Safety Study of Raltitrexed Perfusion in Elderly Patients with Colorectal Cancer and Effect on CEA mRNA in Peritoneal Lavage Fluid.

Background: Intraperitoneal chemotherapy is an effective way to kill free tumor cells in the abdominal cavity. The safety and efficacy of raltitrexed perfusion during radical surgery for elderly patients with colorectal cancer are still unclear. Methods: In accordance with computer-generated random allocation sequences, 116 elderly patients with colorectal cancer who received radical surgery were randomly grouped into the raltitrexed intraperitoneal perfusion group or the saline intraperitoneal perfusion group from January 2020 to December 2021 in the First Affiliated Hospital of Bengbu Medical University. t tests and χ2 tests were used to analyze the difference between the two groups of the clinical characteristics, pathological features, perioperative parameters, and carcinoembryonic antigen mRNA in the peritoneal lavage fluid. Results: No statistically significant differences in postoperative complications after radical surgery were observed between the two groups. No statistically significant differences in peripheral blood indexes were observed between the two groups before surgery or on the first and third days after surgery. One day after radical surgery, the alanine transaminase (54.33 ± 4.93 vs 51.01 ± 5.56) and aspartate transaminase (49.28 ± 4.30 vs 50.99 ± 3.88) in the peripheral blood were higher in the raltitrexed intraperitoneal perfusion group than in the saline intraperitoneal perfusion group. At the same time, no significant difference was found on the third day after surgery. No significant differences in side effects of chemotherapy were observed between the two groups. The positive rate of carcinoembryonic antigen mRNA in the raltitrexed intraperitoneal perfusion group (8.47%) was significantly lower than that in the saline intraperitoneal perfusion group (22.81%) after surgery. Conclusion: Raltitrexed perfusion during radical surgery is safe and feasible for elderly patients with CRC and can reduce the positive rate of carcinoembryonic antigen mRNA in peritoneal lavage fluid, so it can be explored as a treatment option.

Exploring the Synergy: Chinese Female Tennis Players and Chansu-Medicated Serum's Potential in Inhibiting Breast Cancer Cell Proliferation Through Apoptosis and G2 Arrest

This study delves into the synergy between Chinese female tennis players and the potential of Chansu-Medicated Serum in inhibiting breast cancer cell proliferation through apoptosis and G2 arrest. Chinese female tennis players have garnered international recognition for their achievements on the court and their philanthropic endeavors off it. This research investigates the intersection of their impact and the advancement of breast cancer research. Chansu-Medicated Serum, a traditional Chinese medicine derivative, presents promising mechanisms for inhibiting breast cancer cell proliferation, including apoptosis induction and G2 cell cycle arrest. By exploring this conjunction, we aim to shed light on the possible contributions of these athletes and traditional medicine to the ongoing battle against breast cancer. (AU)

Structural Maintenance of Chromosome Protein 4 Promotes the Progression of Cardia Adenocarcinoma via Regulation of the Wnt/ß-catenin Signaling Pathway.

BACKGROUND: Structural maintenance of chromosome protein 4 (SMC4) is crucial for chromosome assembly and separation, but its role and mechanism in cardia adenocarcinoma (CA) are unknown. METHODS: SMC4 expression levels were initially detected by protein profiling in 20 pairs of CA tumor tissues and adjacent normal tissues. The level of SMC4 expression in CA cells was then evaluated using a western blot analysis. Cell proliferation was evaluated by CCK-8 and clone formation tests. Scratch and transwell tests were used to investigate cell migration as well as invasion, while through the flow cytometry, we examined the cell apoptosis and progression of the cell cycle. The regulatory effects of the epithelial-mesenchymal transition (EMT) and the Wnt/ß-catenin pathway were investigated using western blot. A tumorigenesis experiment was used to investigate the influence of SMC4 on tumor development in nude mice. RESULTS: This study showed overexpression of SMC4 in CA tissues and cells. Knockdown of SMC4 can significantly inhibit the proliferation, migration and invasion, stimulate cell apoptosis, induce cell cycle arrest in the G0/G1 phase of CA cells, and inhibit tumor growth in vivo. In addition, down-regulation of SMC4 resulted in decreased expression of Bcl-2, Cyclin D1, CDK4, CDK6, ß-catenin, phosphorylated GSK-3ß, N-cadherin, and Vimentin, with an increased level of proteins, i.e., Bax, cleaved-caspase3, and E-cadherin. When SMC4 was overexpressed, these effects were reversed. CONCLUSION: SMC4 can facilitate the biological progression of CA, suggesting that SMC4 could be a potential therapeutic target for the disease.

