Microjunction-Modulated Selective Ammonia Sensor with P-Type Oxides-Decorated WS2 Microflakes.

In this study, p-type oxides including NiO, Co3O4, and CuO had been heterostructured with WS2 microflakes for chemiresistive-type gas sensors at room temperature. Microjunctions formed between p-type oxides and WS2 microflakes effectively modulated the sensitivities of the sensors to ammonia. In comparison to Co3O4- or CuO-decorated WS2-based sensors in which "deep energy puddles" were formed at the microjunctions between the oxides and WS2, the fabricated NiO/WS2 heterostructure-based sensor without the formed energy puddles exhibited a better sensing performance with improved sensitivity and a faster response to gaseous 1-10 ppm of NH3. It also processes a good selectivity to some volatile organic compounds including HCHO, toluene, CH3OH, C2H5OH, CH3COCH3, and trimethylamine (TMA). The underlying mechanisms for the enhanced responses were examined by employing in situ diffuse reflectance infrared Fourier transform spectroscopy and density functional theory computation. The oxidization of NH3 on NiO/WS2 was much more intensified compared to those occurred on Co3O4/WS2 and CuO/WS2. NiO/WS2 has a stronger adsorption to NH3 and gains more effective charges transferred from NH3 which significantly contributes to the enhanced sensing properties.

Bivalent activity of super-enhancer RNA LINC02454 controls 3D chromatin structure and regulates glioma sensitivity to temozolomide.

Glioma cell sensitivity to temozolomide (TMZ) is critical for effective treatment and correlates with patient survival, although mechanisms underlying this activity are unclear. Here, we reveal a new mechanism used by glioma cells to modulate TMZ sensitivity via regulation of SORBS2 and DDR1 genes by super-enhancer RNA LINC02454. We report that LINC02454 activity increases glioma cell TMZ sensitivity by maintaining long-range chromatin interactions between SORBS2 and the LINC02454 enhancer. By contrast, LINC02454 activity also decreased glioma cell TMZ sensitivity by promoting DDR1 expression. Our study suggests a bivalent function for super-enhancer RNA LINC02454 in regulating glioma cell sensitivity to TMZ.

Scinderin promotes glioma cell migration and invasion via remodeling actin cytoskeleton.

BACKGROUND: Glioma is one of the most common intracranial tumors, characterized by invasive growth and poor prognosis. Actin cytoskeletal rearrangement is an essential event of tumor cell migration. The actin dynamics-related protein scinderin (SCIN) has been reported to be closely related to tumor cell migration and invasion in several cancers. AIM: To investigate the role and mechanism of SCIN in glioma. METHODS: The expression and clinical significance of SCIN in glioma were analyzed based on public databases. SCIN expression was examined using real-time quantitative polymerase chain reaction and Western blotting. Gene silencing was performed using short hairpin RNA transfection. Cell viability, migration, and invasion were assessed using cell counting kit 8 assay, wound healing, and Matrigel invasion assays, respectively. F-actin cytoskeleton organization was assessed using F-actin staining. RESULTS: SCIN expression was significantly elevated in glioma, and high levels of SCIN were associated with advanced tumor grade and wild-type isocitrate dehydrogenase. Furthermore, SCIN-deficient cells exhibited decreased proliferation, migration, and invasion in U87 and U251 cells. Moreover, knockdown of SCIN inhibited the RhoA/focal adhesion kinase (FAK) signaling to promote F-actin depolymerization in U87 and U251 cells. CONCLUSION: SCIN modulates the actin cytoskeleton via activating RhoA/FAK signaling, thereby promoting the migration and invasion of glioma cells. This study identified the cancer-promoting effect of SCIN and provided a potential therapeutic target for the treatment of glioma.

SnTe/SnSe Heterojunction Based Ammonia Sensors with Excellent Withstand to Ambient Humidities.

