Search

In the design of photoelectrocatalytic cells, a key element is effective photogeneration of electron‐hole pairs to drive redox activation of catalysts. Despite recent progress in photoelectrocatalysis, experimental realization of a high‐performance photocathode for multi‐electron reduction of chemicals, such as nitrate reduction to ammonia, has remained a challenge due to difficulty in obtaining efficient electrode configurations for extraction of high‐throughput electrons from absorbed photons. This work describes a new design for catalytic photoelectrodes using chromophore assembly‐functionalized covalent networks for boosting eight‐electron reduction of nitrate to ammonia. Upon sunlight irradiation, the photoelectrode stores a mass of reducing equivalents at the photoexcited chromophore assembly for multielectron reduction of a copper catalyst, enabling efficient nitrate reduction to ammonia. By introducing the new photoelectrode structure, it is demonstrated that the electronic interplay between charge photo‐accumulating assembly and multi‐electron redox catalysts can be optimized to achieve proper balance between electron transfer dynamics and thermodynamic output of photoelectrocatalytic systems. [ABSTRACT FROM AUTHOR]

Although the importance of PIWI-interacting RNAs (piRNAs) in cancer has recently been recognized, studies on the role and functional mechanism of piRNAs in lung adenocarcinoma (LUAD) development and progression are limited. In this study, we identified 10 differently expressed piRNAs in LUAD tissues compared to normal tissues, among which, piR-hsa-211106 expression levels were downregulated in LUAD tissues and cell lines. Furthermore, the effects of piR-hsa-211106 on the malignant phenotypes and chemosensitivity of LUAD cells were detected by gain- and loss-of-function analyses in vitro and in vivo , which showed that piR-hsa-211106 inhibited LUAD cell proliferation, tumor growth, and migration, but promoted apoptosis. Moreover, our finding indicated that piR-hsa-211106 is a potential therapeutic target that synergistically imparts anticancer effects with a chemotherapeutic agent for LUAD-cisplatin. Further mechanistic investigation indicated that piR-hsa-211106 could bind to pyruvate carboxylase (PC) by RNA pull down and RNA immunoprecipitation assays and inhibited PC mRNA and protein expression. Our study demonstrates that piR-hsa-211106 inhibits LUAD progression by hindering the expression and function of PC and enhances chemotherapy sensitivity, suggesting that piR-hsa-211106 is a novel diagnostic and therapeutic target for LUAD. [ABSTRACT FROM AUTHOR]

Radiation-induced heart damage is a serious side effect caused by radiotherapy, especially during the treatment of cancer near the chest. Trimetazidine is effective at reducing inflammation in the heart, but how it affects radiation-induced cardiac fibrosis (RICF) is unknown. To investigate the potential effect and molecular mechanism, we designed this project with a C57BL6 male mouse model supposing trimetazidine could inhibit RICF in mice. During the experiment, mice were randomly divided into six groups including a control group (Con), radiation-damaged model group (Mod) and four experimental groups receiving low-dose (10 mg/kg/day) or high-dose (20 mg/kg/day) trimetazidine before or after radiation treatment. Apart from the control group, all mice chests were exposed to 6 MV X-rays at a single dose of 20 Gy to induce RICF, and tissue analysis was done at 8 weeks after irradiation. Fibroblast or interstitial tissues and cardiac fibrosis-like characteristics were determined using haematoxylin and eosin and Masson staining, which can be used to assess myocardial fibrosis. Immunohistochemical analysis and RT-PCR were used to determine gene expression and study the molecular mechanism. As a result, this study suggests that trimetazidine inhibits RICF by reducing gene expression related to myocyte apoptosis and fibrosis formation, i.e. connective tissue growth factor (CTGF), transforming growth factor (TGF)-β1, smad2 and smad3. In conclusion, by regulating the CTGF/TGF-β1/Smad pathway, trimetazidine could be a prospective drug for clinical treatment of RICF. [ABSTRACT FROM AUTHOR]

