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Mounting evidence has shown that long noncoding RNAs (lncRNAs) play critical roles in carcinogenesis and tumor progression. SNHG12 has been identified in multiple types of malignant tumors. However, the role of SNHG12 in human non‐small cell lung cancer (NSCLC) is poorly characterized, and the relevant underlying mechanism remains unclear. The expression levels of SNHG12, miR‐101‐3p, and CUL4B in collected human NSCLC tumor tissues and NSCLC cell lines were tested via qRT‐PCR. Then, NSCLC cellular proliferation, migration and invasion were determined, followed by MTT, scratch and Transwell assays. Dual‐luciferase reporter assays and RNA pulldown assays were adopted to explore the target site. Moreover, western blotting was performed to detect the relevant protein expression concerning the CUL4B/PI3K/AKT pathway. This study clarified that SNHG12 knockdown significantly reduced proliferation, migration, invasion and EMT of NSCLC cells. Our data indicated that SNHG12 targeted and negatively regulated miR‐101‐3p, and this depletion reversed the inhibitory effect of si‐SNHG12 on NSCLC cells. Furthermore, CUL4B was confirmed as a functional target of miR‐101‐3p, and its knockdown resulted in a strong alleviation of the NSLCL cell phenotype, which was enhanced by the silencing of miR‐101‐3p. Mechanistically, we found that SNHG12 regulated miR‐101‐3p to modulate the PI3K/AKT pathway mediated by CUL4B.These observations suggested that lncRNA SNHG12‐mediated miR‐101‐3p downregulation regulated the malignant phenotype of NSCLC cells by targeting CUL4B through the PI3K/AKT pathway, which may present a path to novel therapeutic strategies for NSCLC therapy.

Currently, the role of Notch signaling during myocardial infarction (MI) remains controversy. In this study we used in vitro and in vivo approaches to investigate the role of Notch signaling in MI. Using cultured human umbilical vein endothelial cells exposed to hypoxia/reoxygenation (H/R), we demonstrated that H/R inhibited the proliferation, VEGF secretion, and tube formation of HUVECs, and these effects were correlated with the inhibition of Notch signaling. Furthermore, these effects were antagonized by overexpression of NICD but aggravated by knockdown of NICD. In addition, in MI model rats we found that heart dysfunction and angiogenesis in model rats was partly improved by NICD overexpression but was aggravated by knockdown of NICD. In conclusion, these data demonstrate that Notch signaling is downregulated in H/R injury in the hearts. Artificial activation of Notch signaling could promote myocardial survival and angiogenesis and improve cardiac function following H/R injury.

This paper develops a family of Markov-switching GARCH (MSG) processes that not only encompasses some specifications in the literature, but also can be regarded as a Markov-switching version of the family of GARCH processes introduced by He and Terasvirta (J. Econometrics, 1999, 92, 173–192). Some structural properties of this new family of MSG processes are considered. First, a sufficient and necessary condition for the existence of the strictly stationary solution of the family of MSG processes is presented. Moreover, we also give a sufficient and necessary condition for the existence of the strictly stationary solution of the family of MSG processes with finite δ-order moment. In particular, a definition of so-called family of integrated MSG processes is introduced and its stationarity is also discussed. Next, the general conditions for the existence of any order moment of the family of MSG processes are derived. Finally, by means of a new renewal theorem, we describe the tail of the marginal distribution of the family of MSG processes.