Evidence map›Paper›PMID 26625315›Full record

ArticleOncotarget2016

The pepper's natural ingredient capsaicin induces autophagy blockage in prostate cancer cells.

Ágata Ramos-Torres, Alicia Bort, Cecilia Morell, Nieves Rodríguez-Henche, Inés Díaz-Laviada

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, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
8.4field-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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.

  1. Guideline
  2. Article
  3. Review
  4. Article
  5. Article
  6. Capsaicin: Emerging Pharmacological and Therapeutic Insights.Current issues in molecular biology · 2024
    Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Exploring the Nutraceutical Potential of Dried PepperAntioxidants (Basel, Switzerland) · 2020
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  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

5 authors at 1 institution in 1 country.

Ágata Ramos-TorresDepartment of System Biology, Biochemistry and Molecular Biology Unit, School of Medicine, Alcala University, Alcala de Henares 28871, Madrid, Spain.
Alicia BortDepartment of System Biology, Biochemistry and Molecular Biology Unit, School of Medicine, Alcala University, Alcala de Henares 28871, Madrid, Spain.
Cecilia MorellDepartment of System Biology, Biochemistry and Molecular Biology Unit, School of Medicine, Alcala University, Alcala de Henares 28871, Madrid, Spain.
Nieves Rodríguez-HencheDepartment of System Biology, Biochemistry and Molecular Biology Unit, School of Medicine, Alcala University, Alcala de Henares 28871, Madrid, Spain.
Inés Díaz-LaviadaDepartment of System Biology, Biochemistry and Molecular Biology Unit, School of Medicine, Alcala University, Alcala de Henares 28871, Madrid, Spain.
Universidad de Alcalá · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Capsaicin, the pungent ingredient of red hot chili peepers, has been shown to have anti-cancer activities in several cancer cells, including prostate cancer. Several molecular mechanisms have been proposed on its chemopreventive action, including ceramide accumulation, endoplasmic reticulum stress induction and NFκB inhibition. However, the precise mechanisms by which capsaicin exerts its anti-proliferative effect in prostate cancer cells remain questionable. Herein, we have tested the involvement of autophagy on the capsaicin mechanism of action on prostate cancer LNCaP and PC-3 cells.The results showed that capsaicin induced prostate cancer cell death in a time- and concentration-dependent manner, increased the levels of microtubule-associated protein light chain 3-II (LC3-II, a marker of autophagy) and the accumulation of the cargo protein p62 suggesting an autophagy blockage. Moreover, confocal microscopy revealed that capsaicin treatment increased lysosomes which co-localized with LC3 positive vesicles in a similar extent to that produced by the lysosomal protease inhibitors E64 and pepstatin pointing to an autophagolysosomes breakdown inhibition. Furthermore, we found that capsaicin triggered ROS generation in cells, while the levels of ROS decreased with N-acetyl-cysteine (NAC), a ROS scavenger. Co-treatment of cells with NAC and capsaicin abrogated the effects of capsaicin on autophagy and cell death. Normal prostate PNT2 and RWPE-1 cells were more resistant to capsaicin-induced cytotoxicity and did not accumulate p62 protein.Taken together, these results suggest that ROS-mediated capsaicin-induced autophagy blockage contributes to antiproliferation in prostate cancer cells, which provides new insights into the anticancer molecular mechanism of capsaicin.

Indexed as

Antineoplastic Agents, PhytogenicAntioxidantsApoptosisAutophagyCapsaicinCapsicumCell Line, TumorCell ProliferationDose-Response Relationship, DrugHumansLysosomesMaleMicrotubule-Associated ProteinsPhosphatidylinositol 3-KinaseProstatic NeoplasmsProto-Oncogene Proteins c-aktAntineoplastic Agents, PhytogenicAntioxidantsCapsaicinMAP1LC3A protein, humanMicrotubule-Associated ProteinsMTOR protein, humanPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktReactive Oxygen SpeciesTOR Serine-Threonine Kinasesautophagycapsaicinprostate cancerreactive oxygen species

Identifiers

PMID26625315
PMCPMC4811481
OpenAlexW2186327842

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.