LncRNA MNX1-AS1 contributes to lung adenocarcinoma progression by targeting the miR-34a/SIRT1 axis.

LncRNA MNX1-AS1 is known to be involved in progression of several tumor types. However, few studies have investigated the molecular mechanism of MNX1-AS1 in lung adenocarcinoma (LAC). To explore the function of MNX1-AS1 in the pathogenesis of LAC, qRT-PCR was performed to show MNX1-AS1 expression. MNX1-AS1 expression in LAC cells was suppressed by siRNA to detect the biologic behavior. The relationships among miR-34a, MNX1-AS1 and SIRT1 were confirmed by pull-down and dual-luciferase reporter assay. Whether MNX1-AS1 was involved in LAC by targeting miR-34a/SIRT1 axis was verified. MNX1-AS1 was up-regulated in LAC, and over-expression of MNX1-AS1 was significantly associated with lymph node metastasis and poor prognosis. In A549 and H1299 cells, cell proliferation, migration, and invasion were suppressed, the cell cycle was regulated, as well as apoptosis was increased after silencing MNX1-AS1. Mechanistically, MNX1-AS1 served as a ceRNA of miR-34a to down-regulate miR-34a expression. SIRT1 is targeted by miR-34a and its expression is regulated by MNX1-AS1 and miR-34a. Up-regulation of SIRT1 salvaged the effect of silencing MNX1-AS1 on A549 and H1299 cells, to some extent. These results showed that MNX1-AS1 contributes to LAC progression by targeting the miR-34a/SIRT1 axis.

Expression and significance of LncRNA MNX1-AS1 in non-small cell lung cancer.

Objective: To investigate the expression of LncRNA MNX1-AS1 in NSCLC and its effect on NSCLC cell lines. Methods: In this experiment, the expression of LncRNA MNX1-AS1 was detected by qRT-PCR in 116 NSCLC samples, and the correlation between MNX1-AS1 and NSCLC patients was further analyzed by chi-square test. The prognostic value of MNX1-AS1 was assessed by Kaplan-Meier survival curve. The expression of MNX1-AS1 in NSCLC cell line A549 was knocked down, and the effects of MNX1-AS1 on proliferation, apoptosis, migration and invasion of NSCLC cells were evaluated. Results: Compared with normal lung tissue, the expression of MNX1-AS1 was significantly increased in lung cancer tissues (p<0.05). The expression level of MNX1-AS1 in NSCLC cell line A549 was significantly higher than that in human normal lung epithelial cell line Beas-2B (p<0.05). MNX1-AS1 expression was significantly associated with TNM stage and lymph node metastasis (p<0.05). Kaplan-Meier survival curve analysis showed that high expression of MNX1-AS1 was associated with a poor prognosis in NSCLC. In addition, knockdown of MNX1-AS1 inhibited proliferation, migration and invasion of the NSCLC cell line A549 and promoted apoptosis. Conclusion: The up-regulation of LncRNA MNX1-AS1 is associated with the progression and prognosis of NSCLC. Knockdown of LncRNA MNX1-AS1 inhibits proliferation, migration and invasion of NSCLC cells and promotes apoptosis.

Roles and activities of chromatin remodeling ATPases in plants.

Chromatin remodeling ATPases and their associated complexes can alter the accessibility of the genome in the context of chromatin by using energy derived from the hydrolysis of ATP to change the positioning, occupancy and composition of nucleosomes. In animals and plants, these remodelers have been implicated in diverse processes ranging from stem cell maintenance and differentiation to developmental phase transitions and stress responses. Detailed investigation of their roles in individual processes has suggested a higher level of selectivity of chromatin remodeling ATPase activity than previously anticipated, and diverse mechanisms have been uncovered that can contribute to the selectivity. This review summarizes recent advances in understanding the roles and activities of chromatin remodeling ATPases in plants.

Calmodulin binds to extracellular sites on the plasma membrane of plant cells and elicits a rise in intracellular calcium concentration.

Calmodulin (CaM) is a highly conserved intracellular calcium sensor. In plants, CaM also appears to be present in the apoplasm, and application of exogenous CaM has been shown to influence a number of physiological functions as a polypeptide signal; however, the existence and localization of its corresponding apoplasmic binding sites remain controversial. To identify the site(s) of action, a CaM-conjugated quantum dot (QD) system was employed for single molecule level detection at the surface of plant cells. Using this approach, we show that QD-CaM binds selectively to sites on the outer surface of the plasma membrane, which was further confirmed by high resolution transmission electron microscopy. Measurements of Ca(2+) fluxes across the plasma membrane, using ion-selective microelectrodes, demonstrated that exogenous CaM induces a net influx into protoplasts. Consistent with these flux studies, calcium-green-dextran and FRET experiments confirmed that applied CaM/QD-CaM elicited an increase in cytoplasmic Ca(2+) levels. These results support the hypothesis that apoplasmic CaM can act as a signaling agent. These findings are discussed in terms of CaM acting as an apoplasmic peptide ligand to mediate transmembrane signaling in the plant kingdom.