Long noncoding RNAs in pancreas cancer: from biomarkers to therapeutic targets.

Long noncoding RNAs (lncRNAs) are noncoding RNA molecules with a heterogeneous structure consisting of 200 or more nucleotides. Because these noncoding RNAs are transcribed by RNA polymerase II, they have properties similar to messenger RNA (mRNA). Contrary to popular belief, the term "ncRNA" originated before the discovery of microRNAs. LncRNA genes are more numerous than protein-coding genes. They are the focus of current molecular research because of their pivotal roles in cancer-related processes such as cell proliferation, differentiation, and migration. The incidence of pancreatic cancer (PC) is increasing around the world and research on the molecular aspects of PC are growing. In this review, it is aimed to provide critical information about lncRNAs in PC, including the biological and oncological behaviors of lncRNAs in PC and their potential application in therapeutic strategies and as diagnostic tumor markers.

mir-221, mir-190b, mir-363-3p, mir-200c are involved in rat liver ischaemia-reperfusion injury through oxidative stress, apoptosis and endoplasmic reticulum stress.

AIM: In this study, it was aimed to investigate the relationship between expression levels of micro-RNAs, endoplasmic reticulum (ER) stress, apoptosis and oxidative stress markers in hepatic ischaemia-reperfusion (IR) injury. METHODS: Sixteen rats were randomised into two groups: Sham and IR groups. In the IR group, portal vein and hepatic artery were totally clamped with an atraumatic microvascular clamp and 60 minutes later unclamped and finally IR model was accomplished (60 minutes ischaemia and 60 minutes reperfusion). After sacrification, serum insulin-like growth factor-1 (IGF-1), tumour necrosis factor-α (TNF-α), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were measured. Liver tissue samples were evaluated histopathologically. The expression levels of IR1-alpha, Perk, Catalase, Gpx-1, Caspase-3, Bcl-2 genes and miR-33a, miR-221, miR-190b, miR-363-3p, miR-200c, miR-223, miR-133b were measured by quantitative real-time polymerase chain reaction method. RESULTS: Biochemical parameters of the IR group showed significantly higher changes compared with the Sham group (P < .01). Histological tissue damage was significantly prominent in the IR group. ER stress, oxidative stress and apoptosis gene expression levels were significantly higher in the IR group (P < .01). Expression levels of miR-221, miR-190b, miR-363-3p and miR-200c were increased in the IR group compared with the Sham group. No significant difference was found between the two groups in terms of miR-33a, miR-133b and miR-223 expression levels (P > .05). CONCLUSION: There is a strong need to enlighten the physiopathological and molecular mechanisms of liver IR injury and to find more specific biomarkers for IR damage, and miR-221, miR-190b, miR-363-3p and miR-200c maybe used as potential biomarkers of hepatic IR injury.

A novel FLCN mutation in family members diagnosed with primary spontaneous pneumothorax.

BACKGROUND: Primary spontaneous pneumothorax (PSP) is a disease characterized by the accumulation of air in the pleural space between the lung and thoracic wall. It is more common in young, tall, thin, and asthenic men. A family history was reported for approximately 11.5% of individuals admitted with PSP. The literature has reported cases diagnosed with familial PSP, who have no manifestations of Birt-Hogg-Dubé (BHD) syndrome but mutations in different exons of the Folliculin (FLCN) gene. The aim of this study is to present a Turkish family in which 13 members from three generations of the same family developed recurrent isolated spontaneous pneumothorax with a novel mutation in the FLCN. METHODS: A male proband was diagnosed with spontaneous pneumothorax in the emergency department of the University of Health Sciences Haydarpasa Numune Training and Research Center, Istanbul, Turkey. His 12 relatives from three generations diagnosed with PSP, as revealed by his family history, were invited to the hospital to give blood samples for mutation analysis. The Sanger sequence data of FLCN were analyzed on the ENSEMBL website using SeqScape 3 and Codon Aligner software. RESULTS: A novel heterozygous mutation c. 1273C>T (p.Gln425Ter) was detected in exon 11 of the FLCN, which caused PSP in the proband and his 12 relatives tested using Sanger sequencing. CONCLUSION: We found that a heterozygous mutation in exon 11 of FLCN c. 1273C>T (p.Gln425Ter), which was identified for the first time in our study, might cause isolated familial spontaneous pneumothorax.