Evidence map›Paper›PMID 30846786›Full record

ArticleScientific reports2019

Differential gene expression induced by Verteporfin in endometrial cancer cells.

Lisa Gahyun Bang, Venkata Ramesh Dasari, Dokyoon Kim, Radhika P Gogoi

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 30% 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

9 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. YAP/TAZ Transcriptional Coactivators Create Therapeutic Vulnerability to Verteporfin in EGFR-mutant Glioblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021
    Article
  6. Article
  7. Article
  8. Review
  9. Verteporfin induced SUMOylation of YAP1 in endometrial cancer.American journal of cancer research · 2020
    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

4 authors at 3 institutions in 1 country.

Lisa Gahyun BangBiomedical and Translational Informatics Institute, Geisinger, Danville, PA, USA.
Venkata Ramesh DasariWeis Center for Research, Geisinger Clinic, Danville, PA, USA.
Dokyoon KimBiomedical and Translational Informatics Institute, Geisinger, Danville, PA, USA.
Radhika P GogoiWeis Center for Research, Geisinger Clinic, Danville, PA, USA. rpgogoi@geisinger.edu.ORCID 0000-0002-8556-829X
Geisinger Medical Center · USGeisinger Neuroscience Institute · USPennsylvania State University · US

Funding

UTAH REGIONAL CANCER CENTERP30CA042014 · NCI · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI KATHARINE S ULLMAN · 1986 to 2026
$72.6M
NCI NIH HHS P30 CA042014
6 · The paper itself

Abstract

Endometrial cancer (EMCA) is a clinically heterogeneous disease. Previously, we tested the efficacy of Verteporfin (VP) in EMCA cells and observed cytotoxic and anti-proliferative effects. In this study, we analyzed RNA sequencing data to investigate the comprehensive transcriptomic landscape of VP treated Type 1 EMCA cell lines, including HEC-1-A and HEC-1-B. There were 549 genes with differential expression of two-fold or greater and P < 0.05 after false discovery rate correction for the HEC-1-B cell line. Positive regulation of TGFβ1 production, regulation of lipoprotein metabolic process, cell adhesion, endodermal cell differentiation, formation and development, and integrin mediated signaling pathway were among the significantly associated terms. A functional enrichment analysis of differentially expressed genes after VP treatment revealed extracellular matrix organization Gene Ontology as the most significant. CDC23 and BUB1B, two genes crucially involved in mitotic checkpoint progression, were found to be the pair with the best association from STRING among differentially expressed genes in VP treated HEC-1-B cells. Our in vivo results indicate that subcutaneous tumors in mice were regressed after VP treatment by inhibiting cell cycle pathway proteins. The present study revealed multiple key genes of pathological significance in EMCA, thereby improving our understanding of molecular profiles of EMCA cells.

Indexed as

AnimalsBlotting, WesternCell Line, TumorEndometrial NeoplasmsFemaleGene Expression Regulation, NeoplasticGenes, NeoplasmHumansMiceNeoplasm TransplantationReal-Time Polymerase Chain ReactionSequence AlignmentTranscriptomeVerteporfinVerteporfin

Identifiers

PMID30846786
PMCPMC6405995
OpenAlexW2918841585

What OpenQuestion holds

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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.