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Background Lung cancer poses a serious threat to human health, but its molecular mechanisms remain unclear. Circular RNAs (circRNAs) are closely associated with tumour progression, and the important role of 8-oxoguanine (o8G) modification in regulating the fate of RNA has been gradually revealed. However, o8G modification of circRNAs has not been reported. We identified circPLCE1, which is significantly downregulated in lung cancer, and further investigated the o8G modification of circPLCE1 and the related mechanism in lung cancer progression. Methods We identified differentially expressed circRNAs by RNA high-throughput sequencing and then conducted methylated RNA immunoprecipitation (MeRIP), immunofluorescence (IF) analysis, crosslinking immunoprecipitation (CLIP) and actinomycin D (ActD) assays to explore circPLCE1 o8G modification. The biological functions of circPLCE1 in vivo and in vitro were clarified via establishing a circPLCE1 silencing/overexpression system. Tagged RNA affinity purification (TRAP), RNA Immunoprecipitation (RIP) and coimmunoprecipitation (Co-IP) assays, and pSIN-PAmCherry-KFERQ-NE reporter gene were used to elucidate the molecular mechanism by which circPLCE1 inhibits lung cancer progression. Results This study revealed that reactive oxygen species (ROS) can induce circPLCE1 o8G modification and that AUF1 can mediate a decrease in circPLCE1 stability. We found that circPLCE1 significantly inhibited lung cancer progression in vitro and in vivo and that its expression was associated with tumour stage and prognosis. The molecular mechanism was elucidated: circPLCE1 targets the HSC70 protein, increases its ubiquitination level, regulates ATG5-dependent macroautophagy via the chaperone-mediated autophagy (CMA) pathway, and ultimately inhibits lung cancer progression. Conclusion o8G-modified circPLCE1 inhibits lung cancer progression through CMA to inhibit macroautophagy and alter cell fate. This study provides not only a new theoretical basis for elucidating the molecular mechanism of lung cancer progression but also potential targets for lung cancer treatment. Graphical abstract ROS induce circPLCE1 o8G modification, and AUF1 specifically recognizes o8G modification, thereby decreases circPLCE1 stability. circPLCE1 targets the HSC70 protein, increases its ubiquitination level, inhibits CMA activity, and promotes ATG5-dependent macroautophagy via the CMA pathway, altering the fate of tumour cells and ultimately inhibiting lung cancer progression.

Background Lung cancer is a serious threat to human life and health, but effective screening and treatment methods are lacking. Circular RNAs (circRNAs) have important biological functions and are closely related to tumour development. Some studies have shown that the 8-oxo-7,8-dihydroguanosine (o8G) modification plays a key role in the disease process, but the effect of the o8G modification on circRNAs has not been elucidated. Moreover, cuproptosis is a novel mode of cell death in which copper ions directly promote protein aggregation and the disruption of cellular metabolic pathways. The present study revealed that the o8G modification of circKIAA1797 occurs and promotes lung cancer development by inhibiting cuproptosis, which provides new perspectives for epitranscriptomic studies and the development of novel therapeutic approaches for lung cancer. Methods circRNA differential expression profiles in lung cancer were revealed via RNA high-throughput sequencing, and circKIAA1797 expression in lung cancer cell lines and tissues was detected using qPCR. Experiments such as o8G RNA immunoprecipitation (o8G RIP) and crosslinking immunoprecipitation (CLIP) were performed to explore the presence of o8G on circKIAA1797. The regulation of circKIAA1797 by the o8G reader Y-box binding protein 1 (YBX1) was explored using nuclear–cytoplasmic fractionation, actinomycin D (Act D) stability experiments and other experiments. circKIAA1797 silencing and overexpression systems were constructed for in vivo and in vitro experiments to study the role of circKIAA1797 in lung cancer development. Tagged RNA affinity purification (TRAP), RNA immunoprecipitation (RIP), coimmunoprecipitation (Co-IP), and immunofluorescence (IF) staining were subsequently conducted to reveal the molecular mechanism by which circKIAA1797 regulates cuproptosis and promotes lung cancer development. Results This study is the first to reveal the presence of o8G on circKIAA1797 and that YBX1 is a reader that recognises ROS-induced circKIAA1797 o8G modifications and increases the stability and cytoplasmic expression of circKIAA1797. circKIAA1797, which is associated with the tumour stage and prognosis, has been shown to significantly promote the biological function of lung cancer development both in vivo and in vitro. This study revealed that circKIAA1797 inhibits intracellular cuproptosis by binding to the ferredoxin 1 (FDX1) mRNA, decreasing FDX1 mRNA stability, inhibiting FDX1 expression, and binding to the signal transducer and activator of transcription 1 (STAT1) protein and inhibiting lipoyltransferase 1 (LIPT1) transcription; moreover, circKIAA1797 promotes the closure of the mitochondrial permeability transition pore (mPTP), inhibits cuproptosis, and ultimately promotes lung cancer development. Conclusions This study revealed the presence of the o8G modification in circKIAA1797, which plays an important role in the development of lung cancer. circKIAA1797 can inhibit cuproptosis by inhibiting key cuproptosis proteins and promoting mPTP closure, ultimately promoting the development of lung cancer. This study provides not only a new theoretical basis for an in-depth understanding of the molecular mechanisms of lung cancer development but also a potential target for lung cancer treatment.

