Evidence map›Paper›PMID 26494557›Full record

ArticleCancer gene therapy2015

Conditioned media from human ovarian cancer endothelial progenitor cells induces ovarian cancer cell migration by activating epithelial-to-mesenchymal transition.

L Teng, S Peng, H Guo, H Liang, Z Xu, Y Su, L Gao

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Cancer gene therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 33% 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

2 citing papers in PubMed, 9 citations in OpenAlex.

  1. Clinical perspectives of BET inhibition in ovarian cancer.Cellular oncology (Dordrecht, Netherlands) · 2021
    Review
  2. 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

7 authors at 3 institutions in 1 country.

L TengDepartment of Clinical Laboratory, Cancer Hospital, Harbin Medical University, Harbin, China.
S PengDepartment of Clinical Laboratory, Cancer Hospital, Harbin Medical University, Harbin, China.
H GuoDepartment of Clinical Laboratory, Cancer Hospital, Harbin Medical University, Harbin, China.
H LiangDepartment of Clinical Laboratory, Cancer Hospital, Harbin Medical University, Harbin, China.
Z XuDepartment of Clinical Laboratory, Cancer Hospital, Harbin Medical University, Harbin, China.
Y SuDepartment of Clinical Laboratory, Cancer Hospital, Harbin Medical University, Harbin, China.
L GaoDepartment of Clinical Laboratory, Nanjing Maternity and Child Health Care Hospital, Nanjing Medical University, Nanjing, China.
Harbin Medical University · CNThird Affiliated Hospital of Harbin Medical University · CNNanjing Maternity and Child Health Care Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bone marrow-derived endothelial progenitor cells (EPCs) migrate to and engraft at ovarian cancer sites. Understanding the interactions between ovarian cancer cells and EPCs is fundamental for determining whether to harness EPC-tumor interactions for delivery of therapeutic agents or target them for intervention. Ovarian cancer cell lines (SKOV-3 and OVCAR-3) were cultured alone or in EPC-conditioned media (EPC-CM). Migration of ovarian cancer cells was detected by transwell chamber. N-cadherin and E-cadherin expression were analyzed by real-time reverse transcription PCR and western blot. EPC-CM can increase transforming growth factor-beta (TGF-β) secretion in SKOV-3 and OVCAR-3 cells. EPC-CM induced loss of ovarian cancer cell-cell junctions, downregulation of E-cadherin, upregulation of N-cadherin and acquisition of a fibroblastic phenotype, consistent with an epithelial-to-mesenchymal transition (EMT). The specific TGF-β inhibitor SB431542 abolished the SKOV-3 and OVCAR-3 ovarian cancer cell migration induced by EPC-CM. In SKOV-3 and OVCAR-3 cells, EPC-CM downregulated E-cadherin and concurrently upregulated N-cadherin. EPC-CM upregulated the expression of transcriptional repressors of E-cadherin, Snail and Twist. Treatment with SB431542 abolished the effects of EPC-CM on the relative expression levels of cadherin, Snail and Twist. This study demonstrates that TGF-β has a role in EPC-CM-induced ovarian cancer migration by activating EMT.

Indexed as

BenzamidesCell Line, TumorCell MovementCells, CulturedCulture Media, ConditionedDioxolesEndothelial Progenitor CellsEpithelial-Mesenchymal TransitionFemaleHumansOvarian NeoplasmsSnail Family Transcription FactorsTranscription FactorsTransforming Growth Factor betaTwist-Related Protein 14-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamideBenzamidesCulture Media, ConditionedDioxolesSnail Family Transcription FactorsTranscription FactorsTransforming Growth Factor betaTwist-Related Protein 1

Identifiers

PMID26494557
OpenAlexW2173157534

What OpenQuestion holds

Textmetadata
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.