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Background Our previous studies identified the calcium-dependent phospholipid binding protein Annexin A7 (ANXA7) as a critical mediator of hepatocellular carcinoma (HCC) lymph node metastasis (LNM) in mice, possibly through c-Jun N-terminal kinase (JNK) signaling. Activating transcription factor-2 (ATF2) is a downstream target of JNK, so we examined if modulation of LNM capacity by ANXA7 and JNK is associated with changes in ATF2 activity and its sequence-related long non-coding (lnc)RNA NONMMUT114121.1. Methods The effects of shRNA-induced ANXA7 and JNK knockdown on HCC cell transwell invasion, HCC cell lymphatic tissue adherence, ATF2 mRNA and protein expression, and ATF2 subcellular distribution were examined in the murine HCC cell line Hca-P. Results Invasive capacity, lymphoid adhesion, and ATF2 expression at both mRNA and protein levels were significantly reduced by ANXA7 or JNK knockdown (all P

Background The expression of Kelch-like protein 18 (KLHL18) in non-small cell lung cancer (NSCLC) is lower than that in normal lung tissue according to the Gene Expression Profiling Interactive Analysis database. KLHL18 is a BTB domain protein and binds cullin 3 (CUL3). However, whether this complex participates in ubiquitination-mediated protein degradation in NSCLC is unclear. Therefore, we aimed to investigate the role of KLHL18 in human NSCLC cells. Results We found that KLHL18 is downregulated in cancer cells and is associated with poor prognosis. Further, its expression was significantly associated with tumor node metastasis (TNM) stage, lymph node metastasis, and tumor size. In vitro analysis of NSCLC cells showed that overexpressing KLHL18 inhibited cell proliferation, migration, and invasion. We found that the tumor-inhibitory effect of the KLHL18 protein was achieved by promoting the ubiquitination and degradation of phosphatidylinositol 3-kinase (PI3K) p85α and inhibiting the expression of PD-L1 protein, ultimately preventing tumor cell immune escape. Conclusions Our results identified the tumor-suppressive mechanism of KLHL18 and suggested that it is closely related to NSCLC occurrence and development. Further investigation of the underlying mechanism may provide new targets for NSCLC treatment.

Analysis of the Gene Expression Profiling Interactive Analysis (GEPIA) database revealed that Kelch-like 17 (KLHL17) is overexpressed in non-small cell lung cancer (NSCLC) including adenocarcinoma (ADC) and squamous cell carcinoma (SCC). We therefore explored the role of KLHL17 in the development and progression of NSCLC. Immunohistochemistry and western blotting showed that KLHL17 expression was significantly higher in the tumor tissues from 173 patients with NSCLC, compared with the corresponding non-neoplastic tissue. In addition, upregulated KLHL17 expression was positively correlated with tumor size, lymph node metastasis and tumor node metastasis (TNM) stage, and affected the overall survival (OS) of patients with NSCLC. Consistent with clinical samples, in vitro studies demonstrated that KLHL17 expression was higher in various cell lines of NSCLC (A549, H1299, H460 and SK cells) as compared to normal human bronchial epithelial cells (HBE cells). Overexpression of KLHL17 in the cell lines of NSCLC with KLHL17-Flag plasmid promoted the proliferation and migration of tumor cells, which was associated with elevated activation of Rat sarcoma/Mitogen-activated protein kinases (Ras/MAPK) signaling and increased expression of cyclin D1, cyclin D-dependent kinases 4 (CDK4), matrix metalloproteinase 2 (MMP2) and Ras homolog gene family member A (RhoA). In contrast, knockdown of KLHL17 in the cell lines of NSCLC using KLHL17 small interfering RNA suppressed the proliferation and migration of tumor cells, in association with reduced activation of Ras/MAPK signaling and decreased expression of cyclin D1, CDK4, MMP2 and RhoA. Moreover, treatment of tumor cells with Ras inhibitor salirasib prevented KLHL17-induced Ras/MAPK activity as well as tumor proliferation and migration. These results suggest that upregulated KLHL17 in NSCLC promotes the proliferation and migration of tumor by activating Ras/MAPK signaling pathway. Therefore, KLHL17 may be a novel therapeutic target for the treatment of NSCLC.