Enhanced film quality of PbS QD solid by eliminating the oxide traps through an in situ surface etching and passivation.

PbS QDs have attracted considerable interest in optoelectronics. However, their high susceptibility to oxidation results in the production of Pb oxides on PbS, which can induce sub-bandgap traps in PbS QDs that are detrimental to the performance of the resultant device. Here we report a facile strategy to enhance the film quality of PbS QD solids through an in situ surface etching and passivation route, carried out by immersing the PbS QD solid film in an I-/I2 solution at room temperature in ambient air. The process is simple and allows for the simultaneous removal of surface Pb oxides and the formation of a PbI2 passivation layer on PbS QDs, leading to the elimination of traps in PbS QDs while preserving their optical properties and film morphology. As a result, charge recombination within the film is suppressed and charge carrier transport is enhanced. When used to fabricate a quantum dot sensitized solar cell, a large increase in cell performance was achieved.

Behaviour of polymer-coated composite nanoparticles at bubble-stabilizing interfaces during bubble coarsening and accelerated coalescence: A Cryo-SEM study.

HYPOTHESIS: Dynamics of polymer-coated silica composite nanoparticles (CPs) during bubble coarsening is highly dominated by the behaviour of the polymer layer, while in-situ particle aggregation would lead to accelerated bubble coalescence. EXPERIMENTS: CPs-stabilized foams were prepared in 0.1 M and 0.55 M Na2SO4 solution, referring to the 0.1 M and 0.55 M foam/bubble respectively. The 0.1 M to 0.55 M transition foam was also prepared. High resolution Cryo-SEM was originally used to investigate the CPs behaviour at the bubble-stabilizing interface during bubble coarsening and accelerated coalescence. FINDINGS: The 0.1 M bubble-stabilizing interface buckles in uniaxial compression due to coarsening, with the CPs being observed to desorb from the interface. While the CPs were visualized to rearrange into crumpled particle multi-layers surrounding the shrinking 0.55 M bubbles, due to the adhesion between interpenetrating polymer chains and the unique lubrication effect of the PVP layers. The 0.1 M to 0.55 M transition foaming behaviour was also studied. Cracks and voids were observed at interfaces surrounding the transition bubbles driven by in-situ particle aggregation, resulting in accelerated bubble coalescence during the transition process.

Long-term exposure to genistein inhibits the proliferation of gallbladder cancer by downregulating the MCM complex.

Soy isoflavones are natural tyrosine kinase inhibitors closely associated with decreased morbidity and mortality of various tumors. The activation of tyrosine kinases such as ERBB2 is the mechanism by which cholecystitis transforms into gallbladder cancer (GBC), therefore, it is important to investigate the relationship between long-term exposure to soy isoflavones and the occurrence and progression of GBC. This case-control study (n = 85 pairs) found that the high level of plasma soy isoflavone-genistein (GEN) was associated with a lower risk of gallbladder cancer (≥326.00 ng/mL compared to ≤19.30 ng/mL, crude odds ratio 0.15, 95% CI 0.04-0.59; P for trend = 0.016), and that the level of GEN exposure negatively correlated with Ki67 expression in GBC tissue (n = 85). Consistent with these results, the proliferation of GBC cells was inhibited in the long-term exposure models of GEN in vitro and in vivo. The long-term exposure to GEN reduced the tyrosine kinase activity of ERBB2 and impaired the function of the PTK6-AKT-GSK3ß axis, leading to downregulation of the MCM complex in GBC cells. In summary, long-term exposure to GEN associated with soy products intake might play a certain role in preventing GBC and even inhibiting the proliferation of GBC cells.

