Evidence map›Paper›PMID 19060920›Full record

ArticleOncogene2009

The pivotal role of c-Jun NH2-terminal kinase-mediated Beclin 1 expression during anticancer agents-induced autophagy in cancer cells.

D-D Li, L-L Wang, R Deng, J Tang, Y Shen, J-F Guo, Y Wang, L-P Xia, G-K Feng, Q Q Liu and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 146 papers.

0numbers the graph read from it
0cells of the map it votes in
146citing papers in PubMed
8.8field-weighted citation impact, top 2% 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

146 citing papers in PubMed, 256 citations in OpenAlex.

  1. Autophagy · 2026
    Review
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Role of CELF2 in ferroptosis: Potential targets for cancer therapy (Review).International journal of molecular medicine · 2023
    Review
  13. Article
  14. Review
  15. The Interplay Between Autophagy and Regulated Necrosis.Antioxidants & redox signaling · 2023
    Review
  16. Article
  17. Review
  18. Review
  19. Review
  20. Review

86 more citing papers are in PubMed but not listed here.

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

13 authors at 3 institutions in 1 country.

D-D LiState Key Laboratory of Oncology in South China, Cancer Center, Sun Yat-Sen University, Guangzhou, China.
L-L Wang
R Deng
J Tang
Y Shen
J-F Guo
Y Wang
L-P Xia
G-K Feng
Q Q Liu
W-L Huang
Y-X Zeng
X-F Zhu
Sun Yat-sen University Cancer Center · CNSun Yat-sen University · CNState Key Laboratory of Oncology in South China

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The c-Jun NH2-terminal kinase (JNK) pathway represents one subgroup of MAP kinases that are activated primarily by cytokines and exposure to environmental stress. Autophagy is a protein-degradation system characterized by the formation of double-membrane vacuoles termed autophagosomes. Autophagy-related gene beclin 1 plays a key role in autophagosome formation. However, the relationships between activation of JNK pathway, autophagy induction and Beclin 1 expression remain elusive. In this study, we used human cancer cell lines CNE2 and Hep3B to investigate the role of JNK-mediated Beclin 1 expression in ceramide-induced autophagic cell death. Ceramide-treated cells exhibited the characteristics of autophagy (that is, acidic vesicular organelle formation and the LC3-II generation). JNK was activated in these two cell lines exposed to ceramide and the phosphorylation of c-Jun also increased. In the meantime, we found that ceramide upregulated Beclin 1 expression in cancer cells. The upregulation of Beclin 1 expression could be blocked by SP600125 (a specific inhibitor of JNK) or a small interfering RNA (siRNA) directed against JNK1/2 or c-Jun. Chromatin immunoprecipitation and luciferase reporter analysis revealed that c-Jun was involved in the regulation of beclin 1 transcription in response to ceramide treatment. In addition, inhibition of JNK activity by SP600125 could inhibit autophagy induction by ceramide. Furthermore, Beclin 1 knockdown by siRNA also inhibited ceramide-mediated autophagic cell death. JNK-mediated Beclin 1 expression was also observed in topotecan-induced autophagy. These data suggest that activation of JNK pathway can mediate Beclin 1 expression, which plays a key role in autophagic cell death in cancer cells.

Indexed as

AutophagyGene Expression Regulation, NeoplasticAnthracenesAntineoplastic AgentsApoptosis Regulatory ProteinsBeclin-1Caspase 3Cell Line, TumorCeramidesEnzyme InhibitorsHumansJNK Mitogen-Activated Protein KinasesMAP Kinase Kinase 4Membrane ProteinsPhagosomesPhosphorylationAnthracenesAntineoplastic AgentsApoptosis Regulatory ProteinsBeclin-1BECN1 protein, humanCaspase 3CeramidesEnzyme InhibitorsJNK Mitogen-Activated Protein KinasesMAP Kinase Kinase 4Membrane ProteinspyrazolanthroneRNA, Small Interfering

Identifiers

PMID19060920
OpenAlexW2085169607

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.