FEBS letters, 2014-05, Vol.588 (9), p.1780-1786
2014
Details
- Autor(en) / Beteiligte
- Titel
- High expression of long non-coding RNA H19 is required for efficient tumorigenesis induced by Bcr-Abl oncogene
- Ist Teil von
- FEBS letters, 2014-05, Vol.588 (9), p.1780-1786
- Ort / Verlag
- England: Elsevier B.V
- Erscheinungsjahr
- 2014
- Link zum Volltext
- Quelle
- Free E-Journal (出版社公開部分のみ）
- Beschreibungen/Notizen
- •H19 is expressed in Bcr-Abl transformants in an Abl kinase-dependent manner.•Silencing H19 expression promotes K562 leukemic cells to undergo apoptosis.•H19 deficiency inhibits the growth of Bcr-Abl-positive tumor in nude mice.•The expression of H19 is regulated by c-Myc in the K562 cells. Dysregulation of non-coding RNA H19 has been observed in various tumors. However, it remains unknown whether H19 is involved in Bcr-Abl-induced leukemia. Here, we demonstrate a critical requirement for H19 in Bcr-Abl-mediated tumorigenesis. H19 was highly expressed in Bcr-Abl-transformed cell lines and primary cells derived from patients in a Bcr-Abl kinase-dependent manner. Silencing H19 expression sensitized leukemic cells to undergo imatinib-induced apoptosis and inhibited Bcr-Abl-induced tumor growth. Furthermore, H19 was shown to be regulated by c-Myc in Bcr-Abl-expressing cells. These results reveal an important role H19 plays in Bcr-Abl-mediated transformation and provide novel insights into complex mechanisms underlying Bcr-Abl-induced cancers.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 0014-5793eISSN: 1873-3468DOI: 10.1016/j.febslet.2014.03.038Titel-ID: cdi_proquest_miscellaneous_1635043049
- Format
- –
- Schlagworte
- Animals, Bcr-Abl, c-Myc, Cell Survival, Cell Transformation, Neoplastic - genetics, Cell Transformation, Neoplastic - metabolism, Female, Fusion Proteins, bcr-abl - genetics, Fusion Proteins, bcr-abl - metabolism, Gene Expression, Gene Expression Regulation, Leukemic, H19, Humans, Jurkat Cells, K562 Cells, Long non-coding RNA, Mice, Mice, Nude, Neoplasm Transplantation, Proto-Oncogene Proteins c-myc - metabolism, RNA, Long Noncoding - genetics, RNA, Long Noncoding - metabolism, Tumorigenesis