Achieving High Efficacy and Low Safety Risk by Balancing Pesticide Deposition on Leaves and Fruits of Chinese Wolfberry (Lycium barbarum L.).

Pesticide residue has become the main technical barrier that restricts the export of Chinese wolfberry. Can we achieve high efficacy and low safety risk by balancing pesticide deposition on the leaves and fruits of Chinese wolfberry? In this research, the structural characteristics and wettability of leaves and fruits of Chinese wolfberry at different growth stages were studied. The adaxial and abaxial surfaces of leaves were hydrophobic, whereas the fruit surfaces were hydrophilic. Adding spray adjuvant could increase the retention of droplets on the leaf surfaces of Chinese wolfberry by 52.28-97.89% and reduce the retention on the fruit surfaces by 21.68-42.14%. A structural equation model analysis showed that the adhesion tension was the key factor affecting the retention of the solutions among various interface behaviors. When the concentrations of Silwet618, AEO-5, Gemini 31551, and 1227 were 2-5 times higher than their CMCs, the retention of pesticide solutions (pyraclostrobin and tylophorine) on Chinese wolfberry leaves significantly increased, and the control efficacies on aphids and powdery mildew also dramatically improved (65.90-105.15 and 41.18-133.06%, respectively). Meanwhile, the retention of pesticides on the fruit of Chinese wolfberry was reduced. This study provides new insights into increasing the utilization of pesticides in controlling pests and improving food safety.

Increased expression of NCAPG (Non-SMC condensing I complex subunit G) is associated with progression and poor prognosis of lung adenocarcinoma.

Recently, studies have shown that the up-regulation of Non-SMC Condensin I Complex Subunit G (NCAPG) in some tumors can promote tumor progression, and its high expression has a strong correlation with the poor prognosis of patients. However, there are few studies on NCAPG in lung adenocarcinoma (LUAD). Our research is to explore the role of NCAPG in LUAD and try to reveal the possible molecular mechanism. We use public databases and tissue samples from LUAD patients to verify that NCAPG is significantly up-regulated in LUAD, and the high expression of NCAPG is related to the poor prognosis of patients. Subsequently, we found that silencing NCAPG can inhibit the proliferation and invasion of LUAD cells in vitro and the growth of subcutaneous tumors in nude mice in vivo. In order to explore the possible molecular mechanism of NCAPG's function, we found out the genes co-expressed with NCAPG through the cBioportal database, and discovered that these genes were significantly enriched in the cell cycle and other pathways through DAVID analysis, which implies the importance of NCAPG in the cell cycle. Finally, we confirmed by flow cytometry that NCAPG affects the conversion of cell cycle mitosis from G1 to S. Taken together, our research results suggest that NCAPG plays a role in the progress of LUAD. Moreover, NCAPG can be used as a potential biomarker for the diagnosis of LUAD, as well as a potential therapeutic target for patients with LUAD.

N6-methyladenosine (m6A)-mediated lncRNA DLGAP1-AS1enhances breast canceradriamycin resistance through miR-299-3p/WTAP feedback loop.

Chemotherapy resistance is identified as an obstacle for breast cancer (BC) therapy, and, besides, increasing evidence indicates that long-noncoding RNAs (lncRNAs) participate in the regulation of BC adriamycin (ADR) resistance. Here, our work shows that lncRNA DLGAP1 antisense RNA 1 (DLGAP1-AS1) is up-regulated in ADR-resistant BC cells (MCF-7/ADR). Clinically, higher DLGAP1-AS1 expression was closely correlated to poorer clinical prognosis. Results showed that DLGAP1-AS1 promoted the ADR IC50 and proliferation of ADR-resistant cells. Moreover, N6-methyladenosine (m6A) methyltransferase WT1 associated protein (WTAP) binds to the m6A modified site of DLGAP1-AS1 and motivates its stability. Mechanistically, DLGAP1-AS1 sponged miR-299-3p through 3'-untranslated region (3'-UTR) binding, which in turn relieved the repression of WTAP and thus upregulated WTAP expression. In conclusion, above findings conclude that lncRNA DLGAP1-AS1 promotes BC ADR-resistance through WTAP/DLGAP1-AS1/miR-299-3p feedback loop.

Parathyroid hormone type 1 receptor regulates osteosarcoma K7M2 Cell growth by interacting with angiotensinogen.

This study aimed to determine the interactions between parathyroid hormone type 1 receptor (PTHR1) and angiotensinogen (AGT) and the effects of these agents on osteosarcoma (OS). We constructed a stably transfected mouse OS K7M2 cell line (shPTHR1- K7M2) using shRNA and knocked down AGT in these cells using siRNA-AGT. The transfection efficiency and expression of AGT, chemokine C-C motif receptor 3 (CCR3), and chemokine (C-C motif) ligand 9 (CCL9) were determined using real-time quantitative PCR. Cell viability and colony formation were assessed using Cell Counting Kit-8 and crystal violet staining, respectively. Cell apoptosis and cycle phases were assessed by flow cytometry, and cell migration and invasion were evaluated using Transwell assays. Interference with PTHR1 upregulated the expression of AGT and CCR3, and downregulated that of CCL9, which was further downregulated by AGT knockdown. Cell viability, migration, invasion and colony formation were significantly decreased, while cell apoptosis was significantly increased in shPTHR1-K7M2, compared with those in K7M2 cells (P < .05 for all). However, AGT knockdown further inhibited cell viability after 72 h of culture but promoted cell migration and invasion. PTHR1 interference decreased and increased the numbers of cells in the G0/G1 and G2/M phases, respectively, compared with those in K7M2 cells. Angiotensinogen knockdown increased the number of cells in the G0/G1 phase compared with that in the shPTHR1-K7M2 cells. Therefore, PTHR1 affects cell viability, apoptosis, migration, invasion and colony formation, possibly by regulating AGT/CCL9 in OS cells.