Non-invasive breath testing has gained increasing importance for early disease screening, spurring research into cheap sensors for detecting trace biomarkers such as ammonia. However, real-life deployment of ammonia sensors remains hindered by susceptibility to humidity-induced interference. The SnTe/SnSe heterojunction-based chemiresistive-type sensor demonstrates an excellent response/recovery to different concentrations of ammonia from 0.1 to 100 ppm at room temperature. The improved sensing properties of the heterojunctions-based sensors compared to single-phased SnTe or SnSe can be attributed to the stronger NH3 adsorptions, more Te vacancies, and hydrophobic surface induced by the formed SnTe/SnSe heterojunctions. The sensing mechanisms are investigated in detail by using in situ techniques such as diffuse reflectance Fourier transform infrared spectroscopy (DRIFTS), Kelvin probe, and a.c. impedance spectroscopy together with the Density-Function-Theory calculations. The formed heterojunctions boost the overall charge transfer efficiency between the ammonia and the sensing materials, thus leading to the desirable sensing features as well, with excellent resistance to ambient humidities.

Design of a SnO2/Zeolite Gas Sensor to Enhance Formaldehyde Sensing Properties: From the Strategy of the Band Gap-Tunable Zeolite.

ZSM-5 zeolite is usually used in gas sensors as an auxiliary material to improve the gas-sensitive properties of other semiconductor materials, such as its molecular sieve properties and surface adsorption properties. Here, the gas-sensitive mechanism analysis of SnO2/zeolite gas sensors is studied for the first time based on the perspective of zeolite as a band gap-tunable semiconductor that was reported recently. The gas-sensing mechanism of the zeolite/semiconductor has been modeled based on the surface charge theory, and the work function of the ZSM-5 zeolite has been revealed for the first time. A heterostructure of Ag and ZSM-5 was designed and compounded to tune the band gap of the ZSM-5 zeolite by the ammonia pool effect method. The band gap width of the zeolite decreases from 4.51 to 3.61 eV. A series of characterization techniques were used to analyze the distribution and morphology of silver nanoparticles in zeolites and the variation of the ZSM-5 band gap. Then, SnO2/Ag@ZSM-5 sensors were fabricated, and the gas-sensing performances were measured. The gas-sensing results show that the SnO2/Ag@ZSM-5 sensor has an improved response to formaldehyde in particular compared to the SnO2 sensor. The response value of the SnO2/Ag@ZSM-5 sensor to 70 ppm formaldehyde reached 29.4, which is a 528% improvement compared to the SnO2 sensor. Additionally, the selectivity was greatly enhanced. This study provides a strategy for designing and developing higher-performance gas sensors.

20-hydroxyecdysone reprograms amino acid metabolism to support the metamorphic development of Helicoverpa armigera.

Amino acid metabolism is regulated according to nutrient conditions; however, the mechanism is not fully understood. Using the holometabolous insect cotton bollworm (Helicoverpa armigera) as a model, we report that hemolymph metabolites are greatly changed from the feeding larvae to the wandering larvae and to pupae. Arginine, alpha-ketoglutarate (α-KG), and glutamate (Glu) are identified as marker metabolites of feeding larvae, wandering larvae, and pupae, respectively. Arginine level is decreased by 20-hydroxyecdysone (20E) regulation via repression of argininosuccinate synthetase (Ass) expression and upregulation of arginase (Arg) expression during metamorphosis. α-KG is transformed from Glu by glutamate dehydrogenase (GDH) in larval midgut, which is repressed by 20E. The α-KG is then transformed to Glu by GDH-like in pupal fat body, which is upregulated by 20E. Thus, 20E reprogrammed amino acid metabolism during metamorphosis by regulating gene expression in a stage- and tissue-specific manner to support insect metamorphic development.

Cuproptosis-related molecular subtypes direct T cell exhaustion phenotypes and therapeutic strategies for patients with lung adenocarcinoma.

