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Background Non-small cell lung cancer (NSCLC) is one of the leading causes of cancer death in the world, and has a relatively low survival rate. Long non-coding RNAs (lncRNAs) have been demonstrated to modulate cancer progression through a variety of molecular mechanisms. We sought to investigate the role and potential mechanism of MYC-induced long non-coding RNA (MINCR) in NSCLC. Methods Expression levels of MINCR was first identified using The Cancer Genome Atlas (TCGA), further confirmed with specimens from 29 NSCLC patients and three cell lines using qRT-PCR. Overexpression and knockdown of MINCR were performed in NSCLC cell lines through MINCR overexpression vectors and synthesized siRNAs, respectively. The roles of MINCR in NSCLC cell lines, such as cell proliferation, cell cycle arrest, and apoptosis, were identified by MTT, flow cytometry, and Western blot. The modulation of MINCR-regulated genes, including c-Myc and its downstream effectors, as well as apoptosis-associated genes, was analyzed using Western blot. Results MINCR expression was increased in NSCLC patients from TCGA datasets, and was also significantly increased in our collected specimens from NSCLC patients and NSCLC cell lines. Knocking down of MINCR greatly inhibited the growth of NSCLC cell lines PC9 and A549. In addition, silencing of MINCR induced cell cycle arrest and apoptosis. Furthermore, silencing of MINCR reduced the expression levels of oncogene c-Myc and its downstream cyclin A, cyclin D, CD4, and CDK2, as well as apoptosis-associated Bcl-2, while significantly increased the expression levels of cleaved PARP-1. In the meantime, overexpression of MINCR remarkably enhanced cell proliferation of PC9 cells and activated c-Myc and its downstream effectors. Conclusion MINCR exerted inhibitory effects on the cell cycle arrest and apoptosis of NSCLC cells by activating c-Myc and its downstream effectors, suggesting that this lncRNA could be used as a potential therapeutic target for the treatment of NSCLC. Electronic supplementary material The online version of this article (10.1186/s12931-019-1174-z) contains supplementary material, which is available to authorized users.

Biomineralization has intrigued researchers for decades. Although mineralization of type I collagen has been universally investigated, this process remains a great challenge due to the lack of mechanistic understanding of the roles of biomolecules. In our study, dentine was successfully repaired using the biomolecule polydopamine (PDA), and the remineralized dentine exhibited mechanical properties comparable to those of natural dentine. Detailed analyses of the collagen mineralization process facilitated by PDA showed that PDA can promote intrafibrillar mineralization with a decreased heterogeneous nucleation barrier for hydroxyapatite (HAP) by reducing the interfacial energy between collagen fibrils and amorphous calcium phosphate (ACP), resulting in the conversion of an increasing amount of nanoprecursors into collagen fibrils. The present work highlights the importance of interfacial control in dentine remineralization and provides profound insight into the regulatory effect of biomolecules in collagen mineralization as well as the clinical application of dentine restoration.

We developed a novel wide-bandgap conjugated polymer PTzBI-O based on an alkoxylated electron-deficient monomer 4,8-di­(thiophen-2-yl)-[1,2,3]­triazolo­[4,5-f]­isoindole-5,7­(2H,6H)-dione (TzBI-O). Regarding that of alkyl-substituted imide-functionalized benzotriazole (TzBI) unit, the incorporation of oxygen atom into the substitution of TzBI-O increased the electronegativity. The resulting polymer PTzBI-O exhibited an absorption onset of 708 nm, corresponding to a bandgap of 1.75 eV. The PTzBI-O:N2200 blend exhibited strong aggregation in toluene solution, resulting in the enhanced absorptivity in thin film compared to those of equivalent films processed with chlorinated solvents. The fabricated all-polymer solar cell based on PTzBI-O:N2200 blend film processed with toluene exhibited an impressive power conversion efficiency of 7.91%. The higher efficiency of the toluene-processed device than those based on films processed with chlorinated solvents can be attributed to more effective charge dissociation, trivial bimolecular recombination, greater charge transportation, and more favorable thin film morphology of the toluene-cast blend film. These findings indicated that the resulting copolymer has great potential for the construction of high-performance all-polymer solar cells.

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Lung cancer is a common disease that is associated with poor prognosis. Fungal immunomodulatory protein from Nectria haematococca (FIP-nha) has potential as a lung cancer therapeutic; as such, illuminating its anti-tumor mechanism is expected to facilitate novel treatment options. Here, we showed that FIP-nha affects lung adenocarcinoma growth ex vivo and in vivo. Comparative quantitative proteomics showed that FIP-nha negatively regulates PI3K/Akt signaling and induces cell cycle arrest, autophagy, and apoptosis. We further demonstrated that FIP-nha suppresses Akt phosphorylation, leading to upregulation of p21 and p27 and downregulation of cyclin B1, cyclin D1, CDK2, and CDK4 expression, ultimately resulting in G1/S and G2/M cell cycle arrest. Meanwhile, FIP-nha-induced PI3K/Akt downregulation promotes A549 apoptosis by increasing the expression ratio of Bax/Bcl-2 and c-PARP and autophagy by decreasing the phosphorylation of mTOR. Thus, we comprehensively revealed the anti-tumor mechanism of FIP-nha, which inhibits tumor growth by modulating PI3K/Akt-regulated cell cycle arrest, autophagy, and apoptosis, and provided the basis for further application of fungal immunomodulatory proteins, especially FIP-nha.