The Long Non-Coding RNA MIR503HG Enhances Proliferation of Human ALK-Negative Anaplastic Large-Cell Lymphoma.
Po-Shuan HuangI-Hsiao ChungYang-Hsiang LinTzu-Kang LinWei-Jan ChenKwang-Huei LinPublished in: International journal of molecular sciences (2018)
Anaplastic lymphoma kinase (ALK)-negative anaplastic large-cell lymphoma (ALCL) is a rare type of highly malignant, non-Hodgkin lymphoma. Currently, only a few gene rearrangements have been linked to ALK-negative ALCL progression. However, the specific molecular mechanisms underlying the growth of ALK-negative ALCL tumors remain unclear. Here, we investigated aberrantly expressed, long non-coding RNAs (lncRNAs) in ALK-negative ALCL and assessed their potential biological function. MIR503HG (miR-503 host gene) was highly expressed in ALK-negative cell lines and was significantly upregulated in tumors in mice formed from ALK-negative ALCL cell lines. Depletion of MIR503HG suppressed tumor cell proliferation in vivo and in vitro; conversely, its overexpression enhanced tumor cell growth. MIR503HG-induced proliferation was mediated by the induction of microRNA-503 (miR-503) and suppression of Smurf2, resulting in stabilization of the tumor growth factor-β receptor (TGFBR) and enhanced tumor cell growth. Collectively, these findings support a potential role for MIR503HG in cancer cell proliferation through the miR-503/Smurf2/TGFBR axis and indicate that MIR503HG is a potential marker in ALK-negative ALCL.
Keyphrases
- long non coding rna
- cell proliferation
- poor prognosis
- long noncoding rna
- advanced non small cell lung cancer
- cell cycle
- growth factor
- endothelial cells
- fluorescent probe
- diffuse large b cell lymphoma
- stem cells
- squamous cell carcinoma
- gene expression
- cell therapy
- type diabetes
- metabolic syndrome
- genome wide
- mass spectrometry
- oxidative stress
- adipose tissue
- single molecule
- aqueous solution
- high resolution
- dna methylation
- bone marrow
- tyrosine kinase
- network analysis