Evidence map›Paper›PMID 33771981›Full record

ArticleCell death discovery2021

Long non-coding RNA ZFAS1 is a major regulator of epithelial-mesenchymal transition through miR-200/ZEB1/E-cadherin, vimentin signaling in colon adenocarcinoma.

Stephen J O'Brien, Casey Fiechter, James Burton, Jacob Hallion, Mason Paas, Ankur Patel, Ajay Patel, Andre Rochet, Katharina Scheurlen, Sarah Gardner and 7 more

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.0field-weighted citation impact, top 4% 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

26 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
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  7. MicroRNA-200c in Cancer Generation, Invasion, and Metastasis.International journal of molecular sciences · 2025
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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

17 authors at 3 institutions in 2 countries.

Stephen J O'BrienPrice Institute of Surgical Research, Hiram C. Polk Jr. MD Department of Surgery, University of Louisville School of Medicine, Louisville, KY, 40202, USA.
Casey FiechterPrice Institute of Surgical Research, Hiram C. Polk Jr. MD Department of Surgery, University of Louisville School of Medicine, Louisville, KY, 40202, USA.
James BurtonPrice Institute of Surgical Research, Hiram C. Polk Jr. MD Department of Surgery, University of Louisville School of Medicine, Louisville, KY, 40202, USA.
Jacob HallionPrice Institute of Surgical Research, Hiram C. Polk Jr. MD Department of Surgery, University of Louisville School of Medicine, Louisville, KY, 40202, USA.
Mason PaasPrice Institute of Surgical Research, Hiram C. Polk Jr. MD Department of Surgery, University of Louisville School of Medicine, Louisville, KY, 40202, USA.
Ankur PatelPrice Institute of Surgical Research, Hiram C. Polk Jr. MD Department of Surgery, University of Louisville School of Medicine, Louisville, KY, 40202, USA.
Ajay PatelPrice Institute of Surgical Research, Hiram C. Polk Jr. MD Department of Surgery, University of Louisville School of Medicine, Louisville, KY, 40202, USA.
Andre RochetPrice Institute of Surgical Research, Hiram C. Polk Jr. MD Department of Surgery, University of Louisville School of Medicine, Louisville, KY, 40202, USA.
Katharina ScheurlenPrice Institute of Surgical Research, Hiram C. Polk Jr. MD Department of Surgery, University of Louisville School of Medicine, Louisville, KY, 40202, USA.
Sarah GardnerPrice Institute of Surgical Research, Hiram C. Polk Jr. MD Department of Surgery, University of Louisville School of Medicine, Louisville, KY, 40202, USA.
Maurice EichenbergerPrice Institute of Surgical Research, Hiram C. Polk Jr. MD Department of Surgery, University of Louisville School of Medicine, Louisville, KY, 40202, USA.
Harshini SarojiniPrice Institute of Surgical Research, Hiram C. Polk Jr. MD Department of Surgery, University of Louisville School of Medicine, Louisville, KY, 40202, USA.
Sudhir SrivastavaDepartment of Bioinformatics and Biostatistics, University of Louisville, Louisville, KY, USA.ORCID http://orcid.org/0000-0003-4990-7693
Shesh RaiDepartment of Bioinformatics and Biostatistics, University of Louisville, Louisville, KY, USA.
Theodore KalbfleischDepartment of Veterinary Science, Gluck Equine Research Center, University of Kentucky, Lexington, KY, USA.ORCID http://orcid.org/0000-0002-2370-8189
Hiram C PolkPrice Institute of Surgical Research, Hiram C. Polk Jr. MD Department of Surgery, University of Louisville School of Medicine, Louisville, KY, 40202, USA.
Susan GalandiukPrice Institute of Surgical Research, Hiram C. Polk Jr. MD Department of Surgery, University of Louisville School of Medicine, Louisville, KY, 40202, USA. susan.galandiuk@louisville.edu.ORCID http://orcid.org/0000-0001-9994-5263
University of Louisville · USIndian Agricultural Statistics Research Institute · INUniversity of Kentucky · US

Funding

University of Louisville Cancer Education ProgramR25CA134283 · NCI · UNIVERSITY OF LOUISVILLE · PI HEIN, DAVID W, KIDD, LA CREIS RENEE · 2011 to 2022
$3.1M
Foundation for the National Institutes of Health (Foundation for the National Institutes of Health, Inc.) NIH 2R25CA134283-06A1NCI NIH HHS R25 CA134283
6 · The paper itself

Abstract

Colon adenocarcinoma is a common cause of cancer-related deaths worldwide. Epithelial-mesenchymal transition is a major regulator of cancer metastasis, and increased understanding of this process is essential to improve patient outcomes. Long non-coding RNA (lncRNA) are important regulators of carcinogenesis. To identify lncRNAs associated with colon carcinogenesis, we performed an exploratory differential gene expression analysis comparing paired colon adenocarcinoma and normal colon epithelium using an RNA-sequencing data set. This analysis identified lncRNA ZFAS1 as significantly increased in colon cancer compared to normal colon epithelium. This finding was validated in an institutional cohort using laser capture microdissection. ZFAS1 was also found to be principally located in the cellular cytoplasm. ZFAS1 knockdown was associated with decreased cellular proliferation, migration, and invasion in two colon cancer cell lines (HT29 and SW480). MicroRNA-200b and microRNA-200c (miR-200b and miR-200c) are experimentally validated targets of ZFAS1, and this interaction was confirmed using reciprocal gene knockdown. ZFAS1 knockdown regulated ZEB1 gene expression and downstream targets E-cadherin and vimentin. Knockdown of miR-200b or miR-200c reversed the effect of ZFAS1 knockdown in the ZEB1/E-cadherin, vimentin signaling cascade, and the effects of cellular migration and invasion, but not cellular proliferation. ZFAS1 knockdown was also associated with decreased tumor growth in an in vivo mouse model. These results demonstrate the critical importance of ZFAS1 as a regulator of the miR-200/ZEB1/E-cadherin, vimentin signaling cascade.

Identifiers

PMID33771981
PMCPMC7998025
OpenAlexW3137575798

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.