The separation of photoinduced electrons and holes can enhance the photocatalytic properties of photocatalysts. A piezoelectric field is created inside piezoelectric materials, such as ZnO and MoS2, by applying strain. The electrons and holes become separated under the driving force of the piezoelectric field. Here, we propose combining piezoelectric MoS2 nanoflowers (NFs) and full solar response Ag2O nanoparticles (NPs) to form a MoS2@Ag2O heterostructure and achieve high efficiency full solar (UV, visible, and near-infrared) photocatalysis. Under both full solar light and ultrasonic excitation, the MoS2@Ag2O heterostructures can rapidly degrade methyl orange (MO) in aqueous solution. A built-in electric field is formed by the spontaneous polarization potential of the MoS2 NFs during this process, and an ultrasonic wave as a driving force can consecutively change the potential created by the piezoelectric effect. Under light irradiation, electrons and holes are generated in the Ag2O NPs, and the photogenerated electrons and holes with opposite signs in the two Ag2O NPs at the two surfaces of the MoS2 NFs, can be separated respectively, along the spontaneous polarized direction. Therefore, the piezoelectric effect-induced enhancement of carrier separation under ultrasonic excitation can improve the full solar photocatalytic performance of the MoS2@Ag2O heterostructures.

The expression pattern, biological functions and the related mechanisms of the ring finger protein 19A (RNF19A) in non‐small cell lung cancer (NSCLC) remain poorly understood. This study aimed to explore the role of RNF19A, as well as the underlying potential mechanism, in the development of NSCLC. Here, we found that RNF19A was overexpressed in NSCLC tissues, and RNF19A expression in NSCLC tissue samples was associated with NSCLC carcinogenesis and poor outcome. RNF19A promoted the proliferation of NSCLC cells and inhibited apoptosis. RNF19A reduced p53, p21 and BAX expression and induced Cyclin D1, CDK4, CDK6 and BCL2 expression. The inhibitory effect of RNF19A knockdown on proliferation was partially rescued by p53 silencing. RNF19A interacted with p53, shortened p53 half‐life and mediated p53 ubiquitin‐degradation. Collectively, we suggest that RNF19A plays a critical oncogenic role in lung carcinogenesis by disrupting the function of p53. RNF19A may serve as a new biomarker and/or target for NSCLC management.

Mitotic spindle organizing protein 2A (MZT2A) is localized at the centrosome and regulates microtubule nucleation activity in cells. This study assessed the role of MZT2A in non–small‐cell lung cancer (NSCLC). Differential MZT2A expression was bioinformatically assessed using TCGA database, the GEPIA database, and Kaplan‐Meier survival data to determine the association between MZT2A expression and NSCLC prognosis. Furthermore, NSCLC tissue specimens were evaluated by immunohistochemistry. MZT2A was overexpressed or knocked down in NSCLC cells using cDNA and siRNA, respectively. The cells were subjected to various assays and treated with the selective Akt inhibitor LY294002 or co‐transfected with galectin‐3‐binding protein (LGALS3BP) siRNA. MZT2A mRNA and protein levels were upregulated in NSCLC lesions and MTZ2A expression was associated with poor NSCLC prognosis. MZT2A protein was also highly expressed in NSCLC cells compared with the expression in normal bronchial cells. MZT2A expression promoted NSCLC cell viability and invasion, whereas MTZ2A siRNA had the opposite effect on NSCLC cells in vitro. At the protein level, MZT2A induced Akt phosphorylation, promoting NSCLC proliferation and invasion (but the selective Akt inhibitor blocked these effects) through upregulation of LGALS3BP via the MTZ2A MOZART2 domain, whereas LGALS3BP siRNA suppressed MTZ2A activity in NSCLC cells. The limited in vivo experiments confirmed the in vitro data. In conclusion, MZT2A exhibits oncogenic activity by activating LGALS3BP and Akt in NSCLC. Future studies will assess MTZ2A as a biomarker to predict NSCLC prognosis or as a target in the control of NSCLC progression., MZT2A induced Akt phosphorylation, promoting NSCLC proliferation and invasion through the upregulation of LGALS3BP via the MTZ2A MOZART2 domain. Future studies will assess MTZ2A as a biomarker to predict NSCLC prognosis or as a target to control NSCLC progression

