Explore the vast range of titles available.

Prostate cancer is one of the most prevalent forms of cancer around the world. Androgen-deprivation treatment and chemotherapy are the curative approaches used to suppress prostate cancer progression. However, drug resistance is extensively and hard to overcome even though remarkable progress has been made in recent decades. Noncoding RNAs, such as miRNAs, lncRNAs, and circRNAs, are a group of cellular RNAs which participate in various cellular processes and diseases. Recently, accumulating evidence has highlighted the vital role of non-coding RNA in the development of drug resistance in prostate cancer. In this review, we summarize the important roles of these three classes of noncoding RNA in drug resistance and the potential therapeutic applications in this disease.

The separation of hydrogen isotopes for applications such as nuclear fusion is a major challenge. Current technologies are energy intensive and inefficient. Nanoporous materials have the potential to separate hydrogen isotopes by kinetic quantum sieving, but high separation selectivity tends to correlate with low adsorption capacity, which can prohibit process scale-up. In this study, we use organic synthesis to modify the internal cavities of cage molecules to produce hybrid materials that are excellent quantum sieves. By combining small-pore and large-pore cages together in a single solid, we produce a material with optimal separation performance that combines an excellent deuterium/hydrogen selectivity (8.0) with a high deuterium uptake (4.7 millimoles per gram).

Nerves are important pathological elements of the microenvironment of tumors, including those in pancreatic, colon and rectal, prostate, head and neck, and breast cancers. Recent studies have associated perineural invasion with tumor progression and poor outcomes. In turn, tumors drive the reprogramming of neurons to recruit new nerve fibers. Therefore, the crosstalk between nerves and tumors is the hot topic and trend in current cancer investigations. Herein, we reviewed recent studies presenting direct supporting evidences for a better understanding of nerve–tumor interactions.

Two-dimensional covalent organic frameworks (2D COFs) are promising for gas sensing owing to the large surface area, abundant active sites, and their semiconducting nature. However, 2D COFs are usually produced in the form of insoluble micro-crystallites. Their poor contacts between grain boundaries severely suppress the conductivity, which are too low for chemresistive gas sensing. Here, we demonstrate that halide perovskites can be employed as electric glues to bond 2D COF crystallites to improve their conductivity by two orders of magnitude, activating them to detect NO 2 with high selectivity and sensitivity. Resonant microcantilever, grand canonical Monte Carlo, density functional theory and sum-frequency generation analyses prove that 2D COFs can enrich and transfer electrons to NO 2 molecules, leading to increased device conductivity. This work provides a facile approach for improving the conductivity of polycrystalline 2D COF films and may expand their applications in semiconductor devices, such as sensors, resistors, memristors and field-emission transistors. 2D COFs are promising for resistance-related applications, but usually form powders where poor contacts at grain boundaries inhibit the conductivity. Here authors show that halide perovskites can act as electric glues to bond 2D COFs to improve their conductivity, activating them to detect NO 2 with high selectivity and sensitivity.

Background Sunitinib resistance can be classified into primary and secondary resistance. While accumulating research has indicated several underlying factors contributing to sunitinib resistance, the precise mechanisms in renal cell carcinoma are still unclear. Methods RNA sequencing and m6A sequencing were used to screen for functional genes involved in sunitinib resistance. In vitro and in vivo experiments were carried out and patient samples and clinical information were obtained for clinical analysis. Results We identified a tumor necrosis factor receptor-associated factor, TRAF1, that was significantly increased in sunitinib-resistant cells, resistant cell-derived xenograft (CDX-R) models and clinical patients with sunitinib resistance. Silencing TRAF1 increased sunitinib-induced apoptotic and antiangiogenic effects. Mechanistically, the upregulated level of TRAF1 in sunitinib-resistant cells was derived from increased TRAF1 RNA stability, which was caused by an increased level of N6-methyladenosine (m6A) in a METTL14-dependent manner. Moreover, in vivo adeno-associated virus 9 (AAV9) -mediated transduction of TRAF1 suppressed the sunitinib-induced apoptotic and antiangiogenic effects in the CDX models, whereas knockdown of TRAF1 effectively resensitized the sunitinib-resistant CDXs to sunitinib treatment. Conclusions Overexpression of TRAF1 promotes sunitinib resistance by modulating apoptotic and angiogenic pathways in a METTL14-dependent manner. Targeting TRAF1 and its pathways may be a novel pharmaceutical intervention for sunitinib-treated patients.

The methyltransferase Wilms’ tumor 1-associated protein (WTAP) has been reported to be dysregulated in various tumors. However, its role in renal cell carcinoma (RCC) remains elusive. Here, we explored whether WTAP was upregulated in RCC specimens compared to normal tissues. Functionally, WTAP promoted RCC cell proliferation and metastasis in vivo and in vitro. Mechanistically, WTAP act as an N6-methyladenosine transferase to regulate the m 6 A modification of long noncoding RNA TEX41. Then, the upregulated m 6 A modification destabilized TEX41 in a YTHDF2-dependent manner. Furthermore, TEX41 interacted with the SUZ12 protein and increased the histone methyltransferase activity of SUZ12, resulting in HDAC1 silencing. Totally, our study demonstrated the oncogenic the role of WTAP/TEX41/SUZ12/HDAC1 axis in RCC progression.