Temperate phages are potential therapeutic agents, but only a few temperate phages infecting multidrug-resistant Acinetobacter baumannii have been identified. In this study, we isolated 5W, a temperate phage that infects multidrug-resistant A. baumannii, from pond water using the enrichment method. A member of the Siphoviridae family, 5W has a narrow host range and infected only four of 19 A. baumannii clinical isolates. It exhibited rapid adsorption (> 90% in 6 min), a latency period of 20 min, and a burst size of ~ 180 plaque-forming units (PFU/cell). 5W contains a linear double-stranded DNA (dsDNA) genome of 43,032 bp with a GC content of 39.85%. The 5W genome contains 61 open reading frames, including lysogen-forming genes, but lacks any known virulence and antibiotic resistance genes. The lysin of 5W is an N-acetyl-β-d-muramidase belonging to the GH_108 family. The α-helical structure and highly positively charged amino acids in the C-terminal region indicate potential antibacterial activity against A. baumannii, and the M/S subunits of the restriction endonuclease are inserted into the lysogenic gene cluster. Comparative genome analysis revealed high similarity with two different prophages in A. baumannii ABCR01, suggesting that 5W may be derived from recombination of other prophages.

Background Lung cancer is the most common malignant tumour and the leading cause of cancer-related death. circular RNAs (circRNAs) have important biological functions and are closely related to tumour development. The 5-methylcytosine (m5C) modification can regulate the molecular fate of RNA molecules and thus influence disease development. Methods High-throughput RNA sequencing was used to construct the differential expression profiles of circRNAs. The m5C modification of circRREB1 was explored through methylated RNA immunoprecipitation (MeRIP) and crosslinking-immunoprecipitation (CLIP). RNA stability experiments, fluorescence in situ hybridization (FISH), and nuclear-cytoplasmic fractionation experiments were performed to explore the effects of the m5C modification on circRREB1. A system for the silencing and overexpression of circRREB1 was established, and in vitro and in vivo experiments were conducted to study the biological functions of circRREB1. Tagged RNA affinity purification (TRAP), RNA immunoprecipitation (RIP), and coimmunoprecipitation (Co-IP) experiments were conducted to reveal the molecular mechanisms of circRREB1. Results In this study, we found that circRREB1 is highly expressed in lung cancer tissues and cells and that patients with high circRREB1 expression have a poor prognosis. We discovered that circRREB1 undergoes the m5C modification mediated by the methyltransferase NSUN2. This modification facilitates its nuclear export via the m5C reader ALYREF. Functional studies demonstrated that circRREB1 promotes lung cancer progression both in vitro and in vivo. Mechanistically, circRREB1 directly binds to HSPA8 and stabilizes it by inhibiting ubiquitin-dependent degradation, thereby inducing mitophagy through the HSPA8/PINK1/Parkin signalling axis and ultimately promoting the development of lung cancer. Conclusions This study revealed the presence of m5C modifications on circRREB1 and showed that m5C-modified circRREB1 can induce mitophagy, ultimately promoting lung cancer. These findings provide not only a theoretical basis for further exploration of the mechanisms underlying lung cancer development but also potential targets for lung cancer therapy. Graphical Abstract

