Micro-mesoporous cobalt phosphosulfide (Co3S4/CoP/NC) nanowires for ultrahigh rate capacity and ultrastable sodium ion battery.

The construction of heterostructure materials has been demonstrated as the promising approach to design high-performance anode materials for sodium ion batteries (SIBs). Herein, micro-mesoporous cobalt phosphosulfide nanowires (Co3S4/CoP/NC) with Co3S4/CoP hetero-nanocrystals encapsulating into N-doped carbon frameworks were successfully synthesized via hydrothermal reaction and subsequent phosphosulfidation process. The obtained micro-mesoporous nanowires greatly improve the charge transport kinetics from the facilitation of the charge transport into the inner part of nanowire. When evaluated as SIBs anode material, the Co3S4/CoP/NC presents outstanding electrochemical performance and battery properties owing to the synergistic effect between Co3S4 and CoP nanocrystals and the conductive carbon frameworks. The electrode material delivers outstanding reversible rate capacity (722.33 mAh/g at 0.1 A/g) and excellent cycle stability with 522.22 mAh/g after 570 cycles at 5.0 A/g. Besides, the Ex-situ characterizations including XRD, XPS, and EIS further revealed and demonstrated the outstanding sodium ion storage mechanism of Co3S4/CoP/NC electrode. These findings pave a promising way for the development of novel metal phosphosulfide anodes with unexpected performance for SIBs and other alkali ion batteries.

ZnSe@NPSC core-shell nanorods for super sodium ion storage induced from an organic polymer derived N, P, S tri-doped carbon framework.

In this work, core-shell structured ZnSe@NPSC nanorods were prepared with a N, P, S hetero-doped carbon shell. The design of the core-shell structure is conducive to facilitating the transport of electrons and buffering the volume expansion during charge/discharge processes, which is favourable for improving the sodium ion storage properties of ZnSe@NPSC. Therefore, it can deliver capacities of 376.67 mA h g-1 after 150 cycles at 0.5 A g-1 and 359.1 mA h g-1 after cycling for 350 cycles at 1.0 A g-1, respectively.

microRNA-651-5p affects the proliferation, migration, and invasion of lung cancer cells by regulating Calmodulin 2 expression.

OBJECTIVE: Lung cancer is prevalent worldwide and a leading contributor to tumor death. This research intends to explore the molecular mechanism of the microRNA-651-5p (miR-651-5p)/Calmodulin 2 (CALM2) axis in the proliferation, migration, and invasion of lung cancer cells. METHODS: Lung cancer tissues and para-cancerous tissues were collected. The expression levels of miR-651-5p and CALM2 in lung cancer tissues and cells were tested, and the connection between miR-651-5p expression and clinicopathological characteristics of lung cancer patients was further analyzed. The binding sites between miR-651-5p and CALM2 were analyzed and validated. Lung cancer cell proliferation, migration, invasion, and apoptosis were examined. RESULTS: miR-651-5p was lowly expressed in lung cancer tissues and cells. miR-651-5p expression had no correlation with patients' age and gender but had a correlation with patients' tumor size, TNM stage, and lymph node metastasis. Overexpression of miR-651-5p repressed proliferative, migratory, and invasive behaviors of lung cancer cells. miR-651-5p targeted and negatively regulated CALM2 expression, and CALM2 reversed the inhibiting effects of miR-651-5p on lung cancer cell malignant behaviors, including proliferation, migration, and invasion. CONCLUSION: This study expounds that miR-651-5p affects the proliferation, migration, and invasion of lung cancer cells by regulating CALM2 expression.

1D hybrid metal coordination polymer-derived hierarchical Co1-xS/MnS/NC nanowires for advanced sodium-ion batteries.

Hierarchical Co1-xS/MnS/NC nanowires have been successfully prepared by a simple hydrothermal reaction and the subsequent annealing process of its one-dimensional (1D) coordination polymer precursors. The Co1-x/MnS/NC heterostructure nanowires can not only buffer the volume expansion during the discharging and charging process but also conspicuously enhance electronic conductivity, which is favourable for improving the rate performance and cycling stability, which can maintain 612.9 mA h g-1 after 100 cycles at 0.5 A g-1 and 544.6 mA h g-1 after 200 cycles at 1.0 A g-1 for SIBs.

