Evidence map›Paper›PMID 35214061›Full record

ArticlePharmaceutics2022

The Natural Chemotherapeutic Capsaicin Activates AMPK through LKB1 Kinase and TRPV1 Receptors in Prostate Cancer Cells.

Belén G Sánchez, Alicia Bort, José M Mora-Rodríguez, Inés Díaz-Laviada

Open access · goldAbstract read
In one paragraph

Article in Pharmaceutics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.0field-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

15 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Salinity-induced capsaicin biosynthesis inIn silico pharmacology · 2025
    Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Capsaicin: a spicy way in liver disease.Frontiers in pharmacology · 2024
    Review
  15. 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

4 authors at 1 institution in 1 country.

Belén G SánchezUniversity of Alcalá, School of Medicine and Health Sciences, Department of Systems Biology, Biochemistry and Molecular Biology Unit, 28871 Alcalá de Henares, Madrid, Spain.
Alicia BortUniversity of Alcalá, School of Medicine and Health Sciences, Department of Systems Biology, Biochemistry and Molecular Biology Unit, 28871 Alcalá de Henares, Madrid, Spain.
José M Mora-RodríguezUniversity of Alcalá, School of Medicine and Health Sciences, Department of Systems Biology, Biochemistry and Molecular Biology Unit, 28871 Alcalá de Henares, Madrid, Spain.
Inés Díaz-LaviadaUniversity of Alcalá, School of Medicine and Health Sciences, Department of Systems Biology, Biochemistry and Molecular Biology Unit, 28871 Alcalá de Henares, Madrid, Spain.ORCID 0000-0001-9704-4373
Universidad de Alcalá · ES

Funding

Fundación Tatiana Pérez de Guzmán Patrocinio 2019-01Instituto de Salud Carlos III PI20/01327
6 · The paper itself

Abstract

The natural bioactive compound capsaicin has been reported to have anticancer activity, although the underlying mechanism of action has not been completely clarified. Herein, we investigated the mechanism whereby capsaicin exerts antitumor effects on prostate cancer cells. We found that capsaicin activated AMP-activated kinase (AMPK) and promoted cell death in the LKB1-expressing prostate cancer cell lines LNCaP and PC3, but not in the liver kinase B1 (LKB1)-null cell line DU-145. Capsaicin treatment stimulated LKB1 phosphorylation and activated AMPK in LKB1-expressing cells. In addition, LKB1 silencing in LNCaP and PC3 cells abrogated capsaicin-induced AMPK activation, while the overexpression of LKB1 by lentiviral infection in DU-145 cells induced capsaicin-triggered AMPK phosphorylation. Moreover, the calcium/calmodulin-dependent kinase kinase 2 (CaMKK2) inhibitor STO-609 did not modify the activation of AMPK induced by capsaicin, suggesting a CaMKK2-independent mechanism. Capsaicin-induced LKB1 phosphorylation was dependent on the transient receptor potential cation channel subfamily V member 1 (TRPV1), since TRPV1 knocked down by shRNA abolished LKB1 and AMPK phosphorylation in LKB1-expressing cells. Altogether, our results showed that capsaicin affected AMPK activity in an LKB1- and TRPV1-dependent fashion, linking TRPV1 with cell fate. These data also suggest that capsaicin may be a rational chemotherapeutic option for prostate tumors.

Indexed as

AMPKcapsaicinDU-145LKB1LNCaPPC3prostate cancerTRPV1

Identifiers

PMID35214061
PMCPMC8880011
OpenAlexW4210793962

What OpenQuestion holds

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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.