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Long noncoding RNAs participate in the progression and initiation of non-small cell lung cancer (NSCLC), although the mechanism remains unknown. The lncRNA identified as small nucleolar RNA host gene 1 ( SNHG1) is a novel lncRNA that is increased in multiple human cancers; however, the regulatory mechanism requires further investigation. In this study, we discovered that SNHG1 was markedly up-regulated in NSCLC tissues and cells and that SNHG1 silencing decreased tumor volumes. Moreover, we explored its regulatory mechanism and found that SNHG1 directly bound to microRNA (miRNA)-145-5p, isolating miR-145-5p from its target gene MTDH. Inhibition of SNHG1 suppressed NSCLC cell viability, proliferation, migration, and invasion in vitro, but its effect was rescued by miR-145-5p inhibition. These results demonstrate that SNHG1 contributes to NSCLC progression by modulating the miR-145-5p/ MTDH axis, and it could potentially be a therapeutic target as well as a diagnostic marker.-Lu, Q., Shan, S., Li, Y., Zhu, D., Jin, W., Ren, T. Long noncoding RNA SNHG1 promotes non-small cell lung cancer progression by up-regulating MTDH via sponging miR-145-5p.

Idiopathic pulmonary fibrosis (IPF) is characterized by lung fibroblasts accumulation and extracellular matrix (ECM) deposition. Recently, long-noncoding RNAs (lncRNAs) have emerged as critical regulators and prognostic markers in several diseases including IPF. In the present study, we found that the expression of H19 was significantly increased in transforming growth factor-β (TGF-β)-induced fibroblast proliferation and bleomycin-(BLM) induced lung fibrosis (p < 0.05). We further demonstrated that H19 was a direct target of miR-196a and was associated with COL1A1 expression by sponging miR-196a. Moreover, downregulation of H19 alleviated fibroblast activation and lung fibrosis, and this effect was blocked by a miR-196a inhibitor. In conclusion, our results suggest that lncRNA H19 has a promotive effect on BLM-induced IPF, and it functions as a molecular sponge of miR-196a, which provides a novel therapeutic target for IPF.

Many biomineralization systems start from transient amorphous precursor phases, but the exact crystallization pathways and mechanisms remain largely unknown. The study of a well-defined biomimetic crystallization system is key for elucidating the possible mechanisms of biomineralization and monitoring the detailed crystallization pathways. In this review, we focus on amorphous phase mediated crystallization (APMC) pathways and their crystallization mechanisms in bio-and biomimetic-mineralization systems. The fundamental questions of biomineralization as well as the advantages and limitations of biomimetic model systems are discussed. This review could provide a full landscape of APMC systems for biomineralization and inspire new experiments aimed at some unresolved issues for understanding biomineralization.

In the ACP-mediated HAP nucleation pathway, the nucleation rate of HAP increases when ACP is in the separated state.

T cell functional exhaustion during chronic hepatitis B virus (HBV) infection may contribute to the failed viral clearance; however, the underlying molecular mechanisms remain largely unknown. Here we demonstrate that jumonji domain-containing protein 6 (JMJD6) is a potential regulator of T cell proliferation during chronic HBV infection. The expression of JMJD6 was reduced in T lymphocytes in chronic hepatitis B (CHB) patients, and this reduction in JMJD6 expression was associated with impaired T cell proliferation. Moreover, silencing JMJD6 expression in primary human T cells impaired T cell proliferation. We found that JMJD6 promotes T cell proliferation by suppressing the mRNA expression of CDKN3. Furthermore, we have identified platelet derived growth factor-BB (PDGF-BB) as a regulator of JMJD6 expression. PDGF-BB downregulates JMJD6 expression and inhibits the proliferation of human primary T cells. Importantly, the expression levels of JMJD6 and PDGF-BB in lymphocytes from CHB patients were correlated with the degree of liver damage and the outcome of chronic HBV infection treatment. Our results demonstrate that PDGF-BB and JMJD6 regulate T cell function during chronic HBV infection and may provide insights for the treatment strategies for CHB patients.

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BackgroundMicroRNAs (miRNAs) have been reported to play crucial roles in multiple cancers including non-small cell lung cancer (NSCLC). Here, we investigated the role of miR-145 and miR-497 in TGF-β-induced epithelial–mesenchymal transition (EMT) process of NSCLC.MethodsWe performed quantitative real time PCR (qRT-PCR) to detect the expression level of miR-145 and miR-497 in NSCLC cell lines. Then in the presence/absence of TGF-β, we transfected miRNA mimics or inhibitor into A549 and H1299 cells and investigated the role of miR-145 and miR-497 in cell migration and invasion using transwell and wound-healing assay. The regulation role of miR-145 and miR-497 on Metadherin (MTDH) was determined by luciferase assay. The expression level of MTDH and EMT markers E-cadherin and vimentin were detected on mRNA and protein level.ResultsIn our study, our results showed that miR-145 and miR-497 were downregulated in NSCLC cell lines. Overexpression of miR-145 and miR-497 inhibited TGF-β-induced EMT and suppressed cancer cell migration and invasion, while the opposite results were observed in cells transfected with miR-145 or miR-497 inhibitor. Moreover, the luciferase assay confirmed that miR-145 and miR-497 attenuated MTDH expression by directly binding 3′-UTR of MTDH mRNA and exert the tumor-suppression role.ConclusionsOverall, we demonstrated that miR-145 and miR-497 functioned as EMT-suppressor in NSCLC by targeting MTDH, provided new evidence that miR-145 and miR-497 as potential therapeutic targets.