Characterizing the Crosstalk of NCAPG with Tumor Microenvironment and Tumor Stemness in Stomach Adenocarcinoma.

Background: Nonstructural maintenance of non-SMC condensin I complex subunit G (NCAPG) exerts critical effects on cancer progression. However, its biological roles in tumorigenesis and metastasis remain unclear. Thus, we aimed to assess the prognostic utility of NCAPG in stomach adenocarcinoma (STAD) and its potential as a tumor biomarker. Methods: Pan-cancer expression profile dataset from public databases and corresponding clinical information were extracted. Single-sample gene set enrichment analysis (ssGSEA) was performed for the evaluation of immune correlations pan-cancer. Subsequently, we focused on STAD and evaluated the methylation profiles, copy number variants (CNVs), and single nucleotide variants (SNVs). Immune features were analyzed between high and low NCAPG expression groups. Differential analysis was performed between high and low expression groups to identify differentially expressed genes (DEGs). Prognostic DEGs were screened by univariate analysis, and an NCAPG-based risk model was constructed based on the prognostic DEGs and LASSO analysis. Results: NCAPG expression in STAD was significantly and positively correlated with four immune checkpoints, namely, CTLA4, PDCD1, LAG3, and CD276, but was negatively correlated with the infiltration of most immune cells. High and low NCAPG expression groups had differential overall survival, tumor mutation burden, and differential enrichment of therapeutic-related pathways. An immune risk scoring model related to NCAPG expression and immune score was constructed which showed a favorable performance in predicting STAD prognosis as well as predicting the response to immunotherapy. In addition, we found a higher mRNA stemness index (mRNAsi) in the high-risk group and a positive correlation between NCAPG expression and mRNAsi. Conclusion: NCAPG was suggested to be involved in the regulation of tumor microenvironment in STAD. High NCAPG expression was related to high tumor stemness and good prognosis. The immune risk model had a potential to predict STAD prognosis and help directing therapeutic treatment.

AIM2 Promotes Gastric Cancer Cell Proliferation via the MAPK Signaling Pathway.

Background: Gastric cancer (GC) is a highly prevalent tumor type. The dysregulated expression of melanoma deficiency factor 2 (AIM2) has been observed in a range of tumor types. Herein, we explore the role of AIM2 in the regulation of GC progression. Methods: Gastric cancer cells BGC-823 and MGC-803 in logarithmic growth phase were divided into blank group (control), Control group (NC) and SH-AIM2 group, respectively. Control group and SH-AIM2 group were transfected with AIM2 NC and SH-AIM2, respectively. Nude mice were divided into blank group (control) and SH-AIM2 group, and the treatment methods were the same as above. Differential AIM2 expression in GC tissues was assessed via bioinformatics analyses, after which western blotting was used for analyzing the AIM2 levels in tumor and paracancerous tissues from five stomach cancer patients. In addition, qPCR and protein imprinting were used to assess AIM2 expression levels in GC cells, and AIM2 knockdown was conducted in MGC-803 and BGC-823cells, after which colony formation and EdU incorporation assay were utilized to assess cell proliferation. The oncogenic role of AIM2 was then assessed in mice and validated through immunohistochemical analyses. Results: GC tissues and cell lines exhibited marked AIM2 overexpression. AIM2 knockdown significantly impaired GC cell proliferation and migration, as confirmed through in vitro assays. In vivo experiments showed that both the increment ability and invasion and migration ability of AIM2 knockdown group were significantly lower than that of control and NC the change of AIM2 protein level would affect the change of MAPK pathway related protein level. Conclusions: AIM2 knockdown markedly suppresses the proliferation, migration, as well as invasion of GC cells via the inhibition of MAPK signaling, thereby slowing tumor progression. Overall, these results suggest that further analyses of AIM2 may offer clinically valuable insights that can aid in the treatment of human GC.

Protocol for a gallbladder cancer registry study in China: the Chinese Research Group of Gallbladder Cancer (CRGGC) study.

