Filamin A increases aggressiveness of human neuroblastoma.

Background: The actin-binding protein filamin A (FLNA) regulates oncogenic signal transduction important for tumor growth, but the role of FLNA in the progression of neuroblastoma (NB) has not been explored.

Methods: We analyzed mRNA expression in the R2 NB-database and FLNA protein expression in human NB tumors. We then silenced expression in human SKNBE2 and IMR32 NB cells by lentiviral vector encoding shRNA and assayed the cells for proliferation, migration, colony, spheroid formation, and apoptosis.

NBAT1/CASC15-003/USP36 control MYCN expression and its downstream pathway genes in neuroblastoma.

Background: has been an attractive therapeutic target in neuroblastoma considering the widespread amplification of the locus in neuroblastoma, and its established role in neuroblastoma development and progression. Thus, understanding neuroblastoma-specific control of expression at the transcriptional and post-transcriptional level would lead to identification of novel -dependent oncogenic pathways and potential therapeutic strategies.

Methods: By performing loss- and gain-of-function experiments of the neuroblastoma hotspot locus 6p22.

Subcellular Distribution of p53 by the p53-Responsive lncRNA Determines Chemotherapeutic Response in Neuroblastoma.

Neuroblastoma has a low mutation rate for the gene. Alternative ways of p53 inactivation have been proposed in neuroblastoma, such as abnormal cytoplasmic accumulation of wild-type p53. However, mechanisms leading to p53 inactivation via cytoplasmic accumulation are not well investigated.

Analysis of copy number alterations reveals the lncRNA ALAL-1 as a regulator of lung cancer immune evasion.

Cancer is characterized by genomic instability leading to deletion or amplification of oncogenes or tumor suppressors. However, most of the altered regions are devoid of known cancer drivers. Here, we identify lncRNAs frequently lost or amplified in cancer.

Sense-Antisense lncRNA Pair Encoded by Locus 6p22.3 Determines Neuroblastoma Susceptibility via the USP36-CHD7-SOX9 Regulatory Axis.

Trait-associated loci often map to genomic regions encoding long noncoding RNAs (lncRNAs), but the role of these lncRNAs in disease etiology is largely unexplored. We show that a pair of sense/antisense lncRNA (6p22lncRNAs) encoded by CASC15 and NBAT1 located at the neuroblastoma (NB) risk-associated 6p22.3 locus are tumor suppressors and show reduced expression in high-risk NBs.

Mega roles of microRNAs in regulation of skeletal muscle health and disease.

Skeletal muscle is a dynamic tissue with remarkable plasticity. Skeletal muscle growth and regeneration are highly organized processes thus it is not surprising that a high degree of complexity exists in the regulation of these processes. Recent discovery of non-coding microRNAs (miRNAs) has prompted extensive research in understanding the roles of these molecules in skeletal muscle.

Myostatin augments muscle-specific ring finger protein-1 expression through an NF-kB independent mechanism in SMAD3 null muscle.

Smad (Sma and Mad-related protein) 2/3 are downstream signaling molecules for TGF-β and myostatin (Mstn). Recently, Mstn was shown to induce reactive oxygen species (ROS) in skeletal muscle via canonical Smad3, nuclear factor-κB, and TNF-α pathway. However, mice lacking Smad3 display skeletal muscle atrophy due to increased Mstn levels.

Myostatin induces DNA damage in skeletal muscle of streptozotocin-induced type 1 diabetic mice.

One of the features of uncontrolled type 1 diabetes is oxidative stress that induces DNA damage and cell death. Skeletal muscle atrophy is also considerable in type 1 diabetes, however, the signaling mechanisms that induce oxidative stress culminating in muscle atrophy are not fully known. Here, we show that in Streptozotocin-induced diabetic wild type mice, hypo-phosphorylation of Akt, resulted in activation of Foxa2 transcription factor in the muscle.

Argonaute identity defines the length of mature mammalian microRNAs.

MicroRNAs (miRNAs) are 19- to 25-nt-long non-coding RNAs that regulate gene expression by base-pairing with target mRNAs and reducing their stability or translational efficiency. Mammalian miRNAs function in association with four closely related Argonaute proteins, AGO1-4. All four proteins contain the PAZ and the MID domains interacting with the miRNA 3' and 5' termini, respectively, as well as the PIWI domain comprising an mRNA 'slicing' activity in the case of AGO2 but not AGO1, AGO3 and AGO4.