Evidence map›Paper›PMID 20388782›Full record

ArticleCancer research2010

Gemcitabine sensitivity can be induced in pancreatic cancer cells through modulation of miR-200 and miR-21 expression by curcumin or its analogue CDF.

Shadan Ali, Aamir Ahmad, Sanjeev Banerjee, Subhash Padhye, Kristin Dominiak, Jacqueline M Schaffert, Zhiwei Wang, Philip A Philip, Fazlul H Sarkar

RetractedOpen access · bronzeAbstract readRetracted Publication
In one paragraph

Article in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 185 papers.

0numbers the graph read from it
0cells of the map it votes in
185citing papers in PubMed
17.6field-weighted citation impact, top 1% 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

185 citing papers in PubMed, 424 citations in OpenAlex.

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  17. MiR-194 promotes hepatocellular carcinoma through negative regulation of CADM1.International journal of clinical and experimental pathology · 2020
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125 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

Shadan AliDivision of Hematology/Oncology, Department of Pathology, Karmanos Cancer Institute, Wayne State University, Detroit, Michigan 48201, USA.
Aamir Ahmad
Sanjeev Banerjee
Subhash Padhye
Kristin Dominiak
Jacqueline M Schaffert
Zhiwei Wang
Philip A Philip
Fazlul H Sarkar
Wayne State University · USThe Barbara Ann Karmanos Cancer Institute · USD.Y. Patil University · IN

Funding

RO1: A novel and targeted approach to inhibit invasion and angiogenesisR01CA131151 · NCI · WAYNE STATE UNIVERSITY · PI SARKAR, FAZLUL H. · 2008 to 2012
$1.8M
Prevention of Tumor Progression by a Novel ApproachR01CA154321 · NCI · WAYNE STATE UNIVERSITY · PI SARKAR, FAZLUL H. · 2011 to 2015
$1.5M
FoxM1: A molecular target in pancreatic cancerR01CA132794 · NCI · WAYNE STATE UNIVERSITY · PI SARKAR, FAZLUL H. · 2009 to 2013
$1.5M
NCI NIH HHS 3R01CA131151-02S1NCI NIH HHS 5R01CA131151NCI NIH HHS 5R01CA132794NCI NIH HHS R01 CA131151NCI NIH HHS R01 CA132794NCI NIH HHS R01 CA154321
6 · The paper itself

Abstract

Curcumin induces cancer cell growth arrest and apoptosis in vitro, but its poor bioavailability in vivo limits its antitumor efficacy. We have previously evaluated the bioavailability of novel analogues of curcumin compared with curcumin, and we found that the analogue CDF exhibited greater systemic and pancreatic tissue bioavailability. In this study, we evaluated the effects of CDF or curcumin alone or in combination with gemcitabine on cell viability and apoptosis in gemcitabine-sensitive and gemcitabine-resistant pancreatic cancer (PC) cell lines. Mechanistic investigations revealed a significant reduction in cell viability in CDF-treated cells compared with curcumin-treated cells, which were also associated with the induction of apoptosis, and these results were consistent with the downregulation of Akt, cyclooxygenase-2, prostaglandin E(2), vascular endothelial growth factor, and NF-kappaB DNA binding activity. We have also documented attenuated expression of miR-200 and increased expression of miR-21 (a signature of tumor aggressiveness) in gemcitabine-resistant cells relative to gemcitabine-sensitive cells. Interestingly, CDF treatment upregulated miR-200 expression and downregulated the expression of miR-21, and the downregulation of miR-21 resulted in the induction of PTEN. These results prompt further interest in CDF as a drug modality to improve treatment outcome of patients diagnosed with PC as a result of its greater bioavailability in pancreatic tissue.

Indexed as

Antineoplastic Combined Chemotherapy ProtocolsApoptosisCell Line, TumorCurcuminDeoxycytidineDinoprostoneDNA, ComplementaryDNA, NeoplasmDrug SynergismGemcitabineGene Expression Regulation, NeoplasticGene SilencingHumansMicroRNAsNF-kappa BOligonucleotides, AntisenseCurcumincycloart-23Z-ene-3 beta,25-diol-3 beta-trans-ferulateDeoxycytidineDinoprostoneDNA, ComplementaryDNA, NeoplasmGemcitabineMicroRNAsMIRN200 microRNA, humanNF-kappa BOligonucleotides, AntisensePTEN PhosphohydrolasePTEN protein, humanTriterpenesVascular Endothelial Growth Factor A

Identifiers

PMID20388782
PMCPMC2978024
OpenAlexW2014442719

What OpenQuestion holds

Textmetadata
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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.