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Background: Long non‐coding RNAs regulate malignant behaviors of nasopharyngeal carcinoma (NPC). We aim to investigate the roles and mechanisms of long non‐coding RNA maternally expressed gene 3 (lnc‐MEG3) in NPC. Methods: The expression levels of lnc‐MEG3 and sequestosome 1 (SQSTM1) in NPC tissues and cell lines were detected by quantitative real‐time polymerase chain reaction (qRT‐PCR). Cell invasion and migration abilities were evaluated using transwell and wound healing assays, respectively. Results: Downregulated lnc‐MEG3 expression and upregulated SQSTM1 expression were found in NPC tissues and cells. Overexpression of lnc‐MEG3 inhibited invasion, migration, and epithelial–mesenchymal transition in NPC cells. Overexpression of lnc‐MEG3 reduced the expression level of SQSTM1, and SQSTM1 expression was inversely correlated with lnc‐MEG3 level in NPC tissues. Besides, overexpression of SQSTM1 reversed the effects of lnc‐MEG3 overexpression. Moreover, knockdown of lnc‐MEG3 enhanced NPC progression while its effects were eased by SQSTM1 silence. Conclusion: Lnc‐MEG3 inhibits malignant behaviors by regulating SQSTM1 expression. It may serve as a therapeutic target to treat NPC. [ABSTRACT FROM AUTHOR]

P articularly i nteresting n ew c ysteine- h istidine-rich protein (PINCH) is a LIM-domain-only adaptor that plays important roles in cytoskeletal organization and extracellular matrix adhesion, migration, proliferation and survival. Mammalian cells have two functional PINCH proteins, PINCH1 and PINCH2. PINCH not only binds to Nck2 and engages in the signaling of growth factor receptors, but also forms a ternary complex with ILK and parvin (IPP complex). Normally, the IPP complex locates to focal adhesions participating in the signaling of integrins and mediating the interaction of cytoskeleton and extracellular matrix (ECM). Accumulative evidence indicates that abnormalities in PINCH signaling are involved in the pathogenesis of important diseases, such as cancers, renal diseases, cardiomyopathy, and HIV. Therefore, clarifying the functions of PINCH and its interactions with key factors is important for better understanding of signaling events both in health and disease. [ABSTRACT FROM AUTHOR]

• TMP protected ucMSCs against H 2 O 2 induced-oxidative damage at a low concentration. • ucMSC migration was improved by TMP via the SDF-1/CXCR4 axis. • At a high dose, TMP induced the differentiation of ucMSCs into neuron-like cells. • The secretion of cytokines was significantly increased by TMP Umbilical cord mesenchymal stem cells (ucMSCs) may serve as a new source for cell therapy in stroke patients; however, the poor efficiency of viability, migration, and differentiation limit the application of ucMSCs. This study determined the dose-dependent effects of tetramethylpyrazine (TMP) on the characteristics of ucMSCs in vitro. The effect on proliferation was determined with Cell Counting kit-8 assays. Cell migration was analyzed with Transwell assays and western blot analysis. Differentiation of ucMSCs was evaluated according to markers and the expression of relevant proteins and genes. Secretion capacity was detected by ELISA analysis. TMP protected ucMSCs against H 2 O 2 induced-oxidative damage but had no influence on ucMSC activity at a low concentration. Furthermore, ucMSC migration was improved by TMP via the SDF-1/CXCR4 axis. The observed effects were dose dependent. At a high dose, however, TMP induced the differentiation of ucMSCs into neuron-like cells that expressed neuron-specific markers. In addition, the secretion of cytokines was significantly increased by TMP. Therefore, TMP pre-treatment of ucMSCs may be an effective strategy to enhance the efficiency of ucMSC transplantation in stroke therapy. [ABSTRACT FROM AUTHOR]