Background: T cell exhaustion (TEX) heterogeneity leads to unfavorable immunotherapeutic responses in patients with cancer. Classification of TEX molecular phenotypes is pivotal to overcoming TEX and improving immunotherapies in the clinical setting. Cuproptosis is a novel form of programmed cell death associated with tumor progression. However, the relation between cuproptosis-related genes (CuRGs) and the different TEX phenotypes has not been investigated in lung adenocarcinoma (LUAD). Methods: Unsupervised hierarchical clustering and principal component analysis (PCA) algorithm were performed to determine CuRGs-related molecular subtypes and scores for patients with LUAD. The tumor immune microenvironment (TIME) landscape in these molecular subtypes and scores was estimated using ESTIMATE and ssGSEA algorithms. Furthermore, TEX characteristics and phenotypes were evaluated in distinct molecular subtypes and scores through GSVA and Spearman correlation analysis. Finally, TIDE scores, immunophenoscore, pRRophetic, GSE78220, and IMvigor210 datasets were employed to appraise the distinguishing capacity of CuRGscore in immunotherapy and pharmacotherapy effectiveness. Results: We identified three CuRGclusters, three geneClusters, and CuRGscore based on 1012 LUAD transcriptional profiles from five datasets. Compared with other molecular subtypes, CuRGcluster B, geneCluster C, and low-CuRGscore group with good prognosis presented fewer TEX characteristics, including immunosuppressive cells infiltration and TEX-associated gene signatures, signal pathways, checkpoint genes, transcription and inflammatory factors. These molecular subtypes were also responsive in distinguishing TEX phenotype in the terminal, GZMK+, and OXPHOS- TEX subtypes, but not the TCF7+ TEX subtype. Notably, copper importer and exporter, SLC31A1 and ATP7B, were remarkably associated with four TEX phenotypes and nine checkpoint genes such as PDCD1, CTLA4, HAVCR2, TIGIT, LAG3, IDO1, SIGLEC7, CD274, PDCD1LG2, indicating that cuproptosis was involved in the development of TEX and immunosuppressive environment in patients with LUAD. Moreover, CuRGscore was significantly related to the TIDE score, immunophenoscore, and terminal TEX score (Spearman R = 0.62, p < 0.001) to effectively predict immunotherapy and drug sensitivity in both training and external validation cohorts. Conclusion: Our study demonstrated the extensive effect of cuproptosis on TEX. CuRGs-related molecular subtypes and scores could illuminate the heterogeneity of TEX phenotype as reliable tools in predicting prognosis and directing more effective immunotherapeutic and chemotherapeutic strategies for patients with LUAD.

UV-Enhanced Formaldehyde Sensor Using Hollow In2O3@TiO2 Double-Layer Nanospheres at Room Temperature.

Hollow In2O3@TiO2 double-layer nanospheres were prepared via a facile water bath method using the sacrifice template of carbon nanospheres. It is shown that the size of the In2O3/TiO2 nanocomposites is 150-250 nm, the thickness of the In2O3 shell is about 10 nm, and the thickness of the TiO2 shell is about 15 nm. The sensing performances of the synthesized In2O3/TiO2 nanocomposites-based chemiresistive-type sensor to formaldehyde (HCHO) gas under UV light activation at room temperature have been studied. Compared to the pure In2O3- and pure TiO2-based sensors, the In2O3/TiO2 nanocomposite sensor exhibits much better sensing performances to formaldehyde. The response of the In2O3/TiO2 nanocomposite-based sensor to 1 ppm formaldehyde is about 3.8, and the response time and recovery time are 28 and 50 s, respectively. The detectable formaldehyde concentration can reach as low as 0.06 ppm. The role of the formed In2O3/TiO2 heterojunctions and the involved chemical reactions activated by UV light have been investigated by AC impedance spectroscopy and the in situ diffuse reflectance Fourier transform infrared spectroscopy. The improvement of the sensing properties of In2O3/TiO2 nanocomposites could be attributed to the nanoheterojunctions between the two components and the "combined photocatalytic effects" of UV-light-emitting diode irradiation. Density functional theory calculations demonstrated that introducing heterojunctions could improve the adsorption energy and charge transfer between formaldehyde and sensing materials.

MXene/SnS2 Heterojunction for Detecting Sub-ppm NH3 at Room Temperature.

