Format

Send to

Choose Destination
Cell Death Dis. 2018 Jul 3;9(7):736. doi: 10.1038/s41419-018-0777-5.

An antisense RNA capable of modulating the expression of the tumor suppressor microRNA-34a.

Author information

1
Department of Oncology and Pathology, Karolinska Institutet, Stockholm, SE-17177, Sweden. jason.serviss@ki.se.
2
Department of Oncology and Pathology, Karolinska Institutet, Stockholm, SE-17177, Sweden.
3
Department of Medical Biochemistry and Cell Biology, Institute of Biomedicine, The Sahlgrenska Academy, University of Gothenburg, SE-405 30, Gothenburg, Sweden.
4
Kennedy Institute of Rheumatology, University of Oxford, Roosevelt Drive, Oxford, OX3 7FY, UK.
5
Rheumatology Unit, Department of Medicine, Karolinska University Hospital, Solna, Karolinska Institutet, Stockholm, Sweden.
6
Laboratory for Experimental Oncology and Radiobiology (LEXOR), Center for Experimental Molecular Medicine (CEMM), Academic Medical Center, Amsterdam, The Netherlands.
7
Ludwig Institute for Cancer Research, Stockholm, Sweden.
8
Department of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden.

Abstract

The microRNA-34a is a well-studied tumor suppressor microRNA (miRNA) and a direct downstream target of TP53 with roles in several pathways associated with oncogenesis, such as proliferation, cellular growth, and differentiation. Due to its broad tumor suppressive activity, it is not surprising that miR34a expression is altered in a wide variety of solid tumors and hematological malignancies. However, the mechanisms by which miR34a is regulated in these cancers is largely unknown. In this study, we find that a long noncoding RNA transcribed antisense to the miR34a host gene, is critical for miR34a expression and mediation of its cellular functions in multiple types of human cancer. We name this long noncoding RNA lncTAM34a, and characterize its ability to facilitate miR34a expression under different types of cellular stress in both TP53-deficient and wild-type settings.

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center