MiRNA-200C expression in Fanconi anemia pathway functionally deficient lung cancers.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
24 02 2021
Historique:
received: 28 12 2019
accepted: 09 02 2021
entrez: 25 2 2021
pubmed: 26 2 2021
medline: 15 12 2021
Statut: epublish

Résumé

The Fanconi Anemia (FA) pathway is essential for human cells to maintain genomic integrity following DNA damage. This pathway is involved in repairing damaged DNA through homologous recombination. Cancers with a defective FA pathway are expected to be more sensitive to cross-link based therapy or PARP inhibitors. To evaluate downstream effectors of the FA pathway, we studied the expression of 734 different micro RNAs (miRNA) using NanoString nCounter miRNA array in two FA defective lung cancer cells and matched control cells, along with two lung tumors and matched non-tumor tissue samples that were deficient in the FA pathway. Selected miRNA expression was validated with real-time PCR analysis. Among 734 different miRNAs, a cluster of microRNAs were found to be up-regulated including an important cancer related micro RNA, miR-200C. MiRNA-200C has been reported as a negative regulator of epithelial-mesenchymal transition (EMT) and inhibits cell migration and invasion by promoting the upregulation of E-cadherin through targeting ZEB1 and ZEB2 transcription factors. miRNA-200C was increased in the FA defective lung cancers as compared to controls. AmpliSeq analysis showed significant reduction in ZEB1 and ZEB2 mRNA expression. Our findings indicate the miRNA-200C potentially play a very important role in FA pathway downstream regulation.

Identifiants

pubmed: 33627769
doi: 10.1038/s41598-021-83884-9
pii: 10.1038/s41598-021-83884-9
pmc: PMC7904768
doi:

Substances chimiques

Cadherins 0
Homeodomain Proteins 0
MicroRNAs 0
Zinc Finger E-box Binding Homeobox 2 0
Zinc Finger E-box-Binding Homeobox 1 0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

4420

Subventions

Organisme : NCI NIH HHS
ID : R01 CA152101
Pays : United States
Organisme : NCI NIH HHS
ID : R21 CA181291
Pays : United States

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Auteurs

Wenrui Duan (W)

Department of Human and Molecular Genetics, Herbert Wertheim College of Medicine, The Florida International University, Miami, FL, 33199, USA. wduan@fiu.edu.
Biomolecular Sciences Institute, The Florida International University, Miami, FL, 33199, USA. wduan@fiu.edu.
Comprehensive Cancer Center at The Ohio State University College of Medicine and Public Health, Columbus, OH, 43210, USA. wduan@fiu.edu.

Shirley Tang (S)

Comprehensive Cancer Center at The Ohio State University College of Medicine and Public Health, Columbus, OH, 43210, USA.

Li Gao (L)

Department of Human and Molecular Genetics, Herbert Wertheim College of Medicine, The Florida International University, Miami, FL, 33199, USA.

Kathleen Dotts (K)

Comprehensive Cancer Center at The Ohio State University College of Medicine and Public Health, Columbus, OH, 43210, USA.

Andrew Fink (A)

Comprehensive Cancer Center at The Ohio State University College of Medicine and Public Health, Columbus, OH, 43210, USA.

Arjun Kalvala (A)

Comprehensive Cancer Center at The Ohio State University College of Medicine and Public Health, Columbus, OH, 43210, USA.

Brittany Aguila (B)

Comprehensive Cancer Center at The Ohio State University College of Medicine and Public Health, Columbus, OH, 43210, USA.

Qi-En Wang (QE)

Department of Radiation Oncology, Comprehensive Cancer Center, The Ohio State University, Columbus, OH, 43210, USA.

Miguel A Villalona-Calero (MA)

Department of Human and Molecular Genetics, Herbert Wertheim College of Medicine, The Florida International University, Miami, FL, 33199, USA. mvillalona@coh.org.
Department of Medical Oncology and Therapeutics Research, City of Hope National Medical Center, Duarte, CA, 91010, USA. mvillalona@coh.org.

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Classifications MeSH