Detection of ultralow concentrations of ammonia is very important in many applications such as fishing, poultry, agriculture, industry, biomedicine, and clinical diagnosis. However, detecting sub-ppm NH3 remains a challenge for chemiresistive-type gas sensors. Two-dimensional (2D) materials display tremendous potential for effective gas detectors that can be used in these applications. The as-developed MXene/SnS2 heterojunction-based chemiresistive-type sensor presents superior gas-sensing performance toward sub-ppm ammonia at room temperature. The sensor can detect NH3 concentrations down to 10 ppb at room temperature. It also displays excellent long-term stability, with a decline in the response at ∼3.4% for 20 days. The developed sensor also displays good selectivity toward NH3 relative to some potential interferents, such as HCHO, C2H5OH, CH3OH, C3H6O, benzene, and NO2. The measured in situ diffuse-reflectance infrared Fourier transform (DRIFT) spectra confirm that the products of nitric oxides during the chemical reactions occurred at the surface of MXene/SnS2. Density functional theory (DFT) based on the first principles was implemented to compute the adsorption ability of NH3 at the surface of the MXene/SnS2 heterostructure. This indicates that the enhancement in the sensing properties of the MXene/SnS2 heterostructure-based chemosensor could be ascribed to the stronger NH3 adsorption, better catalytical activity, and more effective charge transfer bestowed by the formed heterostructure and the electron-redistribution-assisted stronger extraction of electrons from the sensing material.

MiRNA-154-5p inhibits cell proliferation and metastasis by targeting PIWIL1 in glioblastoma.

MicroRNAs (miRNAs) play a critical role in glioblastoma initiation and progression. PIWIL1, a human homolog of the PIWI family, has a critical effect on glioblastoma progression. In present study, we found that the expression of miR-154-5p was significantly lower in glioblastoma. Our results suggested that the overexpression of miR-154-5p suppressed proliferation and metastasis, induced apoptosis, whereas inhibiting the expression of miR-154-5p significantly promoted proliferation and metastasis of glioblastoma. We further proved that miR-154-5p directly integrated with the 3'-UTR of PIWIL1 and reintroduction of PIWIL1 can rescue the phenotype changes induced by miR-154-5p. Taken together, our study reveals that miR-154-5p can counteract the malignant phenotypes of glioblastoma by targeting PIWIL1, which might be beneficial to reveal new therapeutic targets for glioblastoma.

MiR-433-3p suppresses cell growth and enhances chemosensitivity by targeting CREB in human glioma.

Previous studies reported that miR-433 exerts function widely in human tumorigenesis and development. Here, we further investigate the potential role of miR-433 in glioma. Quantitative real-time PCR demonstrated that miR-433-3p and miR-433-5p were low expressed in glioma tissues and cell lines. Functional studies suggested that the overexpression of miR-433-3p suppressed proliferation, induced apoptosis and inhibited invasion and migration of human glioma cells. But the growth and metastasis of glioma cells were not significantly influenced by overexpression of miR-433-5p. In a xenograft model, we also showed that miR-433-3p had an inhibitory effect on the growth of glioma. Bioinformatics coupled with luciferase and western blot assays revealed that CREB is a direct target of miR-433-3p, and the overexpression of CREB can rescue the phenotype changes induced by miR-433-3p overexpression. Besides, miR-433-3p could increase chemosensitivity of glioma to temozolomide by targeting CREB in vitro and in vivo. Taken together, these results suggest that miR-433-3p may function as a potential marker in diagnostic and therapeutic target for glioma.

Silencing HIWI suppresses the growth, invasion and migration of glioma cells.

The HIWI gene is one of the members of the PIWI gene family that is important for stem cell self­renewal and expressed highly in certain human tumors. Some studies have demonstrated that HIWI plays a key role in the development of tumors in cervical, colon and liver cancer. Previous studies have demonstrated that HIWI is associated with prognosis of patients with glioma. However, there is no report on the analysis of HIWI in the biological characteristics of glioma cells. The aim of the study was to investigate whether HIWI plays an important role in the progress of glioma. Silencing HIWI inhibited cell proliferation by promoting apoptosis and increased cell cycle arrest. The expression of proteins related to apoptosis and the cell cycle, including p21, cyclin D1, Bcl-2, and Bax was significantly altered. Moreover, knockdown of HIWI inhibited the migration and invasion of glioma cells by reducing the expression of MMP-2 and MMP­9. Furthermore, we found that reduction of HIWI inhibited tumor growth in vivo. These findings suggest that HIWI is an oncogene involved in the progression of glioma.