Proliferation, apoptosis and invasion of human lung cancer cells are associated with NFATc1.

The expression of nuclear factor of activated T cells c1 (NFATc1) is closely associated with the progression of numerous types of cancer. When NFATc1 expression becomes dysregulated in some types of cancer, this alteration can promote malignant transformation and thereby progression of cancer. NFATc1 expression has been demonstrated to be upregulated in lung cancer cells. This suggests that knockdown of NFATc1 in lung cancer cells may be a therapeutic marker for the treatment of cancer. In the present study, the effects of NFATc1 on the proliferation, apoptosis, invasion and migration of NCI-H1299 and A549 lung cancer cell lines were explored. Lentivirus infection was used to establish a cell model of NFATc1 knockdown in A549 and NCI-H1299 lung cancer cells. Reverse transcription-quantitative PCR was subsequently performed to detect NFATc1 expression in these human lung cancer cells. MTT, wound healing, colony formation and Transwell invasion assays, and flow cytometry were then performed to measure the proliferation, invasion, apoptosis and cell cycle of the cells. Finally, western blot analysis was performed to investigate the mechanism underlying the involvement of NFATc1 in these processes. NFATc1 knockdown was found to significantly inhibit the proliferation, clone formation, migration and invasion of the cells. Furthermore, the cell cycle was arrested at the G1 phase and the expression levels of the target proteins located downstream in the signaling pathway, namely CDK4, c-Myc, ERK, p38 and N-cadherin, were decreased. Following NFATc1 knockdown, the percentages of apoptotic cells were increased, and the expression levels of Bax, cleaved caspase-3 and E-cadherin were also increased. Taken together, the results of the present study suggested that NFATc1 serves an oncogenic role in lung cancer. In terms of the underlying mechanism, NFATc1 promoted the proliferation of lung cancer cells by inhibiting the MAPK and epithelial-to-mesenchymal transition signaling pathways, suggesting that NFATc1 may be a novel target for therapeutic intervention for the treatment of lung cancer.

Effects of the microRNA-99a-5p/VLDLR axis in lung cancer cell sensitivity to chemotherapy and its mechanism

Abstract Lung cancer is a major cause of cancer-related death worldwide. This study investigated the regulatory effects of the microRNA-99a-5p (miR-99a-5)/VLDLR axis on lung cancer cell sensitivity to chemotherapy and its mechanism. miR-99a-5p and VLDLR expression levels were quantified using RT-qPCR and western blotting, respectively. The IC50 value of cisplatin (DDP) was determined using a CCK-8 assay. Lung cancer cell proliferation and apoptosis were measured using the CCK-8 assay and flow cytometry, respectively. The mRNA expression levels of apoptosis-related factors (Bax, Bcl-2, and Caspase-3) were evaluated using RT-qPCR. The direct relationship between miR-99a-5p and VLDLR was validated using dual-luciferase reporter gene and RIP assays. miR-99a-5p was weakly expressed in DDP-resistant lung cancer cells. Overexpression of miR-99a-5p promoted DDP sensitivity, suppressed proliferation and colony formation, and promoted apoptosis of A549/DDP cells in vitro. Mechanistically, miR-99a-5p restrained VLDLR expression by binding to VLDLR 3'UTR, and miR-99a-5p mediated inhibition of VLDLR regulated the DDP sensitivity, proliferation, and apoptosis of A549/ DDP cells. Overexpression of miR-99a-5p inhibited the growth of A549 cells and increased chemosensitivity of A549 cells to DDP in vivo. In conclusion, miR-99a-5p overexpression promotes sensitivity to DDP and cell apoptosis by downregulating VLDLR expression in A549/ DDP cells.

A Pyroptosis-Related Signature Predicts Overall Survival and Immunotherapy Responses in Lung Adenocarcinoma.

