Background & Objective: One of the most prevalent endocrine system cancers is papillary thyroid carcinoma, with complicated predisposing factors and pathogenesis. YAP1 (Yes-associated protein 1) is a well-known oncogene,its activity is increased in a variety of human malignancies and has recently been paid great attention. The present study examines YAP1 and P53 immunohistochemical expression in papillary thyroid carcinoma and investigates the association of their expression with the available clinicopathological risk factors to assess their possible prognostic role. Methods: The current study used paraffin blocks of 60 cases of papillary thyroid carcinoma, which were immunohistochemically assessed for YAP1 and p53 expression. The study examined the association of their expression with clinicopathological characteristics. Results: YAP1 expression was observed in 70% of papillary thyroid carcinoma cases. A statistically significant relation was observed between YAP1 expression and tumor size, tumor stage, tumor focality, lymph node metastases, and extrathyroidal extension (P-values were =0. 003, > 0. 001, 0. 037, 0. 025, and 0. 006), respectively. p53 expression was observed in 85% of papillary thyroid carcinoma cases. A statistically significant relation was observed between p53 expression and tumor size (P=0. 001) and tumor stage (P>0. 001). A statistically significant relation was noticed between YAP1 and P53 expression (P=0. 009). Conclusion: YAP1 expression was found to be associated with many high-risk clinicopathological characteristics in patients with papillary thyroid carcinoma and with p53 expression,thus, it seems that YAP1 may have a specific impact on the patient's outcome.

Background: Pathological hypertrophy is one of the negative consequences of cardiac sympathetic hyperactivity. Recent studies have shown that YAP1 plays a critical role in cardiomyocytes hypertrophy. Considering the preventive role of exercise training in cardiovascular diseases, the present study was conducted to examine the effect of aerobic exercise training on YAP1 gene expression and its upstream components. Methods: Eighteen male Wistar rats were randomly divided into aerobic training and control groups. Aerobic training was performed one hour/day, five days per week, for eight weeks, on a treadmill at 65‑ 75% VO2 max. Pathological hypertrophy was induced by injecting 3 mg/kg‑ 1 of isoproterenol for seven days. The left ventricle was separated, and YAP1, 3‑ mercaptopyruvate sulfurtransferase (MST), large tumor suppressor (LATS), and mitogen‑ activated protein 4 kinase (MAP4K) gene expressions were assessed and YAP1 protein levels were also assessed by western blotting. Cell apoptosis was detected by TUNEL assays. The between‑ group differences were evaluated using the T‑ test and P value <0. 05 was considered statistically significant. Results: There were no significant between‑ group differences in MST gene expression (P = 0. 061); meanwhile, in the training group, LATS and Map4K expressions were suppressed, followed by a significant increase in YAP1 expression (P < 0. 001). Compared to the control group, the left ventricular weight increased significantly in the training group while the cardiomyocyte apoptosis decreased. Conclusions: The results showed that, by reducing LATS, aerobic training‑ induced YAP1 upregulation can help prevent the propagation of cardiomyocyte apoptosis due to pathological conditions.

Objective: Although growing evidences have showed that long non-coding RNA (lncRNAs) plasmacytoma variant translocation 1 (PVT1) plays a critical role in the progression of non-small cell lung cancer (NSCLC), there are still many unsolved mysteries remains to be deeply elucidated. This study aimed to find a new underlying mechanism of PVT1 in regulating the tumorigenesis and development of NSCLC. Materials and Methods: In this experimental study, Quantitative reverse transcription polymerase chain reaction (qRTPCR) was used to profile the expression of PVT1 in NSCLC tissues and cells. The effects of PVT1 on cell growth, migration and invasion were detected by colony formation assay, Matrigel-free transwell and Matrigel transwell assays, respectively. Changes of the key protein expression in Hippo and NOTCH signaling pathways, as well as epithelialmesenchymal transition (EMT) markers, were analyzed using western blot. Interaction of PVT1 with enhancer of zeste homolog 2 (EZH2) was verified by RNA pull-down, and their binding to the downstream targets was detected by Chromatin Immunoprecipitation (ChIP) assays. Results: These results showed that PVT1 was up-regulated in NSCLC tissue and cell lines, promoting NSCLC cell proliferation, migration and invasion. Knockdown of PVT1 inhibited the expression of Yes-associated protein 1 (YAP1) and NOTCH1 signaling activation. Further, we have confirmed that PVT1 regulated expression of YAP1 through EZH2-mediated miR-497 promoter methylation resulting in the inhibition of miR-497 transcription and its target YAP1 upregulation, and finally NOTCH signaling pathway was activated, which promoted EMT and invasion and metastasis. Conclusions: These results suggested that lncRNA PVT1 promotes NSCLC metastasis through EZH2-mediated activation of Hippo/NOTCH1 signaling pathways. This study provides a new opportunity to advance our understanding in the potential mechanism of NSCLC development.