The existing analysis methods for the silicon gyroscope drive loop, such as the perturbation method and period average method, cannot analyze the dynamic characteristics of the system. In this work, a linearized amplitude control model of the silicon gyroscope drive loop was established to analyze the stability and set-up time of the drive loop, and the vibration conditions of the silicon gyro were obtained. According to the above results, a new silicon gyroscope interface circuit was designed, using a 0.35 μm Bipolar-CMOS-DMOS (BCD) process, and the chip area was 4.5 mm × 4.0 mm. The application-specific integrated circuit (ASIC) of the silicon gyroscope was tested in combination with the sensitive structure with a zero stability of 1.14°/hr (Allen). The test results for the ASIC and the whole machine prove the correctness of the theoretical model, which reflects the effectiveness of the stability optimization of the closed-loop controlled drive loop of the silicon gyroscope circuit.

Porous liquids (PLs), integrating porous hosts into flowing liquids through intermolecular interactions, attract significant attention, while their controlled synthesis remains challenging. Here we report a controllable in-situ transformation strategy to fabricate distinct types of PLs from the same supramolecular framework (SMF). Two isomorphic polyethylene-glycol-based ionic liquids, IL-Br and IL-NTf 2 , differing only in anions, exhibit contrasting electrostatic interactions with the SMF. Strong attraction between IL-Br and the SMF disrupts the ionic bonds within the framework, yielding a type II PL, PL2(SMF-Br), while electrostatic repulsion in IL-NTf 2 preserves the framework, producing a type III PL, PL3(SMF-NTf 2 ). These tailored host–solvent interactions endow PL2(SMF-Br) with over twice the CO 2 uptake and photoresponsivity of its counterpart, as well as record-high CO 2 capacity among reported type II PLs. In this work, we establish a general strategy for tunable PL construction through electrostatically guided host–solvent design. Porous liquids show potential as material for carbon dioxide capture but their controlled synthesis remains challenging. Here the authors report a controlled in-situ transformation strategy to fabricate distinct types of porous liquids from one type of supramolecular framework.

Lactylation, a post-translational modification characterized by the attachment of lactate to protein lysine residues on proteins, plays a pivotal role in cancer progression and immune evasion. However, its implications in immunity regulation and prostate cancer prognosis remains poorly understood. This study aims to systematically examine the impact of lactylation-related genes (LRGs) on prostate cancer. Single-cell and bulk RNA sequencing data from patients with prostate cancer were analyzed. Data were sourced from TCGA-PRAD, GSE116918, and GSE54460, with batch effects mitigated using the ComBat method. LRGs were identified from exisiting literature, and unsupervised clustering was applied to assess their prognostic siginificance. The tumor microenvironment and functional enrichment of relevant pathways were also evaluated. A prognostic model was developed using integrative machine learning techniques, with drug sensitivy analysis included. The mRNA expression profiles of the top ten genes were validated in clinical samples. Single-cell RNA sequencing revealed distinct lactylation signatures across various cell types. Bulk RNA-seq analysis identified 56 prognostic LRGs, classifying patients into two distinct clusters with divergent prognoses. The high-risk cluster exhibited reduced immune cell infiltration and increased resistance to specific targeted therapies. A machine learning-based prognostic signature was developed, demonstrating robust predictive accuracy for treatment responses and disease outcomes. This study offers a comprehensive analysis of lactylation in prostate cancer, identifying potential prognostic biomarkers. The proposed prognostic signature provides a novel approach to personalized treatment strategies, deepening our understanding of the molecular mechanisms driving prostate cancer and offering a tool for predicting therapeutic responses and clinical outcomes.

Background Circular RNA (circRNA) is a novel class noncoding RNA (ncRNA) that plays a critical role in various cancers, including prostate cancer (PCa). However, the clinical significance, biological function, and molecular mechanisms of circRNAs in prostate cancer remain to be elucidated. Methods A circRNA array was performed to identified the differentially expressed circRNAs. circPDE5A was identified as a novel circRNA which downregulated in clinical samples. Functionally, the in vitro and in vivo assays were applied to explore the role of circPDE5A in PCa metastasis. Mechanistically, the interaction between circPDE5A and WTAP was verified using RNA pulldown followed by mass spectrometry, RNA Immunoprecipitation (RIP) assays. m 6 A methylated RNA immunoprecipitation sequencing (MeRIP-seq) was then used to identified the downstream target of circPDE5A. Chromatin immunoprecipitation assay (ChIP) and dual-luciferase reporter assay were used to identified transcriptional factor which regulated circPDE5A expression. Results circPDE5A was identified downregulated in PCa tissues compared to adjacent normal tissue and was negatively correlated with gleason score of PCa patients. circPDE5A inhibits PCa cells migration and invasion both in vitro and in vivo. circPDE5A blocks the WTAP-dependent N6-methyladenisine (m 6 A) methylation of eukaryotic translation initiation factor 3c (EIF3C) mRNA by forming the circPDE5A-WTAP complex, and finally disrupts the translation of EIF3C. Moreover, the circPDE5A-dependent decrease in EIF3C expression inactivates the MAPK pathway and then restrains PCa progression. Conclusions Our findings demonstrate that FOXO4-mediated upregulation of circPDE5A controls PCa metastasis via the circPDE5A-WTAP-EIF3C-MAPK signaling pathway and could serve as a potential therapeutic targer for PCa.