Accumulating evidence indicates that circular RNAs (circRNAs) are inextricably linked to cancer development. However, the function and mechanism of nucleus‐localized circRNAs in hepatocellular carcinoma (HCC) still require investigation. Here, qRT‐PCR and receiver‐operating characteristic curve were used to detect the expression and diagnostic potential of circSLC39A5 for HCC. The biological function of circSLC39A5 in HCC was investigated in vitro and in vivo. Nucleoplasmic separation assay, fluorescence in situ hybridization, RNA pulldown, RNA immunoprecipitation, the HDOCK Server, the NucleicNet Webserver, crosslinking‐immunoprecipitation, MG132 treatment, and chromatin immunoprecipitation were utilized to explore the potential molecular mechanism of circSLC39A5 in HCC. The results showed that circSLC39A5 was downregulated in both HCC tissues and plasma and was associated with satellite nodules and lymph node metastasis/vascular invasion. CircSLC39A5 was stably expressed in plasma samples under different storage conditions, showing good diagnostic potential for HCC (AUC = 0.915). CircSLC39A5 inhibited proliferation, migration, and invasion, facilitated the apoptosis of HCC cells, and was associated with low expression of Ki67 and CD34. Remarkably, circSLC39A5 is mainly localized in the nucleus and binds to the transcription factor signal transducer and activator of transcription 1 (STAT1), affecting its stabilization and expression. STAT1 binds to the promoter of thymine DNA glycosylase (TDG). Overexpression of circSLC39A5 elevates TDG expression and reverses the increase of proliferating cell nuclear antigen (PCNA) expression and the overactive cell proliferation caused by TDG silencing. Our findings uncovered a novel plasma circRNA, circSLC39A5, which may be a potential circulating diagnostic marker for HCC, and the mechanism by which nucleus‐localized circSLC39A5 exerts a transcriptional regulatory role in HCC by affecting STAT1/TDG/PCNA provides new insights into the mechanism of circRNAs.

Lung cancer is the primary cause of cancer-related death worldwide, and its global incidence and mortality rates remain high. The differential expression of circular RNAs (circRNAs) can affect the development of cancer, but the mechanisms by which circRNAs regulate lung cancer progression remain unclear. In this study, we identified circSORBS1, a circRNA that has not been previously described in lung cancer and is significantly underexpressed in lung cancer tissues, blood and cell lines, and the low expression of circSORBS1 correlated with tumour grade and prognosis. In vitro and in vivo functional experiments revealed that circSORBS1 overexpression inhibited cell proliferation and migration while enhancing apoptosis. Mechanistically, circSORBS1 acts as a sponge for miR-6779-5p, indirectly inhibiting RUFY3 mRNA degradation. Simultaneously, it binds to RUFY3 mRNA to enhance its stability. This dual regulatory mechanism leads to an increase in RUFY3 protein levels, which ultimately activates the YWHAE/BAD/BCL2 apoptotic signalling pathway and suppresses lung cancer progression. Our findings not only increase the knowledge about the regulatory pattern of circRNA expression but also provide new insights into the mechanisms by which circRNAs regulate lung cancer development.

Garlic (Allium sativum) is an important economic crop in China. In terms of using remote sensing technology to identify it, there is still room for improvement, and the high-precision classification of garlic has become an important issue. However, to the best of our knowledge, few studies have focused on garlic area mapping. Here, we propose a method for identifying garlic crops using samples and a multi-feature dataset under limited conditions. The results indicate the following: (1) In the land-use classification of the Erhai Lake Basin, the importance ranking of the characteristic bands, from high to low, is as follows: spectral features, vegetation features, texture features, and terrain features. (2) The random forest method based on feature selection demonstrates high accuracy in land-use classification within the Erhai Lake Basin in Yunnan Province. The overall classification accuracy reached 95.79%, with a Kappa coefficient of 0.95. (3) From 1999 to 2023, the expansion of garlic cultivation in the Erhai Lake Basin showed a trend of initially strengthening from north to south, which was followed by weakening. The vertical development of garlic cultivation reached saturation, showing a slow trend toward horizontal expansion between 2005 and 2018. The planting distributions in various townships in the Erhai Lake Basin gradually shifted from relatively uniform distributions to upstream development. This study utilized the Google Earth Engine (GEE) cloud computing platform and machine learning algorithms to compensate for the lack of statistical data on garlic cultivation in the Erhai Lake Basin. Moreover, it accurately, rapidly, and efficiently extracted planting information, demonstrating significant potential for practical applications.

