Background Circular RNAs (circRNAs) are a novel type of noncoding RNAs and play important roles in tumorigenesis, including gastric cancer (GC). However, the functions of most circRNAs remain poorly understood. In our study, we aimed to investigate the functions of a new circRNA circ-DONSON in GC progression. Methods The expression of circ-DONSON in gastric cancer tissues and adjacent normal tissues was analyzed by bioinformatics method, qRT-PCR, Northern blotting and in situ hybridization (ISH). The effects of circ-DONSON on GC cell proliferation, apoptosis, migration and invasion were measured by using CCK8, colony formation, EdU, immunofluorescence (IF), FACS and Transwell assays. qRT-PCR and Western blotting were utilized to validate how circ-DONSON regulates SOX4 expression. ChIP, DNA fluorescence in situ hybridization (DNA-FISH) and DNA accessibility assays were used to investigate how circ-DONSON regulates SOX4 transcription. The interaction between circ-DONSON and NURF complex was evaluated by mass spectrum, RNA immunoprecipitation (RIP), pulldown and EMSA assays. Xenograft mouse model was used to analyze the effect of circ-DONSON on GC growth in vivo. Results Elevated expression of circ-DONSON was observed in GC tissues and positively associated with advanced TNM stage and unfavorable prognosis. Silencing of circ-DONSON significantly suppressed the proliferation, migration and invasion of GC cells while promoting apoptosis. circ-DONSON was localized in the nucleus, recruited the NURF complex to SOX4 promoter and initiated its transcription. Silencing of the NURF complex subunit SNF2L, BPTF or RBBP4 similarly attenuated GC cell growth and increased apoptosis. circ-DONSON knockdown inhibited GC growth in vivo. Conclusion circ-DONSON promotes GC progression through recruiting the NURF complex to initiate SOX4 expression. Electronic supplementary material The online version of this article (10.1186/s12943-019-1006-2) contains supplementary material, which is available to authorized users.
Lanthanide (Ln3+)‐doped luminescent nanoparticles (NPs) with emission in the second near‐infrared (NIR‐II) biological window have shown great promise but their applications are currently limited by the low absorption efficiency of Ln3+ owing to the parity‐forbidden 4f→4f electronic transition. Herein, we developed a strategy for the controlled synthesis of a new class of NIR‐II luminescent nanoprobes based on Ce3+/Er3+ and Ce3+/Nd3+ co‐doped CaS NPs, which can be effectively excited by using a low‐cost blue light‐emitting diode chip. Through sensitization by the allowed 4f→5d transition of Ce3+, intense NIR‐II luminescence from Er3+ and Nd3+ with quantum yields of 9.3 % and 7.7 % was achieved, respectively. By coating them with a layer of amphiphilic phospholipids, these NPs exhibit excellent stability in water and can be exploited as sensitive NIR‐II luminescent nanoprobes for the accurate detection of an important disease biomarker, xanthine, with a detection limit of 32.0 nm.
Supportinginformation and the ORCID identification number(s) for the author(s) of this article can be found under: https://doi.
A broadband NIR photostimulated luminescence nanoprobe with an ultralow power density threshold is developed based on CaS:Eu2+,Sm3+ nanocrystals.
Doping is an effective strategy for tailoring the optical properties of 0D Cs 4 PbX 6 (X = Cl, Br, and I) perovskite nanocrystals (NCs) and expanding their applications. Herein, a unique approach is reported for the controlled synthesis of pure-phase Mn 2+-doped Cs 4 PbCl 6 perovskite NCs and the excited-state dynamics of Mn 2+ is unveiled through temperature-dependent steady-state and transient photoluminescence (PL) spectroscopy. Because of the spatially confined 0D structure of Cs 4 PbCl 6 perovskite, the NCs exhibit drastically different PL properties of Mn 2+ in comparison with their 3D CsPbCl 3 analogues, including significantly improved PL quantum yield in solid form (25.8%), unusually long PL lifetime (26.2 ms), large exciton binding energy, strong electron-phonon coupling strength, and an anomalous temperature evolution of Mn 2+-PL decay from a dominant slow decay (in tens of ms scale) at 300 K to a fast decay (in 1 ms scale) at 10 K. These findings provide fundamental insights into the excited-state dynamics of Mn 2+ in 0D Cs 4 PbCl 6 NCs, thus laying a foundation for future design of 0D perovskite NCs through metal ion doping toward versatile applications.
Colorectal carcinoma (CRC) is the third most commonly diagnosed cancer in the world. Phytochemicals have become a research hotspot in recent years as cancer prevention and treatment agents due to their low toxicity and limited side-effects. Ellagic acid (EA), a natural phenolic constituent, displays various biological activities, including anticancer effects. However, the detailed anticancer mechanisms of EA remain unclear. In the present study, we found that EA inhibited the growth of HCT-116 colon cancer cells. Moreover, we identified differentially expressed genes (DEGs) by microarray profiling of HCT-116 cells treated with EA. A total of 857 DEGs (363 upregulated and 494 downregulated) were identified with a >1.5-fold change in expression after treatment with EA for 72 h. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis showed that a large number of cellular functions were modified by EA including proliferation, apoptosis, cell cycle and angiogenesis. Interaction network analysis using DEGs provided details of their interactions and predicted the key target pathways of EA. To verify the result of cDNA microarray, 10 selected DEGs related to proliferation, apoptosis or cell cycle were further confirmed by real-time RT-PCR. Based on microarray data, we identified several crucial functions of EA. These results provide important new data for EA in anti-CRC research.
Colorectal carcinoma (CRC) is one of the most prevalent malignant tumors worldwide. Screening and early diagnosis are critical for the clinical management of this disease. DNA methylation changes have been regarded as promising biomarkers for CRC diagnosis. Here, we map DNA methylation profiling on CRC in six CRCs and paired normal samples using a 450 K bead array. Further analysis confirms the methylation status of candidates in two data sets from the Gene Expression Omnibus. Receiver operating characteristic (ROC) curves are calculated to determine the diagnostic performances. We identify 1549 differentially methylated regions (DMRs) showing differences in methylation between CRC and normal tissue. Two genes (ADD2 and AKR1B1), related to the DMRs, are selected for further validation. ROC curves show that the areas under the curves of ADD2 and AKR1B1 are higher than that of SEPT9, which has been clinically used as a screening biomarker of CRC. Our data suggests that aberrant DNA methylation of ADD2 and AKR1B1 could be potential screening markers of CRC.
DNA methylation was regarded as the promising biomarker for rectal cancer diagnosis. However, the optimal methylation biomarkers with ideal diagnostic performance for rectal cancer are still limited. To identify new molecular markers for rectal cancer, we mapped DNA methylation and transcriptomic profiles in the six rectal cancer and paired normal samples. Further analysis revealed the hypermethylated probes in cancer prone to be located in gene promoter. Meanwhile, transcriptome analysis presented 773 low-expressed and 1,161 over-expressed genes in rectal cancer. Correction analysis identified a panel of 36 genes with an inverse correlation between methylation and gene expression levels, including 10 known colorectal cancer related genes. From the other 26 novel marker genes, GFRA1 and GSTM2 were selected for further analysis on the basis of their biological functions. Further experiment analysis confirmed their methylation and expression status in a larger number (44) of rectal cancer samples, and ROC curves showed higher AUC than SEPT9, which has been used as a biomarker in rectal cancer. Our data suggests that aberrant DNA methylation of contiguous CpG sites in methylation array may be potential diagnostic markers of rectal cancer.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.