Background: Lung adenocarcinoma (LUAD) is a highly malignant cancer with a bleak prognosis. Pyroptosis is crucial in LUAD. The present study investigated the prognostic value of a pyroptosis-related signature in LUAD. Methods: LUAD's genomic data were downloaded from TCGA and GEO databases. K-means clustering was used to classify the data based on pyroptosis-related genes (PRGs). The features of tumor microenvironment were compared between the two subtypes. Differentially expressed genes (DEGs) were identified between the two subtypes, and functional enrichment and module analysis were carried out. LASSO Cox regression was used to build a prognostic model. Its prognostic value was assessed. Results: In LUAD, genetic and transcriptional changes in PRGs were found. A total of 30 PRGs were found to be differentially expressed in LUAD tissues. Based on PRGs, LUAD patients were divided into two subgroups. Subtype 1 has a higher overall survival rate than subtype 2. The tumor microenvironment characteristics of the two subtypes differed significantly. Compared to subtype 1, subtype 2 had strong immunological infiltration. Between the two groups, 719 DEGs were discovered. WGCNA used these DEGs to build a co-expression network. The network modules were analyzed. A prognostic model based on seven genes was developed, including FOSL1, KRT6A, GPR133, TMPRSS2, PRDM16, SFTPB, and SFTA3. The developed model was linked to overall survival and response to immunotherapy in patients with LUAD. Conclusion: In LUAD, a pyroptosis-related signature was developed to predict overall survival and treatment responses to immunotherapy.

Prediction of Pleural Invasion in Challenging Non-Small-Cell Lung Cancer Patients Using Serum and Imaging Markers.

Introduction. Preoperative detection of pleural invasion in lung cancer patients is key to curative surgical treatment. We tried to predict pleural invasion in non-small-cell lung cancer patients with <100 ml pleural fluid. METHODS: Patients admitted from August 1, 2011, to December 31, 2018, were retrospectively retrieved. Records of serum and imaging markers were analyzed. RESULTS: Among 7004 patients who received surgery, 43 cases with <100 ml pleural fluid who had pleural invasion were included, and another 108 cases without pleural invasion were enrolled as controls. There were no differences in squamous cell carcinoma antigen (SCC) or neuron-specific enolase (NSE) values between the pleural invasion and noninvasion groups (p = 0.30 and 0.14, respectively), but there were significant differences in carcinoembryonic antigen (CEA) and cytokeratin 19 fragment (CYFRA21-1) values (p = 0.30 and 0.14, respectively), but there were significant differences in carcinoembryonic antigen (CEA) and cytokeratin 19 fragment (CYFRA21-1) values (p = 0.30 and 0.14, respectively), but there were significant differences in carcinoembryonic antigen (CEA) and cytokeratin 19 fragment (CYFRA21-1) values (p = 0.30 and 0.14, respectively), but there were significant differences in carcinoembryonic antigen (CEA) and cytokeratin 19 fragment (CYFRA21-1) values (p = 0.30 and 0.14, respectively), but there were significant differences in carcinoembryonic antigen (CEA) and cytokeratin 19 fragment (CYFRA21-1) values (p = 0.30 and 0.14, respectively), but there were significant differences in carcinoembryonic antigen (CEA) and cytokeratin 19 fragment (CYFRA21-1) values (p = 0.30 and 0.14, respectively), but there were significant differences in carcinoembryonic antigen (CEA) and cytokeratin 19 fragment (CYFRA21-1) values (. CONCLUSIONS: Serum CEA and CYFRA21-1, location of original lung cancer (right mid lobe), maximum diameter, CT-detectable pleural fluid, pleural sign by CT, and PET/CT-predicted pleural invasion were good markers for the prediction of pleural invasion in non-small-cell lung cancer patients.

Runt-related transcription factor 1 contributes to lung cancer development by binding to tartrate-resistant acid phosphatase 5.

