inhibitor approved for chronic myelogenous leukemia. This study investigated the effect of nilotinib on HCC. Nilotinib did not induce cellular apoptosis. Instead, staining with acridine orange and microtubule-associated protein 1 light chain 3 revealed that nilotinib induced autophagy in a dose- and time-dependent manner in HCC cell lines, including PLC5, Huh-7, and Hep3B. Moreover, nilotinib up-regulated the phosphryaltion of AMP-activated kinase (AMPK) and protein phosphatase PP2A inactivation were detected after nilotinib treatment. Up-regulating PP2A activity suppressed nilotinib-induced AMPK phosphorylation and autophagy, suggesting that PP2A mediates the effect of nilotinib on AMPK phosphorylation and autophagy. Our data indicate that nilotinib-induced AMPK activation is mediated by PP2A, and AMPK activation and subsequent autophagy might be a major mechanism of action of nilotinib. Growth of PLC5 tumor xenografts in BALB/c nude mice was inhibited by daily oral treatment with nilotinib. Western blot analysis showed both increased phospho-AMPK expression and decreased PP2A activity in vivo. Together, our results reveal that nilotinib induces autophagy, but not apoptosis in HCC, and that the autophagy-inducing activity is associated with PP2A-regulated AMPK phosphorylation.

Indexed as

Administration, OralAMP-Activated Protein KinasesAnimalsAutophagyBlotting, WesternCarcinoma, HepatocellularCell Line, TumorCell SurvivalDose-Response Relationship, DrugEnzyme ActivationHumansLiver NeoplasmsMiceMice, Inbred BALB CMice, NudePhosphorylationAMP-Activated Protein KinasesnilotinibProtein Phosphatase 2PyrimidinesAMP-activated Kinase (AMPK)ApoptosisAutophagyHCCNilotinibSerine Threonine Protein PhosphataseTyrosine Protein Kinase (Tyrosine Kinase)

Identifiers

PMID23677989
PMCPMC3689967
OpenAlexW2080885354

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.