Covalent triazine frameworks (CTFs) with donor–acceptor motifs have been identified as prospective semiconducting materials for photocatalysis. Though donor–acceptor motifs can favor forward intramolecular charge separation, some cases still suffer from backward charge recombination, resulting in the decrease of the photocatalytic activity. Herein, acetylene-bridged CTFs bearing an extended donor−π–acceptor motif was fabricated to prompt exciton dissociation. Experimental investigations and density functional theory calculations prove that the acetylene moiety can suppress backward charge recombination, minimize exciton binding energy, and enhance charge carrier lifetime, thereby prompting forward charge transfer/separation in comparison to the analogous one without acetylene. Thus, the acetylene-bridged CTFs showcased a higher photocatalytic activity for metal-free photocatalytic oxidative amines coupling with oxygen under visible-light irradiation, and apparent quantum efficiency at 420 nm was achieved up to 32.3%, that is, twofold higher than the one without acetylene. Furthermore, the acetylene moieties can adsorb oxygen molecules and provide active sites to lower the energy barrier and thus significantly enable the photoredox catalysis. This work provides alternative insights into the design and construction of high-performance CTFs, with prospective applications in solar-to-chemical energy conversion.

Covalent organic frameworks (COFs) are appealing platforms for photocatalysts because of their structural diversity and adjustable optical band gaps. The construction of efficient COFs for heterogeneous photocatalysis of organic transformations is highly desirable. Herein, we constructed a photoactive COF containing benzothiadiazole and triazine (BTDA−TAPT), for which the morphology and crystallinity might be easily tuned by slight synthetic variation. To unveil the relationship of photocatalytic properties between the structure and morphology, analogous COFs were synthesized by precisely tailoring building blocks. Systematic investigations indicated that tuning the structure and morphology might greatly impact photoelectric properties. The BTDA−TAPT featuring ordered alignment and perfect crystalline nature was more beneficial for promoting charge transfer and separation, which exhibited superior photocatalytic activity for visible light-driven oxidative coupling of amines. Outcomes from this study reveal the intrinsic synergy effects between the structure and morphology of COFs for photocatalysis.

Background Non-small cell lung cancer (NSCLC) is the leading cause of cancer deaths primarily due to chemoresistance. Somatic mutation of TP5 3 (36%) and epidermal growth factor receptor ( EGFR ; > 30%) are major contributors to cisplatin (CDDP) resistance. Substantial evidence suggests the elevated levels of reactive oxygen species (ROS) is a key determinant in cancer. The elevated ROS can affect the cellular responses to chemotherapeutic treatments. Although the role of EGFR in PI3K/Akt signaling cascade in NSCLC is extensively studied, the molecular link between EGFR and p53 and the role of ROS in pathogenesis of NSCLC are limitedly addressed. In this study, we investigated the role of p53 in regulation of ROS production and EGFR signaling, and the chemosensitivity of NSCLC. Methods In multiple NSCLC cell lines with varied p53 and EGFR status, we compared and examined the protein contents involved in EGFR-Akt-P53 signaling loop (EGFR, P-EGFR, Akt, P-Akt, p53, P-p53) by Western blot. Apoptosis was determined based on nuclear morphological assessment using Hoechst 33258 staining. Cellular ROS levels were measured by dichlorofluorescin diacetate (DCFDA) staining followed by flow cytometry analysis. Results We have demonstrated for the first time that activation of p53 sensitizes chemoresistant NSCLC cells to CDDP by down-regulating EGFR signaling pathway and promoting intracellular ROS production. Likewise, blocking EGFR/PI3K/AKT signaling with PI3K inhibitor elicited a similar response. Our findings suggest that CDDP-induced apoptosis in chemosensitive NSCLC cells involves p53 activation, leading to suppressed EGFR signaling and ROS production. In contrast, in chemoresistant NSCLC, activated Akt promotes EGFR signaling by the positive feedback loop and suppresses CDDP-induced ROS production and apoptosis. Conclusion Collectively, our study reveals that the interaction of the p53 and Akt feedback loops determine the fate of NSCLC cells and their CDDP sensitivity. Electronic supplementary material The online version of this article (10.1186/s12935-019-0910-2) contains supplementary material, which is available to authorized users.

Background: N6-methyladenosine (m6A)-mediated ribonucleic acid (RNA) methylation is considered to be the most significant and abundant epigenetic modification in eukaryotic cells, and plays an essential role in the carcinogenesis and molecular pathogenesis of hepatocellular carcinoma (HCC). However, the relationship between m6A regulation and immune cell infiltration of the tumor immune microenvironment (TIME) has not yet been clarified. We aimed to investigate the roles of m6A RNA gene regulators in HCC immune regulation and prognosis.Methods: The Cancer Genome Atlas (TCGA) database was used, and unsupervised clustering of 21 m6A regulators was performed based on differential gene expression. Gene Set Variation Analysis (GSVA), singlesample Gene Set Enrichment Analysis (ssGSEA), the empirical Bayes method, and m6A scores were used in our analyses.Results: Of 433 samples, 101 (23.22%) had m6A regulatory factor mutations. From these, we identified three m6A subtypes, which correlated with different TIME phenotypes: immune rejection, immune infiltration, and immune deficiency. Tumors with low methyltransferase-like 3 (METTL3) expression had increased infiltration of dendritic cells (DCs) in the TIME. Reduced METTL3 expression also led to an overall increase in expression of major histocompatibility complex (MHC) molecules, costimulatory molecules, and adhesion molecules. The m6A subtypes were scored and analyzed for correlations. Patients with epithelial-mesenchymal transition (EMT) subtypes had lower m6A scores than the other three molecular subtypes. Survival analysis found that patients with low m6A scores had better overall survival [hazard ratio (HR) 1.6 (1.1-2.3)] and a 1.16 times better 5-year survival rate than patients with high m6A scores (56% vs. 48%). Conclusions:Our results demonstrated that three different m6A modification subtypes contribute to immune regulation in HCC and have potential as novel prognostic indicators and immune therapeutic targets.

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