The tripartite motif (TRIM) family proteins play a great role in carcinogenesis. However, the expression pattern, prognostic value and biological functions of tripartite motif containing 23 (TRIM23) in colorectal cancer (CRC) are poorly understood. Here, we found that TRIM23 is up‐regulated and associated with tumour size, lymph node metastasis, American Joint Committee on Cancer (AJCC) stage and poor prognosis in CRC. Multivariate Cox regression analyses revealed that TRIM23 overexpression could be identified as an independent prognostic factor for CRC. TRIM23 could promote the proliferation of CRC cell in vitro and in vivo; additionally, TRIM23 depletion induced G1-phase arrest. Gene set enrichment analysis (GSEA) revealed that P53 and cell cycle signalling pathway‐related genes were enriched in patients with high TRIM23 expression levels. We show in this study that TRIM23 physically binds to P53 and enhances the ubiquitination of P53, thereby promoting tumour proliferation. Thus, our data indicated that TRIM23 acts as an oncogene in colorectal carcinogenesis and may provide a novel therapeutic target for CRC management. [ABSTRACT FROM AUTHOR]

Retinoblastoma-binding protein 7 (RBBP7) is an important component of several complexes that regulate chromatin metabolism. It is overexpressed in certain cancer types and serves conflicting roles in tumor progression. In the present study, the expression and roles of RBBP7 were explored in esophageal squamous cell carcinoma (ESCC). Immunohistochemical staining was used to detect RBBP7 expression in ESCC tissues. The mRNA sequencing profiles from the Cancer Genome Atlas and Genotype-Tissue Expression databases were mined to analyze the mRNA expression of RBBP7 in tissues. Proliferation, clone formation, apoptosis and Transwell invasion/migration assays were performed to explore the roles of RBBP7 in ESCC. RBBP7 was highly expressed in ESCC tissues. The protein and mRNA expression levels of RBBP7 were significantly elevated in tumor tissues compared with paired adjacent normal tissues. RBBP7 overexpression was associated with a poor overall survival in patients with ESCC. Furthermore, higher RBBP7 expression was significantly correlated with poor tumor differentiation, advanced regional lymph node involvement, and pathological TNM staging. Knockdown of RBBP7 in ESCC cells did not affect tumor apoptosis or tumor growth. However, the overexpression of RBBP7 significantly enhanced the invasion and migration of ESCC cells, whereas the knockdown of RBBP7 resulted in significantly decreased invasion and migration. The present study indicated that RBBP7 is a novel biomarker and prognosticator for patients with ESCC. Furthermore, RBBP7 serves crucial roles in promoting ESCC invasion and migration. [ABSTRACT FROM AUTHOR]

Fucoidan is a sulfated polysaccharide that is extracted from brown algae seaweed. This study was designed to evaluate the protective and immunomodulatory effects of dietary fucoidan on 7,12-dimethyl benz[a]anthracene (DMBA)-induced experimental mammary carcinogenesis in rats. Sixty Sprague-Dawley rats were randomly assigned to four equal groups: the control group (control group), the cancer model group (model group), and the F1 and F2 groups, which were fed fucoidan at concentrations of 200 and 400 mg/kg·body weight, respectively. We found that fucoidan treatment decreased the tumor incidence and mean tumor weight and prolonged the tumor latency. Flow cytometric analyses revealed that the number of blood natural killer cells was higher after fucoidan treatment and that the proportions of CD4 and CD8 T cells were also increased. The serum levels of interleukin (IL)-6, IL-12p40, and interferon (IFN)-γ were higher in the rats treated with fucoidan compared to those of model rats. Moreover, the percentage of CD3+ Foxp3+ regulatory T cells in the blood and the levels of IL-10 and transforming growth factor β in the serum were lower in the rats treated with fucoidan. Furthermore, fucoidan treatment decreased the expression of Foxp3 and programmed cell death 1 ligand 1 (PDL1) in tumor tissues. The levels of p-phosphatidyl inositol kinase 3 and p-AKT in tumor tissues were also lower than those of model rats. These results suggest that a fucoidan-supplemented diet can inhibit DMBA-induced tumors in rats. This study provides experimental evidence toward elucidating the immune enhancement induced by fucoidan through the programmed cell death 1/PDL1 signaling pathway. The immunomodulatory effect is one of the possible mechanisms of the protective effect of fucoidan against mammary carcinogenesis. [ABSTRACT FROM PUBLISHER]