INTRODUCTION: Gallbladder cancer (GBC), the sixth most common gastrointestinal tract cancer, poses a significant disease burden in China. However, no national representative data are available on the clinical characteristics, treatment and prognosis of GBC in the Chinese population. METHODS AND ANALYSIS: The Chinese Research Group of Gallbladder Cancer (CRGGC) study is a multicentre retrospective registry cohort study. Clinically diagnosed patient with GBC will be identified from 1 January 2008 to December, 2019, by reviewing the electronic medical records from 76 tertiary and secondary hospitals across 28 provinces in China. Patients with pathological and radiological diagnoses of malignancy, including cancer in situ, from the gallbladder and cystic duct are eligible, according to the National Comprehensive Cancer Network 2019 guidelines. Patients will be excluded if GBC is the secondary diagnosis in the discharge summary. The demographic characteristics, medical history, physical examination results, surgery information, pathological data, laboratory examination results and radiology reports will be collected in a standardised case report form. By May 2021, approximately 6000 patient with GBC will be included. The clinical follow-up data will be updated until 5 years after the last admission for GBC of each patient. The study aimed (1) to depict the clinical characteristics, including demographics, pathology, treatment and prognosis of patient with GBC in China; (2) to evaluate the adherence to clinical guidelines of GBC and (3) to improve clinical practice for diagnosing and treating GBC and provide references for policy-makers. ETHICS AND DISSEMINATION: The protocol of the CRGGC has been approved by the Committee for Ethics of Xinhua Hospital, Shanghai Jiao Tong University School of Medicine (SHEC-C-2019-085). All results of this study will be published in peer-reviewed journals and presented at relevant conferences. TRIAL REGISTRATION NUMBER: NCT04140552, Pre-results.

Overexpression of NCAPG inhibits cardia adenocarcinoma apoptosis and promotes epithelial-mesenchymal transition through the Wnt/ß-catenin signaling pathway.

BACKGROUND: Cardia adenocarcinoma (CA) is a distinct form of gastric cancer, and the optimal means of treating it remains controversial. At present, the role of the condensation complex gene non-SMC condensin I complex subunit G (NCAPG) in CA is uncertain, and as such the present study was designed to elucidate its importance in this oncogenic context. METHODS: We first used bioinformatics approaches to assess NCAPG expression profiles in CA using public databases. Protein profiling was also used to examine the expression of this protein in CA tumors and adjacent tissues from 20 patients. Then the expression of NCAPG in CA samples was quantified via qRT-PCR and Western blotting. NCAPG knockdown and overexpression in the SGC-7901 and AGS cell lines were subsequently performed, after which the expression of key proteins associated with epithelial-mesenchymal transition (EMT; E-cadherin, vimentin, N-cadherin, Snail, Slug) and the regulation of apoptotic responses (caspase-3, Bax, Bcl-2) was measured. The mechanistic role of NCAPG in CA was additionally studied by analyzing proteins associated with Wnt/ß-catenin signaling including Wnt1, phosphorylated GSK3ß, ß-catenin, and phosphorylated ß- catenin. The impact of NCAPG on the migration, survival, and invasion of CA cells was further examined. RESULTS: CA samples exhibited high NCAPG expression. When this gene was overexpressed in cell lines, it reduced caspase-3, Bax, and E-cadherin levels whereas it elevated Bcl-2, vimentin, N-cadherin, Snail, and Slug levels. NCAPG overexpression also resulted in the enhanced expression of Wnt1, phosphorylated GSK3ß, and total ß-catenin and the reduced expression of phosphorylated ß-catenin. The knockdown of NCAPG, in contrast, yielded the opposite phenotype. At a functional level, the overexpression of NCAPG improved the apoptotic resistance of CA cells while driving them to undergo EMT and to become more invasive and migratory. CONCLUSIONS: NCAPG overexpression can promote EMT and suppress tumor cell apoptosis via the activation of Wnt/ß-catenin signaling.

NCAPG Induces Cell Proliferation in Cardia Adenocarcinoma via PI3K/AKT Signaling Pathway.

