Evidence map›Paper›PMID 27129171›Full record

ArticleOncotarget2016

Emblica officinalis extract downregulates pro-angiogenic molecules via upregulation of cellular and exosomal miR-375 in human ovarian cancer cells.

Alok De, Benjamin Powers, Archana De, Jianping Zhou, Siddarth Sharma, Peter Van Veldhuizen, Ajay Bansal, Ramratan Sharma, Mukut Sharma

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

21 citing papers in PubMed, 33 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 2 institutions in 1 country.

Alok DeKansas City VA Medical Center and Midwest Biomedical Research Foundation, Kansas City, MO 64128, United States.
Benjamin PowersKansas City VA Medical Center and Midwest Biomedical Research Foundation, Kansas City, MO 64128, United States.
Archana DeKansas City VA Medical Center and Midwest Biomedical Research Foundation, Kansas City, MO 64128, United States.
Jianping ZhouKansas City VA Medical Center and Midwest Biomedical Research Foundation, Kansas City, MO 64128, United States.
Siddarth SharmaKansas City VA Medical Center and Midwest Biomedical Research Foundation, Kansas City, MO 64128, United States.
Peter Van VeldhuizenKansas City VA Medical Center and Midwest Biomedical Research Foundation, Kansas City, MO 64128, United States.
Ajay BansalKansas City VA Medical Center and Midwest Biomedical Research Foundation, Kansas City, MO 64128, United States.
Ramratan SharmaKansas City VA Medical Center and Midwest Biomedical Research Foundation, Kansas City, MO 64128, United States.
Mukut SharmaKansas City VA Medical Center and Midwest Biomedical Research Foundation, Kansas City, MO 64128, United States.
Kansas City VA Medical Center · USBiomedical Research Foundation · US

Funding

Cytokine based murine focal glomerulosclerosis model a prelude to novel therapyI01BX001037 · VA · KANSAS CITY VA MEDICAL CENTER · PI SAVIN, VIRGINIA J. · 2011 to 2014
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BLRD VA I01 BX001037
6 · The paper itself

Abstract

Ovarian cancer (OC) is highly resistant to current treatment strategies based on a combination of surgery, chemotherapy and radiation therapy. We have recently demonstrated the anti-neoplastic effect of Amla extract (Emblica officinalis, AE) on OC cells in vitro and in vivo. We hypothesized that AE attenuates growth of OC through microRNA (miR)-regulated mechanism(s). The inhibitory effect of AE on proliferation, migration and invasiveness (P≤0.001) of SKOV3 cells and >90% attenuation of tumor growth in a xenograft mouse model suggested multiple targets. RT-qPCR analysis of microRNAs associated with OC showed a >2,000-fold increase in the expression of miR-375 in AE-treated SKOV3 cells that was blocked by an exogenous miR-375 inhibitor (P≤0.001). AE also decreased the gene and protein expression of IGF1R, a target of miR-375 (P≤0.001), and SNAIL1 (P≤0.002), an EMT-associated transcription factor that represses E-cadherin expression (P≤0.003). AE increased E-cadherin expression (P≤0.001). Treatment of SKOV3 cells with AE resulted in increased miR-375 in exosomes in the medium (P≤0.01). Finally, AE significantly decreased the expression of IGF1R and SNAIL1 proteins during attenuation of SKOV3-derived xenograft tumor. Together, these results show that AE modulates cancer cells and the tumor microenvironment via activation of miR-375 and by targeting IGF1R and SNAIL1 in OC cells.

Indexed as

Antigens, CDCadherinsCell Line, TumorDown-RegulationExosomesFemaleGene Expression Regulation, NeoplasticHumansMicroRNAsOvarian NeoplasmsPhyllanthus emblicaPlant ExtractsReceptor, IGF Type 1Receptors, SomatomedinSnail Family Transcription FactorsTumor BurdenAntigens, CDCadherinsCDH1 protein, humanIGF1R protein, humanMicroRNAsMIRN375 microRNA, humanPlant ExtractsReceptor, IGF Type 1Receptors, SomatomedinSNAI1 protein, humanSnail Family Transcription FactorsEmblica officinalisexosomesIGF1RmicroRNA-375ovarian cancer

Identifiers

PMID27129171
PMCPMC5058772
OpenAlexW2343680311

What OpenQuestion holds

Textmetadata
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.