MicroRNAs (miRNAs) have emerged as critical regulators of neuronal survival during cerebral ischemia/reperfusion injury. Accumulating evidence has shown that miR-211 plays a crucial role in regulating apoptosis and survival in various cell types. However, whether miR-211 is involved in regulating neuronal survival during cerebral ischemia/reperfusion injury remains unknown. In this study, we aimed to explore the biological role of miR-211 in regulating neuronal injury induced by oxygen-glucose deprivation/reoxygenation (OGD/R) and transient cerebral ischemia/reperfusion (I/R) injury in vitro and in vivo . We found that miR-211 expression was significantly downregulated in PC12 cells in response to OGD/R and in the penumbra of mouse in response to MCAO. Overexpression of miR-211 alleviated OGD/R-induced PC12 cell apoptosis, whereas miR-211 inhibition facilitated OGD/R-induced PC12 cell apoptosis in vitro . Moreover, overexpression of miR-211 reduced infarct volumes, neurologic score, and neuronal apoptosis in vivo, whereas miR-211 inhibition increased infarct volumes, neurologic score and neuronal apoptosis in vivo. Notably, our results identified P53-up-regulated modulator of apoptosis (PUMA) as a target gene of miR-211. Our findings suggested that miR-211 may protect against MCAO injury by targeting PUMA in rats, which paves a potential new way for the therapy of cerebral I/R injury.

Downregulation of lncRNA H19 (H19) expression is associated with an unfavorable prognosis in some cancers. However, little was known as to whether there was an association between H19 and minimally invasive follicular thyroid carcinoma (MI-FTC). In our study, we used quantitative real-time polymerase chain reaction (qRT-PCR) to determine H19 expression in 186 patients with MI-FTC who underwent initial surgery. Of the 186 patients with MI-FTC, 21 patients show distant metastasis (M+)at the initial operation established the diagnosis of MI-FTC. Of the 165 patients who did not show distant metastasis at diagnosis during the follow-up period (≥10 years), 28 patients undergone M+ and 137 patients has no distant metastasis(M-)after the initial operation. Low H19 expression was associated with large tumor size, vascular invasion, and distant metastasis. Univariate analysis showed that gender (male), age (45 years or older), primary tumor size (4 cm or more), vascular invasion and H19 level (<1.12) were significant prognostic factors related to postoperative distant metastases. Multivariate analysis showed that age, primary tumor size (4 cm or more) and vascular invasion was a significant prognostic factor for survival. Patients with low H19 expression showed a poorer outcome in MI-FTC patients. Receiver-operating characteristic (ROC) curve analysis demonstrated H19 could distinguish M+ from M-patientswith a value of area under the curve (AUC). Our findings suggest that H19 is a potential prognostic factor for evaluating prognosis and the metastatic potential of MI-FTC at an initial operation stage. ARTICLE HISTORY

Anaplastic thyroid carcinoma (ATC) are resistant to standard therapies and has no effective treatment. Eukaryotic translation initiation factor 5A2 (EIF5A2) has shown to be upregulated inmany malignant tumors and proposed to be a critical gene involved in tumor metastasis. In thisstudy, we aim to investigate the expression status of EIF5A2 in human ATC tissues, and to study therole and mechanisms of EIF5A2 in ATC tumorigenesis in vitro and in vivo. Expression of EIF5A2protein were analyzed in paraffin-embedded human ATC tissues and adjacent nontumorous tissues(ANCT) (n=24) by immunochemistry. Expression of EIF5A2 mRNA and protein were analyzed infresh-matched ATC and ANCT (n=23) and ATC cell lines by real-time PCR and western blotting. Theeffect of targeting EIF5A2 with short hairpin RNA (shRNA) or EIF5A2 overexpression on the ATCtumorigenesis and TGF-&beta;/Smad2/3 signals in vitro and in vivo was investigated. Expression ofEIF5A2 was significantly upregulated in ATC tissues and cell lines compared with ANCT and normalfollicular epithelial cell line. Functional studies found that targeting EIF5A2 induced SW1736 celldeath in vitro and in vivo, followed by significantly downregulated phosphorylation of Smad2/3(p-Smad2/3) in SW1736 cells at the protein level. Ectopic expression of EIF5A2 could promoted8505C cell growth in vitro and in vivo, followed by significantly upregulated p-Smad3 at the proteinlevel. Recombinant human TGF-&beta;1 (hTGF-β1) treatment decreased the anti-proliferative activity ofthe EIF5A2 downexpressing 8505C cells through reversing p-Smad2/3. Using the specific inhibitorSB431542 to block TGF-&beta; pathway or Smad3 siRNA to knockdown of Smad3 increased theanti-proliferative activity of the EIF5A2 overexpressing 8505C cells through inhibiting p-Smad2/3.Our findings indicated that EIF5A2 controled cell growth in ATC cells, and EIF5A/TGF-&beta;/Smad2/3signal may be as a potential therapeutic target for ATC treatment.