PURPOSE: Previous studies have shown that non-SMC condensin I complex subunit G (NCAPG) overexpression is correlated to poor prognosis of multiple cancer types. Herein, we explored the underlying mechanism of NCAPG-mediated cardia adenocarcinoma (CA) proliferation and cell cycle regulation. METHODS: The protein profiling technology was used to analyze the gene expression in 20 CA and adjacent tissue samples. Differential genes were identified by bioinformatic analysis. Western blot and qRT-PCR-based analysis assessed the NCAPG expression levels in multiple CA cell lines. CA cell lines, SGC-7901 and AGS, were transfected with Lip 2000, and stably transfected cell lines were screened for NCAPG overexpression and downregulation. MTT and clone formation assays were employed to detect cell proliferation, and cell cycle phases were analyzed using flow cytometry. Western blot was performed to determine the NCAPG gene expression levels. Finally, we studied the tumorigenic effects of NCAPG in the mouse model and validated the cell experiment results using immunohistochemistry. RESULTS: A significant overexpression of NCAPG was found in CA tissues and CA cell lines. The outcomes of MTT and clone formation assays showed that NCAPG upregulation promoted cell proliferation. The outcomes of these analyses were further validated using nude mice as an in vivo tumor model. As per the outcome of Western blot and flow cytometry analysis, NCAPG regulated the G1 phase through the cyclins (CDK4, CDK6, and cyclin D1) overexpression and cell cycle inhibitors (P21 and P27) downregulation. Overexpressed NCAPG and silenced NCAPG, both in vitro and in vivo, resulted in abnormal activation of the PI3K/AKT signaling pathway in CA cells. We observed that NCAPG overexpression increased the levels of phosphorylated PI3K, AKT, and GSK3ß; however, their total protein levels remained unchanged in CA cells. CONCLUSION: As a CA oncogene, NCAPG promoted cell proliferation and regulated cell cycle through PI3K/AKT signaling pathway activation.

A High-Performance Transmitarray Antenna with Thin Metasurface for 5G Communication Based on PSO (Particle Swarm Optimization).

A 5G metasurface (MS) transmitarray (TA) feed by compact-antenna array with the performance of high gain and side-lobe level (SLL) reduction is presented. The proposed MS has two identical metallic layers etched on both sides of the dielectric substrate and four fixed vias connecting two metallic layers that works at 28 GHz to increase the transmission phase shift range. The proposed planar TA consisting of unit cells with different dimensional information can simulate the function as an optical lens according to the Fermat's principle, so the quasi-spherical wave emitted by the compact Potter horn antenna at the virtual focal point will transform to the quasi-plane wave by the phase-adjustments. Then, the particle swarm optimization (PSO) is introduced to optimize the phase distribution on the TA to decrease the SLL further. It is found that the optimized TA could achieve 27 dB gain at 28 GHz, 11.8% 3 dB gain bandwidth, -30 dB SLL, and aperture efficiency of 23% at the operating bandwidth of 27.5-29.5 GHz, which performs better than the nonoptimized one. The advanced particularities of this optimized TA including low cost, low profile, and easy to configure make it great potential in paving the way to 5G communication and radar system.

Glutathione Peroxidase 8 as a Prognostic Biomarker of Gastric Cancer: An Analysis of The Cancer Genome Atlas (TCGA) Data.

BACKGROUND Glutathione peroxidase 8 (GPX8) has previously been shown to play a role in Keshan disease. In the present study, we explored the prognostic relevance of GPX8 expression in patients with gastric cancer (GC) based upon The Cancer Genome Atlas (TCGA) data. MATERIAL AND METHODS We assessed the relationship between the expression of GPX8 and clinicopathological findings in GC patients via logistic regression analyses, Kruskal-Wallis tests, and Wilcoxon signed-rank tests. We further assessed the prognostic relevance of specific variables using Kaplan-Meier and Cox regression analyses. We lastly conducted gene set enrichment analyses (GSEA). RESULTS We detected a significant association between elevated GPX8 levels and more advanced GC tumor stage (OR=5.92 for I vs. IV), as well as more advanced T (OR=22.91 for T1 vs. T4) and N classification (OR=1.82 for N0 vs. N3). We found worse prognosis in patients expressing high levels of GPX8 relative to those with lower expression of this gene (P=0.021). In a univariate analysis, we found high GPX8 expression was strongly correlated with worse OS (hazard ratio [HR]: 1.05; 95% confidence interval [CI]: 1.01-1.08; P=0.018), and multivariate analysis confirmed that GPX8 expression independently predicts GC patient OS (HR: 1.04; CI: 1.00-1.08, P=0.041). GSEA revealed that elevated GPX8 expression was associated with enrichment of pathways consistent with MAPK signaling, JAK/STAT signaling, TGF-ß signaling, melanoma, and basal cell carcinoma. CONCLUSIONS The expression of GPX8 may have prognostic relevance, being positively associated with worse OS in GC patients.

