Evidence map›Paper›PMID 27015684›Full record

ArticleMolecular and cellular biochemistry2016

Amblyomin-X induces ER stress, mitochondrial dysfunction, and caspase activation in human melanoma and pancreatic tumor cell.

Katia L P Morais, Mario Thiego Fernandes Pacheco, Carolina Maria Berra, Rosemary V Bosch, Juliana Mozer Sciani, Roger Chammas, Renata de Freitas Saito, Asif Iqbal, Ana Marisa Chudzinski-Tavassi

Open access · hybridAbstract read
In one paragraph

Article in Molecular and cellular biochemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.5field-weighted citation impact, top 13% 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

12 citing papers in PubMed, 20 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

9 authors at 3 institutions in 1 country.

Katia L P MoraisBiochemistry and Biophysics Laboratory, Butantan Institute, Av. Vital Brazil, 1500, São Paulo, SP, 05503-900, Brazil.
Mario Thiego Fernandes PachecoBiochemistry and Biophysics Laboratory, Butantan Institute, Av. Vital Brazil, 1500, São Paulo, SP, 05503-900, Brazil.
Carolina Maria BerraBiochemistry Department, Institute of Chemistry, University of São Paulo, São Paulo, Brazil.
Rosemary V BoschBiochemistry and Biophysics Laboratory, Butantan Institute, Av. Vital Brazil, 1500, São Paulo, SP, 05503-900, Brazil.
Juliana Mozer ScianiBiochemistry and Biophysics Laboratory, Butantan Institute, Av. Vital Brazil, 1500, São Paulo, SP, 05503-900, Brazil.
Roger ChammasExperimental Oncology Medical Investigation Laboratory - LIM/24, University of São Paulo School of Medicine, São Paulo, SP, Brazil.
Renata de Freitas SaitoExperimental Oncology Medical Investigation Laboratory - LIM/24, University of São Paulo School of Medicine, São Paulo, SP, Brazil.
Asif IqbalBiochemistry and Biophysics Laboratory, Butantan Institute, Av. Vital Brazil, 1500, São Paulo, SP, 05503-900, Brazil.
Ana Marisa Chudzinski-TavassiBiochemistry and Biophysics Laboratory, Butantan Institute, Av. Vital Brazil, 1500, São Paulo, SP, 05503-900, Brazil. ana.chudzinski@butantan.gov.br.
Instituto Butantan · BRUniversidade de São Paulo · BRUniversidade Federal de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During the last two decades, new insights into proteasome function and its role in several human diseases made it a potential therapeutic target. In this context, Amblyomin-X is a Kunitz-type FXa inhibitor similar to endogenous tissue factor pathway inhibitor (TFPI) and is a novel proteasome inhibitor. Herein, we have demonstrated Amblyomin-X cytotoxicity to different tumor cells lines such as pancreatic (Panc1, AsPC1BxPC3) and melanoma (SK-MEL-5 and SK-MEL-28). Of note, Amblyomin-X was not cytotoxic to normal human fibroblast cells. In addition, Amblyomin-X promoted accumulation of ER stress markers (GRP78 and GADD153) in sensitive (SK-MEL-28) and bortezomib-resistant (Mia-PaCa-2) tumor cells. The intracellular calcium concentration [Ca(2+)] i was slightly modulated in human tumor cells (SK-MEL-28 and Mia-PaCa-2) after 24 h of Amblyomin-X treatment. Furthermore, Amblyomin-X induced mitochondrial dysfunction, cytochrome-c release, PARP cleavage, and activation of caspase cascade in both human tumor (SK-MEL-28 and Mia-PaCa-2) cells. These investigations might help in further understanding of the antitumor properties of Amblyomin-X.

Indexed as

Arthropod ProteinsCaspasesCell Line, TumorEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressEnzyme ActivationHumansMelanomaMitochondriaPancreatic NeoplasmsRecombinant ProteinsSalivary Proteins and PeptidesAmblyomin-X protein, Amblyomma cajennenseArthropod ProteinsCaspasesEndoplasmic Reticulum Chaperone BiPHSPA5 protein, humanRecombinant ProteinsSalivary Proteins and PeptidesAmblyomin-XAntitumor drug candidateEndoplasmic reticulum stressKunitz-type inhibitorProteasome inhibitor

Identifiers

PMID27015684
PMCPMC4819916
OpenAlexW2306197593

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Registered trials

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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.