Evidence map›Paper›PMID 27626172›Full record

ArticleOncotarget2016

Nestin suppression attenuates invasive potential of endometrial cancer cells by downregulating TGF-β signaling pathway.

Amber A Bokhari, Tabari M Baker, Batsukh Dorjbal, Sana Waheed, Christopher M Zahn, Chad A Hamilton, G Larry Maxwell, Viqar Syed

RetractedOpen access · diamondAbstract readRetracted Publication
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. It has been retracted, and should not be counted. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.1field-weighted citation impact, top 19% 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

15 citing papers in PubMed, 19 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 1 country.

Amber A BokhariUniformed Services University, Department of Obstetrics and Gynecology, Bethesda, MD 20814, USA.
Tabari M BakerUniformed Services University, Department of Obstetrics and Gynecology, Bethesda, MD 20814, USA.
Batsukh DorjbalUniformed Services University, Department of Obstetrics and Gynecology, Bethesda, MD 20814, USA.
Sana WaheedUniformed Services University, Department of Obstetrics and Gynecology, Bethesda, MD 20814, USA.
Christopher M ZahnAmerican College of Obstetricians and Gynecologists, Washington, DC 20024, USA.
Chad A HamiltonUniformed Services University, Department of Obstetrics and Gynecology, Bethesda, MD 20814, USA.
G Larry MaxwellWomen's Health Integrated Research Center at Inova Health System, Department of Defense Gynecologic Cancer Center of Excellence, Annandale, VA 22003, USA.
Viqar SyedUniformed Services University, Department of Obstetrics and Gynecology, Bethesda, MD 20814, USA.
Uniformed Services University of the Health Sciences · USAmerican Congress of Obstetricians and Gynecologists · USInova Fairfax Hospital · USInova Health System · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nestin, an intermediate filament protein and a stem cell marker is expressed in several tumors. Until recently, little was known about the expression levels and the role of Nestin in endometrial cancer. Compared to the immortalized endometrial epithelial cell line EM-E6/E7-TERT, endometrial cancer cell lines express high to moderate levels of Nestin. Furthermore, endometrial tumors and tumor cell lines have a cancer stem-like cell subpopulation expressing CD133. Among the cancer lines, AN3CA and KLE cells exhibited both a significantly higher number of CD133+ cells and expressed Nestin at higher levels than Ishikawa cells. Knockdown of Nestin in AN3CA and KLE increased cells in G0/G1 phase of the cell cycle, whereas overexpression in Ishikawa decreased cells in G0/G1 phase and increased cells in S-phase. Nestin knockdown cells showed increased p21, p27, and PNCA levels and decreased expression of cyclin-D1 and D3. In contrast, Nestin overexpression revealed an inverse expression pattern of cell cycle regulatory proteins. Nestin knockdown inhibited cancer cell growth and invasive potential by downregulating TGF-β signaling components, MMP-2, MMP-9, vimentin, SNAIL, SLUG, Twist, N-cadherin, and upregulating the epithelial cell marker E-cadherin whereas the opposite was observed with Nestin overexpressing Ishikawa cells. Nestin knockdown also inhibited, while overexpression promoted invadopodia formation and pFAK expression. Knockdown of Nestin significantly reduced tumor volume in vivo. Finally, progesterone inhibited Nestin expression in endometrial cancer cells. These results suggest that Nestin can be a therapeutic target for cancer treatment.

Indexed as

CadherinsCell Line, TumorDown-RegulationEndometrial NeoplasmsEpithelial-Mesenchymal TransitionFemaleG1 Phase Cell Cycle CheckpointsHumansNeoplasm InvasivenessNestinProgesteroneSignal TransductionTransforming Growth Factor betaCadherinsNestinProgesteroneTransforming Growth Factor betaangiogenesiscell proliferationepithelial-mesenchymal-transitionmatrix metalloproteinasesprogesterone

Identifiers

PMID27626172
PMCPMC5342511
OpenAlexW2514949913

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.