MTH1 Inhibitor TH287 Suppresses Gastric Cancer Development Through the Regulation of PI3K/AKT Signaling.

Background: Cancer cells evade oxidative stress through the MutT homologue-1 (MTH1), a member of the Nudix family. MTH1 maintains genome integrity and the viability of tumor cells. A new class of MTH1 inhibitors have attracted interest as anticancer agents, but their mechanisms of action remain poorly characterized. In this study, the authors evaluated the anticancer effects of the MTH1 inhibitor TH287 on gastric cancer (GCa) cells. Materials and Methods: BGC-823 and SGC-7901 cells were treated with TH287 and CCK-8, and colony-forming assays were performed. Cell migration was assessed through Transwell and scratch assays. Apoptotic status was measured via flow cytometry and 5,5',6,6'-tetrachloro-1,1',3,3'-tetraethylbenzimidazolyl-carbocyanine iodide (JC-1) staining. Cell cycle status was assessed by propidium iodide (PI) staining. The expression of PI3K/AKT signaling-related proteins was verified by western blotting. Results: TH287 inhibited cell viability, reduced cell proliferation, inhibited apoptosis, induced G2/M arrest, and suppressed cell migration. A loss of mitochondrial membrane potential and reduced Bcl-2/Bax expression were also observed in TH287-treated cells. These effects were mediated through the inhibition of pro-oncogenic PI3K/AKT signaling. Conclusions: These findings indicate that the MTH1 inhibitor TH287 mediates an array of anticancer effects in GCa cells through its effects on mitochondrial function and PI3K/AKT signaling. Collectively, these data highlight the promise of TH287 as a novel therapeutic option for GCa cells.

LncRNA H19 interacted with miR-130a-3p and miR-17-5p to modify radio-resistance and chemo-sensitivity of cardiac carcinoma cells.

The current investigation explored the synthetic contribution of lncRNA H19, miR-130a-3p, and miR-17-5p to radio-resistance and chemo-sensitivity of cardiac cancer cells. Totally 284 human cardiac cancer tissues were gathered, and they have been pathologically diagnosed. The cardiac cancer cells were isolated with utilization of the mechanic method. Moreover, cisplatin, adriamycin, mitomycin, and 5-fluorouracil were designated as the chemotherapies, and single-dose X-rays were managed as the radiotherapy for cardiac cancer cells. We also performed luciferase reporter gene assay to verify the targeted relationship between H19 and miR-130a-3p, as well as between H19 and miR-17-5p. Finally, mice models were established to examine the functions of H19, miR-130a-3p, and miR-17-5p on the development of cardiac cancer. The study results indicated that H19, miR-130a-3p, and miR-17-5p expressions within cardiac cancer tissues were significantly beyond those within adjacent nontumor tissues (P < 0.05), and H19 expression was positively correlated with both miR-130a-3p (rs  = 0.43) and miR-17-5p (rs  = 0.49) expressions. The half maximal inhibitory concentrations (IC50) of cisplatin, adriamycin, mitomycin, and 5-fluorouracil for cardiac cancer cells were, respectively, determined as 2.01 µg/mL, 8.35 µg/mL, 24.44 µg/mL, and 166.42 µg/mL. The overexpressed H19, miR-130a-3p, and miR-17-5p appeared to improve the survival rate and viability of cardiac cancer cells that were exposed to chemotherapies and X-rays (all P < 0.05). It was also drawn from luciferase reporter gene assay that H19 could directly target miR-130a-3p and miR-17-5p, thereby modifying the sensitivity of cardiac cancer cells to drugs and X-rays (P < 0.05). Finally, the mice models also produced larger tumor size and higher tumor weight, when H19, miR-130a-3p, or miR-17-5p expressions were up-regulated within them (P < 0.05). In conclusion, H19 could act on miR-130a-3p or miR-17-5p to alter the radio- and chemo-sensitivities of cardiac cancer cells, helping to improve the radio-/chemotherapies for cardiac cancer.

