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Exosome-shuttled bioactive long non-coding RNA, as novel non-invasive biomarkers for cancer diagnosis, has received increasing attention. Here, we aimed to investigate the expression of serum exosomal long non-coding RNA pcsk2-2:1 (Exo-Lnc RNApcsk2-2:1) in patients of gastric cancer and evaluate its diagnostic value as a marker. Patients and methods: Exosomes were isolated from serum sample of gastric cancer using HiPure Exosomekits and identified via transmission electron microscopy, Western blotting, and nanoparticle tracking analysis. The total exosomal RNA was extracted and reverse transcribed to cDNA. The expression of Exo-Lnc RNA PCSK2-2:1 was detected in serum exosomes of 29 healthy people and 63 gastric cancer patients by real-time quantitative reverse transcription PCR (qRT-PCR), and the relationship between the expression level of Exo-Lnc RNA PCSK2-2:1 and clinicopathological parameters of patients was analyzed. Finally, a receiver operating characteristic curve was used to evaluate the clinical value of Exo-Lnc RNA PCSK2-2:1 as an auxiliary diagnostic marker for gastric cancer. Results: Transmission electron microscopy, nanoparticle size analysis, and Western blotting showed successful separation of serum exosomes. qRT-PCR results revealed that compared with the healthy control, Lnc RNA PCSK2-2:1 expression level in serum exosomes of gastric cancer patients was significantly downregulated (p=0.006). Moreover, the expression level of Exo-Lnc RNA PCSK2-2:1 was correlated with tumor size (p=0.0441), tumor stage (p=0.0061), and venous invasion (p=0.0367). The area under the curve of Exo-Lnc RNA PCSK2-2:1 was 0.896. At the optimal cutoff value, the diagnostic sensitivity and specificity were 84% and 86.5%, respectively. Conclusion: Our data indicate that Exo-Lnc RNA PCSK2-2:1 may perform a vital role in the progression of gastric cancer and can be used as a potential marker for the diagnosis of gastric cancer.

Neonatal hypoxic-ischemic (HI) brain injury is a devastating disease that often leads to death and detrimental neurological deficits. The present study was designed to evaluate the ability of metformin to provide neuroprotection in a model of neonatal hypoxic-ischemic brain injury and to study the associated molecular mechanisms behind these protective effects. Here, we found that metformin treatment remarkably attenuated brain infarct volumes and brain edema at 24 h after HI injury, and the neuroprotection of metformin was associated with inhibition of neuronal apoptosis, suppression of the neuroinflammation and amelioration of the blood brain barrier breakdown. Additionally, metformin treatment conferred long-term protective against brain damage at 7 d after HI injury. Our study indicates that metformin treatment protects against neonatal hypoxic-ischemic brain injury and thus has potential as a therapy for this disease.

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