Evidence map›Paper›PMID 26471237›Full record

ArticleScientific reports2015

EGCG antagonizes Bortezomib cytotoxicity in prostate cancer cells by an autophagic mechanism.

Alice Modernelli, Valeria Naponelli, Maria Giovanna Troglio, Martina Bonacini, Ileana Ramazzina, Saverio Bettuzzi, Federica Rizzi

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
5.5field-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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

Alice ModernelliDepartment of Biomedicine, Biotechnology and Translational Research, University of Parma, Via Volturno 39/a, 43125 Parma, Italy.
Valeria NaponelliDepartment of Biomedicine, Biotechnology and Translational Research, University of Parma, Via Volturno 39/a, 43125 Parma, Italy.
Maria Giovanna TroglioDepartment of Biomedicine, Biotechnology and Translational Research, University of Parma, Via Volturno 39/a, 43125 Parma, Italy.
Martina BonaciniDepartment of Biomedicine, Biotechnology and Translational Research, University of Parma, Via Volturno 39/a, 43125 Parma, Italy.
Ileana RamazzinaDepartment of Biomedicine, Biotechnology and Translational Research, University of Parma, Via Volturno 39/a, 43125 Parma, Italy.
Saverio BettuzziDepartment of Biomedicine, Biotechnology and Translational Research, University of Parma, Via Volturno 39/a, 43125 Parma, Italy.
Federica RizziDepartment of Biomedicine, Biotechnology and Translational Research, University of Parma, Via Volturno 39/a, 43125 Parma, Italy.
University of Parma · ITIstituto Nazionale Biostrutture e Biosistemi · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The proteasome inhibitors Bortezomib (BZM) and MG132 trigger cancer cell death via induction of endoplasmic reticulum (ER) stress and unfolded protein response. Epigallocatechin gallate (EGCG), the most bioactive green tea polyphenol, is known to display strong anticancer properties as it inhibits proteasome activity and induces ER stress. We investigated whether combined delivery of a proteasome inhibitor with EGCG enhances prostate cancer cell death through increased induction of ER stress. Paradoxically, EGCG antagonized BZM cytotoxicity even when used at low concentrations. Conversely, the MG132 dose-response curve was unaffected by co-administration of EGCG. Moreover, apoptosis, proteasome inhibition and ER stress were inhibited in PC3 cells simultaneously treated with BZM and EGCG but not with a combination of MG132 and EGCG; EGCG enhanced autophagy induction in BZM-treated cells only. Autophagy inhibition restored cytotoxicity concomitantly with CHOP and p-eIF2α up-regulation in cells treated with BZM and EGCG. Overall, these findings demonstrate that EGCG antagonizes BZM toxicity by exacerbating the activation of autophagy, which in turn mitigates ER stress and reduces CHOP up-regulation, finally protecting PC3 cells from cell death.

Indexed as

Antineoplastic AgentsAutophagyBortezomibCatechinCell Line, TumorEndoplasmic Reticulum StressEukaryotic Initiation Factor-2HumansLeupeptinsMaleMicrotubule-Associated ProteinsProstatic NeoplasmsProteasome InhibitorsTranscription Factor CHOPUp-RegulationAntineoplastic Agentsbenzyloxycarbonylleucyl-leucyl-leucine aldehydeBortezomibCatechinDDIT3 protein, humanepigallocatechin gallateEukaryotic Initiation Factor-2LeupeptinsMAP1LC3B protein, humanMicrotubule-Associated ProteinsProteasome InhibitorsTranscription Factor CHOP

Identifiers

PMID26471237
PMCPMC4607952
OpenAlexW2410130988

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.