A wheat NAC interacts with an orphan protein and enhances resistance to Fusarium head blight disease.

Taxonomically-restricted orphan genes play an important role in environmental adaptation, as recently demonstrated by the fact that the Pooideae-specific orphan TaFROG (Triticum aestivum Fusarium Resistance Orphan Gene) enhanced wheat resistance to the economically devastating Fusarium head blight (FHB) disease. Like most orphan genes, little is known about the cellular function of the encoded protein TaFROG, other than it interacts with the central stress regulator TaSnRK1α. Here, we functionally characterized a wheat (T. aestivum) NAC-like transcription factor TaNACL-D1 that interacts with TaFROG and investigated its' role in FHB using studies to assess motif analyses, yeast transactivation, protein-protein interaction, gene expression and the disease response of wheat lines overexpressing TaNACL-D1. TaNACL-D1 is a Poaceae-divergent NAC transcription factor that encodes a Triticeae-specific protein C-terminal region with transcriptional activity and a nuclear localisation signal. The TaNACL-D1/TaFROG interaction was detected in yeast and confirmed in planta, within the nucleus. Analysis of multi-protein interactions indicated that TaFROG could form simultaneously distinct protein complexes with TaNACL-D1 and TaSnRK1α in planta. TaNACL-D1 and TaFROG are co-expressed as an early response to both the causal fungal agent of FHB, Fusarium graminearum and its virulence factor deoxynivalenol (DON). Wheat lines overexpressing TaNACL-D1 were more resistant to FHB disease than wild type plants. Thus, we conclude that the orphan protein TaFROG interacts with TaNACL-D1, a NAC transcription factor that forms part of the disease response evolved within the Triticeae.

The contrary functions of lncRNA HOTAIR/miR-17-5p/PTEN axis and Shenqifuzheng injection on chemosensitivity of gastric cancer cells.

This study was implemented to figure out whether lncRNA HOTAIR/miR-17-5p/PTEN axis played a role that was opposite to Shenqifuzheng (SQFZ) injection in regulating the chemosensitivity of gastric cancer cells. The gastric cancer tissues were gathered and four gastric cancer cell lines were prepared, including BGC-823, MGC-803, SGC-7901, and MKN28. Moreover, cisplatin, adriamycin, mitomycin, and 5-fluoroura were managed as the chemo-therapeutics, and SQFZ was prepared as a Chinese medicine. Striking distinctions of HOTAIR, miR-17-5p, and PTEN expressions were observed between gastric cancer tissues and para-carcinoma normal tissues (P < 0.05). MKN28 was associated with the highest resistance to cisplatin, adriamycin, mitomycin, and 5-fluoroura among all the cell types, and SQFZ significantly improved the MKN28 cells' sensitivity to the drugs (P < 0.05). The over-expressed HOTAIR and miR-17-5p, as well as under-expressed PTEN tended to significantly facilitate the viability, EMT process and proliferation of MKN28 cells that were subject to treatment of chemo-therapies (P < 0.05). SQFZ could amplify the effects of si-HOTAIR, miR-17-5p inhibitor, and pcDNA-PTEN on boosting the chemosensitivity of gastric cancer cells (P < 0.05). In addition, HOTAIR was also found to directly target miR-17-5p, and PTEN appeared to be subject to the modification of HOTAIR and miR-17-5p in its acting on the viability, proliferation, EMT process, and apoptosis of gastric cancer cells. The HOTAIR/miR-17-5p/PTEN axis could be regarded as the potential treatment targets for gastric cancer, and adjuvant therapy of SQFZ injection could assist in further improving the treatment efficacy of chemo-therapies for gastric cancer.