Lung cancer (LC) is one of the malignant tumors with growing morbidity and mortality. The involvement of runt-related transcription factor 1 (RUNX1) in LC patients has been elucidated. We intended to research mechanisms of RUNX1 and tartrate-resistant acid phosphatase 5 (ACP5) in LC. Firstly, ACP5 levels in LC tissues, paracancerous tissues, LC cells and tracheal epithelial cells were detected. RUNX1 overexpression plasmid and interference plasmid were constructed and transfected into 95C cells and A549 cells, respectively. The binding of RUNX1 to ACP5 promoter was tested. Additionally, the gain- and loss-of-function were performed to explore the effects of ACP5 and RUNX1 on LC biological process. The xenograft tumor in nude mice was constructed in vivo to verify in vitro results. Functional rescue experiment was performed by adding MAPK-specific activator P79350 to A549 cells with si-ACP5 to measure the effects of ERK/MAPK axis on LC progression. Consequently, we found ACP5 expression was higher in LC tissues and cells, and ACP5 silencing suppressed LC cell growth. Overexpression of ACP5 promoted malignant biological behavior of LC cells. RUNX1 could bind to ACP5 promoter, and overexpressed RUNX1 promoted ACP5 expression and LC cell growth. Moreover, ACP5 upregulated the ERK/MAPK axis and thus promoted LC progression. The results of xenograft tumor in nude mice showed that silencing ACP5 could inhibit the growth of LC cells in vivo. To conclude, silenced RUNX1 inhibits LC progression through the ERK/MAPK axis by binding to ACP5. This study may provide new approaches for LC treatment.

Alcohol accumulation promotes esophagitis via pyroptosis activation.

Gastroesophageal reflux impairs the mucosal barrier in the distal esophagus, allowing chronic exposure of the squamous epithelium to multitudinous stimulations and inducing chronic inflammation. Esophagitis is a response to inflammation of the esophageal squamous mucosa. Our study clarified that alcohol accumulation could aggravate the progress of esophagitis by inducing pyroptosis; however, Ac-YVAD-CMK, an inhibitor of caspase-1, could effectively suppress the expression of IL-1ß and IL-18 both in vivo and in vitro, reducing the inflammatory response, which is promised to be an agent to inhibit the progression of esophagitis. Additionally, caspase-1-derived pyroptosis is involved in esophageal cancer.

Fast-track surgery improves postoperative clinical recovery and cellular and humoral immunity after esophagectomy for esophageal cancer.

BACKGROUND: Our aim was to investigate the influence of FTS on human cellular and humoral immunity using a randomized controlled clinical study in esophageal cancer patients. METHODS: Between October 2013 and December 2014, 276 patients with esophageal cancer in our department were enrolled in the study. The patients were randomized into two groups: FTS pathway group and conventional pathway group. The postoperative hospital stay, hospitalization expenditure, and postoperative complications were recorded. The markers of inflammatory and immune function were measured before operation as well as on the 1st, 3rd, and 7th postoperative days (POD), including serum level of interleukin-6 (IL-6), C-reactive protein (CRP), serum globulin, immunoglobulin G (IgG), immunoglobulin M (IgM), immunoglobulin A (IgA) and lymphocyte subpopulations (CD3 lymphocytes, CD4 lymphocytes, CD8 lymphocytes and the CD4/CD8 ratio) in the patients between the two groups. RESULTS: In all, 260 patients completed the study: 128 in the FTS group and 132 in the conventional group. We found implementation of FTS pathway decreases postoperative length of stay and hospital charges (P < 0.05). In addition, inflammatory reactions, based on IL-6 and CRP levels, were less intense following FTS pathway compared to conventional pathway on POD1 and POD3 (P < 0.05). On POD1 and POD3, the levels of IgG, IgA, CD3 lymphocytes, CD4 lymphocytes and the CD4/CD8 ratio in FTS group were significantly higher than those in control group (All P < 0.05). However, there were no differences in the level of IgM and CD8 lymphocytes between the two groups. CONCLUSIONS: FTS improves postoperative clinical recovery and effectively inhibited release of inflammatory factors via the immune system after esophagectomy for esophageal cancer. TRIAL REGISTRATION: ChiCTR-TRC-13003562 , the date of registration: August 29, 2013.

