作者: Po-Shuan Huang , I-Hsiao Chung , Yang-Hsiang Lin , Tzu-Kang Lin , Wei-Jan Chen
DOI: 10.3390/IJMS19051463
关键词:
摘要: Anaplastic lymphoma kinase (ALK)-negative anaplastic large-cell (ALCL) is a rare type of highly malignant, non-Hodgkin lymphoma. Currently, only few gene rearrangements have been linked to ALK-negative ALCL progression. However, the specific molecular mechanisms underlying growth tumors remain unclear. Here, we investigated aberrantly expressed, long non-coding RNAs (lncRNAs) in and assessed their potential biological function. MIR503HG (miR-503 host gene) was expressed cell lines significantly upregulated mice formed from lines. Depletion suppressed tumor proliferation vivo vitro; conversely, its overexpression enhanced growth. MIR503HG-induced mediated by induction microRNA-503 (miR-503) suppression Smurf2, resulting stabilization factor-β receptor (TGFBR) Collectively, these findings support role for cancer through miR-503/Smurf2/TGFBR axis indicate that marker ALCL.