Background Many studies have shown that circular RNAs (circRNAs) are abnormally expressed in various tumor tissues and served as a key regulator in the occurrence and development of cancer. However, in hepatocellular carcinoma (HCC), the molecular mechanism of circRNAs in body fluids remains to be further explored. Methods The expression levels of genes and proteins were detected by quantitative real‐time polymerase chain reaction (qRT‐PCR) and western blotting, respectively. Cell counting Kit‐8 (CCK‐8), 5‐Ethynyl‐2'‐deoxyuridine (EdU), wound healing assay, Transwell assays, flow cytometry, and tumor formation models in nude mice were conducted to investigate the effects of circFAM114A2 on HCC cells both in vitro and in vivo. RNA antisense purification (RAP), dual luciferase reporter assays and rescue assays were carried out to verify the interaction between circFAM114A2, miR‐630 and HHIP. Results CircFAM114A2 was significantly downregulated in HCC tissues and was associated with microvascular invasion and lymph node metastasis of HCC patients. We also observed that circFAM114A2 was lowly expressed in HCC plasma, which may serve as an effective biomarker to screen HCC patients from healthy controls (area under curve (AUC)=0.922). In vitro, circFAM114A2 overexpression significantly blunted HCC cell proliferation, migration, invasion, and promoted apoptosis, whereas circFAM114A2 silencing posed opposite effects. In vivo, circFAM114A2 overexpression inhibited the growth of HCC cells. Mechanistically, circFAM114A2 could increase the expression of the tumor suppressor HHIP via acting as a sponge for miR‐630. Conclusions CircFAM114A2 exerts a tumor suppressor role in HCC through miR‐630/HHIP axis, and may be served as a potential diagnostic and therapeutic biomarker for HCC patients. CircFAM114A2 exerts a tumor suppressor role in hepatocellular carcinoma (HCC) through miR‐630/HHIP axis and may be served as a potential diagnostic and therapeutic biomarker for HCC patients.

Graphene/silicon hybrid photodetector operating at communication wavelength has attracted enormous attention recently due to its potential to realize bandwidth larger than 100 GHz. However, the responsivity is intrinsically limited by the low absorption from the atomic-thick graphene monolayer, which imposes significant obstacles towards its practical application. Although plasmonic structures has been widely applied to enhance the responsivity, it may induce the metallic absorption thus limit the responsivity lower than 0.6 A/W. Twisted bilayer graphene (TBG) has been reported to hold the ability to dramatically enhance the optical absorption due to the unique twist-angle-dependent van Hove singularities. In this article, we present a design of a silicon/TBG hybrid photodetector with a responsivity higher than 1 A/W and bandwidth exceeding 100 GHz. The enhanced responsivity is achieved by tuning the twisted angle of TBG to increase the absorption within the 1550 nm as well as utilizing the silicon slot waveguide to boost the mode overlap with TBG. The fabrication process of proposed design is also discussed demonstrating the advantages of low fabrication complexity. The proposed silicon/TBG photodetector could not only exhibit superior performance compared to previously reported silicon/monolayer graphene photodetector, but also pave the way for the practical application of graphene-based silicon optoelectronic devices.

The N7-methylguanosine (m7G) modification and circular RNAs (circRNAs) have been shown to play important roles in the development of lung cancer. However, the m7G modification of circRNAs has not been fully elucidated. This study revealed the presence of the m7G modification in circFAM126A. We propose the novel hypothesis that the methyltransferase TRMT10C mediates the m7G modification of circFAM126A and that the stability of m7G-modified circFAM126A is reduced. circFAM126A is downregulated in lung cancer and significantly inhibits lung cancer growth both in vitro and in vivo. The expression of circFAM126A correlates with the stage of lung cancer and with the tumour diameter, and circFAM126A can be used as a potential molecular target for lung cancer. The molecular mechanism by which circFAM126A increases HSP90 ubiquitination and suppresses AKT1 expression to regulate cellular glycolysis, ultimately inhibiting the progression of lung cancer, is elucidated. This study not only broadens the knowledge regarding the expression and regulatory mode of circRNAs but also provides new insights into the molecular mechanisms that regulate tumour cell metabolism and affect tumour cell fate from an epigenetic perspective. These findings will facilitate the development of new strategies for lung cancer prevention and treatment.Graphical Headlights• circRNA can undergo m7G modification. The methyltransferase TRMT10C mediates circFAM126A m7G modification, thereby enhancing circFAM126A stability.• m7G-modified circFAM126A can perform a biological function in inhibiting lung cancer progression by regulating cellular glycolysis.• circFAM126A increases ubiquitination of HSP90 and inhibits AKT1 expression to regulate cellular glycolysis.