Overexpression of pituitary tumor transforming gene (PTTG) is associated with tumor progression and poor prognosis in patients with esophageal squamous cell carcinoma.

Pituitary tumor transforming gene (PTTG) is a newly identified proto-oncogene that has been shown to be aberrantly overexpressed in a subset of human cancers. The aim of the present study was to examine PTTG expression in patients with esophageal squamous cell cancer (ESCC) and explore its clinical significance. PTTG protein expression was analyzed in 108 archived, paraffin-embedded primary ESCC specimens by immunohistochemistry and correlated with clinicopathological parameters and patients' outcome. Overexpression of PTTG was observed in 38.0% (41/108) of primary ESCC tissues and significantly correlated with differentiation, TNM stage, lymph node metastasis, and depth of invasion (P<0.05). Kaplan-Meier curves showed that ESCC patients with tumors expressing high levels of PTTG had substantially shorter overall survival compared with patients expressing low levels of PTTG (P=0.022, log-rank test). Cox multivariate regression analysis revealed that overexpression of PTTG was an independent prognostic factor in overall survival for ESCC patients (hazard ratio was 2.35, P=0.009). Overall, our data suggest that overexpression of PTTG may contribute to the malignant progression of ESCC and serve as a novel prognostic indicator for patients with ESCC.

High expression of M3 muscarinic acetylcholine receptor is a novel biomarker of poor prognostic in patients with non-small cell lung cancer.

We assessed the expression of M3 receptor in non-small cell lung cancer (NSCLC) and determined its relationship with clinicopathological features and its impact on patient outcome. Specimens from 192 patients with NSCLC were investigated by immunohistochemistry for M3 receptor and Ki67 expression. Correlation between the expression of M3 receptor and Ki67 and various clinicopathological features of NSCLC patients was analyzed. We found that M3 receptor expression was gradually elevated from normal to metaplasia/dysplasia tissues to cancer tissues. Furthermore, there was a similar trend for Ki67 expression. Statistical analysis revealed that M3 receptor expression in tumor cells were correlated significantly with stage (P < 0.0001), histology type (P = 0.0003), Ki67 expression (P < 0.0001), tumor size (P < 0.0001), lymph node status (P < 0.0001), LVS invasion (P = 0.0002), and histology grade (P < 0.0001). Patients with M3 receptor high expression showed far lower disease-free survival (DFS) and overall survival (OS) rates than those with M3 receptor low expression. Multivariate Cox regression analysis demonstrated that high M3 receptor expression was an independent prognostic factor for both DFS and OS. High M3 receptor expression correlates with poor survival in NSCLC patients. M3 receptor expression may be related with tumor progression in NSCLC, indicating that M3 receptor may be a novel antineoplastic target in the future.

MicroRNA-378 is associated with non-small cell lung cancer brain metastasis by promoting cell migration, invasion and tumor angiogenesis.

Lung cancer is the leading cause of cancer deaths in the world. Brain metastasis (BM) can affect about 25% of non-small cell lung cancer (NSCLC) patients during their lifetime. Efforts to characterize patients that will develop BM have been disappointing. MicroRNAs (miRNAs) play a role in regulating a variety of targets and, consequently, multiple pathways, which make them a powerful tool for early detection of disease, risk assessment and prognosis. In this study, using RT-PCR and further northern blot validation, we confirmed that miR-378 was significantly differentially expressed in the matched NSCLC from 8 patients with BM and 21 without BM. Our study showed evidences that miR-378 is associated with non-small cell lung cancer brain metastasis by promoting cell migration, invasion and tumor angiogenesis. MiR-378 may be a potential biomarker for characterizing non-small cell lung cancer brain metastasis and assisting clinicians in stratifying the high-risk patients on a clinical trial for either prophylactic cranial irradiation or a new intervention that may mitigate BM development, ultimately leading to a new standard of care for NSCLC patients.