Evidence map›Paper›PMID 27537898›Full record

ArticleMarine drugs2016

Tumor Protein (TP)-p53 Members as Regulators of Autophagy in Tumor Cells upon Marine Drug Exposure.

Edward A Ratovitski

Open access · goldAbstract read
In one paragraph

Article in Marine drugs, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

19 citing papers in PubMed, 33 citations in OpenAlex.

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  15. Chromomycin AThe Journal of general physiology · 2018
    Article
  16. Article
  17. Article
  18. Anticancer Effects of the Marine SpongeEvidence-based complementary and alternative medicine : eCAM · 2017
    Article
  19. 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

1 author at 1 institution in 1 country.

Edward A RatovitskiHead and Neck Cancer Research Division, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA. eratovi1@jhmi.edu.
Johns Hopkins Medicine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Targeting autophagic pathways might play a critical role in designing novel chemotherapeutic approaches in the treatment of human cancers, and the prevention of tumor-derived chemoresistance. Marine compounds were found to decrease tumor cell growth in vitro and in vivo. Some of them were shown to induce autophagic flux in tumor cells. In this study, we observed that the selected marine life-derived compounds (Chromomycin A2, Psammaplin A, and Ilimaquinone) induce expression of several autophagic signaling intermediates in human squamous cell carcinoma, glioblastoma, and colorectal carcinoma cells in vitro through a transcriptional regulation by tumor protein (TP)-p53 family members. These conclusions were supported by specific qPCR expression analysis, luciferase reporter promoter assay, and chromatin immunoprecipitation of promoter sequences bound to the TP53 family proteins, and silencing of the TP53 members in tumor cells.

Indexed as

Antineoplastic AgentsApoptosisAquatic OrganismsAutophagyCell Line, TumorCell SurvivalChromatin ImmunoprecipitationDisulfidesHumansPlicamycinQuinonesReal-Time Polymerase Chain ReactionRNA InterferenceRNA, Small InterferingSesquiterpenesSignal TransductionAntineoplastic Agentschromomycin A2DisulfidesilimaquinonePlicamycinpsammaplin AQuinonesRNA, Small InterferingSesquiterpenesTumor Suppressor Protein p53Tyrosineautophagycancermarine drugsp53 family memberstranscription

Identifiers

PMID27537898
PMCPMC4999915
OpenAlexW2508615560

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.