A wheat cytochrome P450 enhances both resistance to deoxynivalenol and grain yield.

The mycotoxin deoxynivalenol (DON) serves as a plant disease virulence factor for the fungi Fusarium graminearum and F. culmorum during the development of Fusarium head blight (FHB) disease on wheat. A wheat cytochrome P450 gene from the subfamily CYP72A, TaCYP72A, was cloned from wheat cultivar CM82036. TaCYP72A was located on chromosome 3A with homeologs present on 3B and 3D of the wheat genome. Using gene expression studies, we showed that TaCYP72A variants were activated in wheat spikelets as an early response to F. graminearum, and this activation was in response to the mycotoxic Fusarium virulence factor deoxynivalenol (DON). Virus induced gene silencing (VIGS) studies in wheat heads revealed that this gene family contributes to DON resistance. VIGS resulted in more DON-induced discoloration of spikelets, as compared to mock VIGS treatment. In addition to positively affecting DON resistance, TaCYP72A also had a positive effect on grain number. VIGS of TaCYP72A genes reduced grain number by more than 59%. Thus, we provide evidence that TaCYP72A contributes to host resistance to DON and conclude that this gene family warrants further assessment as positive contributors to both biotic stress resistance and grain development in wheat.

Sijunzi decoction-treated rat serum induces apoptosis of side population cells in gastric carcinoma.

Sijunzi decoction (SJZD) is a traditional Chinese herbal medicine. Previous studies have indicated that SJZD exhibits antitumor activity. However, the underlying molecular mechanism has not been fully elucidated. To explore the antitumor mechanism of SJZD, the effects of serum from rats treated with SJZD on the proliferation of MKN-28 and HGC-27 gastric carcinoma cell lines were systematically investigated. It was found that SJZD-treated rat serum significantly inhibited the growth of MKN-28 and HGC-27 cells in vitro. The results obtained from a colony formation assay showed that SJZD-treated rat serum decreased the colony formation ability of MKN-28 and HGC-27 cells. The apoptosis rate in MKN-28 and HGC-27 cells was also increased following treatment with SJZD-treated rat serum. Flow cytometry with cell sorting revealed the presence of side population (SP) cells in MKN-28 and HGC-27 cells though Hoechst 33342 staining, and verapamil reduced the SP percentage. Further analysis showed that SJZD-treated rat serum promoted the apoptosis of SP cells in MKN-28 and HGC-27 cell lines by upregulating Bax, caspase-3 and PARP and downregulating bcl-2. These data revealed the therapeutic effect of SJZD-treated rat serum on gastric carcinoma. Following the preliminary identification of the inhibitory effect on the growth of gastric cancer cells in vitro, the growth inhibitory effect of SJZD-treated rat serum on SP cells was confirmed, and this inhibition particularly involved the induction of cell apoptosis.

Ginsenoside-Rh2 Inhibits Proliferation and Induces Apoptosis of Human Gastric Cancer SGC-7901 Side Population Cells.

OBJECTIVES: To observed the effects of ginsenoside -Rh2 (GS-Rh2) on proliferation and apoptosis of side population (SP) human gastric cancer SGC-7901 cells. MATERIALS AND METHODS: SGC-7901 SP and Non-SP cells were sorted by flow cytometry and assessed using the cck-8 method. Expression of apoptosis-related proteins Bax and Bcl-2 of SP before and after the intervention was determined by Western-blotting. RESULTS: It was found that the proliferation of SP was significantly faster than that of NSP (<0.05). In addition, GS-Rh2 inhibited proliferation of gastric cancer SP cells, induced cell cycle arrest and cell apoptosis, and changed the expression of BAX/Bcl-2 proteins in a time-dependent and concentration-dependent manner (<0.05). CONCLUSIONS: With increase of GS-Rh2 dose, GS-Rh2 gradually inhibit the proliferation of SGC-7901 SP cells, which have high proliferation rate, through G1/G0 phase arrest, followed by apoptosis which involves the up-regulation of Bax and the down-regulation of Bcl-2.