Evidence map›Paper›PMID 23449353›Full record

ArticleBritish journal of cancer2013

Marked improvement of cytotoxic effects induced by docetaxel on highly metastatic and androgen-independent prostate cancer cells by downregulating macrophage inhibitory cytokine-1.

M Mimeault, S L Johansson, S K Batra

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.8field-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

25 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
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  12. Research advances of secretory proteins in malignant tumors.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2021
    Article
  13. Review
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  16. A biodistribution study of solid lipid-polyethyleneimine hybrid nanocarrier for cancer RNAi therapy.European journal of pharmaceutics and biopharmaceutics : official journal of Arbeitsgemeinschaft fur Pharmazeutische Verfahrenstechnik e.V · 2016
    Article
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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

3 authors at 2 institutions in 1 country.

M MimeaultDepartment of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE, USA. mmimeault@unmc.edu
S L Johansson
S K Batra
University of Nebraska Medical Center · USNebraska Medical Center · US

Funding

Novel deregulated genes in the etiology and progression of human prostate cancerR01CA138791 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BATRA, SURINDER K. · 2010 to 2014
$1.9M
NCI NIH HHS R01 CA138791NCI NIH HHS R01CA138791
6 · The paper itself

Abstract

backgroundOverexpression of macrophage inhibitory cytokine-1 (MIC-1) frequently occurs during the progression of prostate cancer (PC) to androgen-independent (AI) and metastatic disease states and is associated with a poor outcome of patients.

methodsThe gain- and loss-of-function analyses of MIC-1 were performed to establish its implications for aggressive and chemoresistant phenotypes of metastatic and AI PC cells and the benefit of its downregulation for reversing docetaxel resistance.

resultsThe results have indicated that an enhanced level of secreted MIC-1 protein in PC3 cells is associated with their acquisition of epithelial-mesenchymal transition features and higher invasive capacity and docetaxel resistance. Importantly, the downregulation of MIC-1 in LNCaP-LN3 and PC3M-LN4 cells significantly decreased their invasive capacity and promoted the antiproliferative, anti-invasive and mitochrondrial- and caspase-dependent apoptotic effects induced by docetaxel. The downregulation of MIC-1 in PC3M-LN4 cells was also effective in promoting the cytotoxic effects induced by docetaxel on the side population (SP) endowed with stem cell-like properties and the non-SP cell fraction from PC3M-LN4 cells.

conclusionThese data suggest that the downregulation of MIC-1 may constitute a potential therapeutic strategy for improving the efficacy of current docetaxel-based chemotherapies, eradicating the total mass of PC cells and thereby preventing disease relapse and the death of PC patients.

Indexed as

Drug Resistance, NeoplasmAndrogen AntagonistsAndrogensAntineoplastic AgentsApoptosisCell Line, TumorCell ProliferationDocetaxelDown-RegulationEpithelial-Mesenchymal TransitionGrowth Differentiation Factor 15HumansMaleNeoplasm InvasivenessNeoplasm MetastasisProstatic NeoplasmsAndrogen AntagonistsAndrogensAntineoplastic AgentsDocetaxelGrowth Differentiation Factor 15Taxoids

Identifiers

PMID23449353
PMCPMC3619053
OpenAlexW2042811466

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.