Additional file 1: Figure S1. MS/MS spectrum of PI3Kp85α protein related peptids. Figure S2. Changes in levels of EMT pathway-related proteins in NCI-A549 and NCI-H1299 cells. The lower graph is a gray value statistical graph, *P

To improve the tribological properties of substrate surfaces, tungsten carbide composite layers were deposited on an iron-based alloy by diffusion-controlled in situ reaction (DIR) at different temperatures. The microstructure, phase composition and worn morphology of the composite layer were characterized by utilizing scanning electron microscopy/energy-dispersive spectroscopy (SEM/EDS), X-ray diffraction (XRD) and confocal laser scanning microscopy (CLSM). A thin tungsten carbide layer with an interface crack was obtained at 1000 °C. At 1100 °C, the structure of the optimized composite layer contains a thin tungsten plate, a thicker tungsten carbide layer (300 μm) and a broad composite zone (2.5 mm) from top to bottom. The indexed phase composition for the carbide layer includes WC and α-Fe, and the composite zone consists of α-Fe, Fe6W6C, FeC and graphite. The tribological properties and mechanical properties of the composite layers were evaluated by using a ball-on-disk tribometer and a nanoindentation hardness tester. The average nanohardness of the tungsten plate, carbide layer, composite region and substrate is approximately 6.4 ± 1.0 GPa, 24.1 ± 3.4 GPa, 13.5 ± 2.4 GPa and 9.6 ± 1.2 GPa, respectively. Friction wear tests of all samples against GCr15 balls were performed at room temperature under 5, 10, 15 and 20 N normal loads. The carbide layer exhibits an average coefficient of friction of 0.39–0.63, which is higher than that of the substrate under an identical load due to the lubricating effect of the flake graphite phase in the substrate during the wear process. The specific wear rate of the carbide layer with a value of 2.69–4.33 is 18.5–34.3% of that of the substrate. The results of the worn morphology presence of particle deformation, extraction and crushing reveal that abrasive wear is a dominant abrasion mechanism for the carbide layer. For the substrate, adhesive wear plays an important role and is accompanied by abrasive wear.

The Polycomb Group Ring Finger 3 (PCGF3) protein has been reported to be significantly upregulated in pancreatic islet tumors and related to signal transduction; however, its detailed mechanisms and biological roles in other tumors, including non-small cell lung cancer (NSCLC), remain unclear. This study investigated the function of PCGF3 in NSCLC and further elucidated its mechanism of action. The immunohistochemical analysis of 86 selected lung cancer tissues revealed that PCGF3 was highly expressed in NSCLC tissues and positively correlated with lymph node metastasis and p-TNM staging. Additionally, PCGF3 promoted cell proliferation in lung cancer by regulating CyclinB1, CyclinD1, and CDK4 expression, and also promoting their migration by regulating RhoA, RhoC, and CDC42. Furthermore, PCGF3 affected both the proliferation and migration of lung cancer cells by regulating the PI3K/AKT pathway, as verified by inhibiting this pathway using LY294002. The findings of this study suggested that PCGF3 is associated with poor prognosis in patients with NSCLC and could therefore be an important biomarker for treating and preventing NSCLC.

The separation of photoinduced electrons and holes can enhance the photocatalytic properties of photocatalysts. A piezoelectric field is created inside piezoelectric materials, such as ZnO and MoS