Evidence map›Paper›PMID 33811561›Full record

ArticleApoptosis : an international journal on programmed cell death2021

Ca

Michela Raimondi, Fabrizio Fontana, Monica Marzagalli, Matteo Audano, Giangiacomo Beretta, Patrizia Procacci, Patrizia Sartori, Nico Mitro, Patrizia Limonta

Open access · hybridAbstract read
In one paragraph

Article in Apoptosis : an international journal on programmed cell death, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 2 pooled it
4.7field-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

54 citing papers in PubMed, 2 syntheses or guidelines pooled it, 84 citations in OpenAlex.

  1. Pooled it
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  6. Article
  7. pH-responsive CaCOiScience · 2026
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  15. Mitochondrial bioenergetics and networks in melanoma: an update.Apoptosis : an international journal on programmed cell death · 2025
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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

9 authors at 1 institution in 1 country.

Michela Raimondi *Department of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Milan, Italy.
Fabrizio Fontana *Department of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Milan, Italy.
Monica MarzagalliDepartment of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Milan, Italy.
Matteo AudanoDepartment of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Milan, Italy.
Giangiacomo BerettaDepartment of Environmental Science and Policy, Università degli Studi di Milano, Milan, Italy.
Patrizia ProcacciDepartment of Biomedical Sciences for Health, Università degli Studi di Milano, Milan, Italy.
Patrizia SartoriDepartment of Biomedical Sciences for Health, Università degli Studi di Milano, Milan, Italy.
Nico MitroDepartment of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Milan, Italy.
Patrizia LimontaDepartment of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Milan, Italy. patrizia.limonta@unimi.it.
University of Milan · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Melanoma is an aggressive tumor with still poor therapy outcomes. δ-tocotrienol (δ-TT) is a vitamin E derivative displaying potent anti-cancer properties. Previously, we demonstrated that δ-TT triggers apoptosis in human melanoma cells. Here, we investigated whether it might also activate paraptosis, a non-canonical programmed cell death. In accordance with the main paraptotic features, δ-TT was shown to promote cytoplasmic vacuolization, associated with endoplasmic reticulum/mitochondrial dilation and protein synthesis, as well as MAPK activation in A375 and BLM cell lines. Moreover, treated cells exhibited a significant reduced expression of OXPHOS complex I and a marked decrease in oxygen consumption and mitochondrial membrane potential, culminating in decreased ATP synthesis and AMPK phosphorylation. This mitochondrial dysfunction resulted in ROS overproduction, found to be responsible for paraptosis induction. Additionally, δ-TT caused Ca

Indexed as

Antineoplastic AgentsCalciumCell Line, TumorEndoplasmic ReticulumHumansMelanomaMembrane Potential, MitochondrialMitochondriaMitochondrial SwellingMitogen-Activated Protein KinasesReactive Oxygen SpeciesRegulated Cell DeathSignal TransductionVitamin EAntineoplastic AgentsCalciumMitogen-Activated Protein KinasesReactive Oxygen Speciestocotrienol, deltaVitamin ECa2+ overloadMelanomaMitochondrial impairmentParaptosisROS productionTocotrienols

Identifiers

PMID33811561
PMCPMC8197726
OpenAlexW3145666903

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.