Circular RNA circRNF20 promotes breast cancer tumorigenesis and Warburg effect through miR-487a/HIF-1α/HK2.

Compelling evidence has demonstrated the potential functions of circular RNAs (circRNAs) in breast cancer (BC) tumorigenesis. Nevertheless, the underlying mechanism by which circRNAs regulate BC progression is still unclear. The purpose of present research was to investigate the novel circRNA circRNF20 (hsa_circ_0087784) and its role in BC. CircRNA microarray sequencing revealed that circRNF20 was one of the upregulated transcripts in BC samples. Increased circRNF20 level predicted the poor clinical outcome in BC specimens. Functionally, circRNF20 promoted the proliferation and Warburg effect (aerobic glycolysis) of BC cells. Mechanistically, circRNF20 harbor miR-487a, acting as miRNA sponge, and then miR-487a targeted the 3'-UTR of hypoxia-inducible factor-1α (HIF-1α). Moreover, HIF-1α could bind with the promoter of hexokinase II (HK2) and promoted its transcription. In conclusion, this finding illustrates the vital roles of circRNF20 via the circRNF20/ miR-487a/HIF-1α/HK2 axis in breast cancer progress and Warburg effect, providing an interesting insight for the BC tumorigenesis.

Prognostic significance of ACP5 expression in patients with lung adenocarcinoma.

INTRODUCTION: Tartrate-resistant acid phosphatase 5 (ACP5), which is essential for bone resorption and osteoclast differentiation, promotes cell motility through the modulation of focal adhesion kinase phosphorylation. This study seeks to elucidate the association of ACP5 expression and the clinicopathologic characteristics of patients with lung adenocarcinoma (AD). METHODS: The expression of ACP5 was measured by Immunohistochemistry and Western blot analysis in lung AD and matched tumor-adjacent tissues, and the χ2 test was applied to analyze the correlation between ACP5 expression and clinicopathologic features. Using the Kaplan-Meier method, univariate and multivariate regression analysis was to explore the correlation between ACP5 expression and overall survival (OS). RESULTS: We found that ACP5 was frequently upregulated in lung AD tissues. The high expression of ACP5 was significantly related to lymph node status, tumor-node-metastasis (TNM) stage, and differentiation. From the results of univariate survival analysis, it indicated that the patients with high expression of ACP5 expression had a significantly lower OS than the patients with low expression of ACP5 expression. As it showed in Multivariate Cox regression analysis, the high expression of ACP5 expression was an independent prognostic factor for OS. CONCLUSIONS: Our results suggest that high expression of ACP5 correlates with tumor progression and may serve as a potential prognostic biomarker in lung AD.

Transcriptomic analyses reveal the underlying pro-malignant functions of PTHR1 for osteosarcoma via activation of Wnt and angiogenesis pathways.

BACKGROUND: Increasing evidence has indicated parathyroid hormone type 1 receptor (PTHR1) plays important roles for the development and progression of osteosarcoma (OS). However, its function mechanisms remain unclear. The goal of this study was to further illuminate the roles of PTHR1 in OS using microarray data. METHODS: Microarray data were available from the Gene Expression Omnibus database under the accession number GSE46861, including six tumors from mice with PTHR1 knockdown (PTHR1.358) and six tumors from mice with control knockdown (Ren.1309). Differentially expressed genes (DEGs) between PTHR1.358 and Ren.1309 were identified using the LIMMA method, and then, protein-protein interaction (PPI) network was constructed using data from STRING database to screen crucial genes associated with PTHR1. KEGG pathway enrichment analysis was performed to investigate the underlying functions of DEGs using DAVID tool. RESULTS: A total of 1163 genes were identified as DEGs, including 617 downregulated (Lef1, lymphoid enhancer-binding factor 1) and 546 upregulated genes (Dkk1, Dickkopf-related protein 1). KEGG enrichment analysis indicated upregulated DEGs were involved in Renin-angiotensin system (e.g., Agt, angiotensinogen) and Wnt signaling pathway (e.g., Dkk1), while downregulated DEGs participated in Basal cell carcinoma (e.g., Lef1). A PPI network (534 nodes and 2830 edges) was constructed, in which Agt gene was demonstrated to be the hub gene and its interactive genes (e.g., CCR3, CC chemokine receptor 3; and CCL9, chemokine CC chemokine ligand 9) were inflammation related. CONCLUSIONS: Our present study preliminarily reveals the pro-malignant effects of PTHR1 in OS cells may be mediated by activating Wnt, angiogenesis, and inflammation pathways via changing the expressions of the crucial enriched genes (Dkk1, Lef1, Agt-CCR3, and Agt-CCL9).

Circular RNA expression profiles reveal that hsa_circ_0018289 is up-regulated in cervical cancer and promotes the tumorigenesis.

Circular RNAs (circRNAs) are a type of non-coding RNAs that have been identified as critical regulators in various diseases, especially in cancers. However, the expression profiles and functions of circRNAs in cervical cancer are still unclear. In present study, human circRNAs microarray were performed to screen the circRNAs expression in cervical cancer tissue. Microarray analysis revealed 45 significantly expressed circRNAs with 4 fold change. Among these up-regulated circRNAs, hsa_circ_0018289 was validated to be significantly up-regulated in 35 pairs of cervical cancer tissue compared with adjacent normal tissue and cell lines. Loss-of-function experiments revealed that, in vitro and in vivo, hsa_circ_0018289 knockdown inhibited the proliferation, migration and invasion of cervical cancer cells. Via bioinformatics prediction program and luciferase reporter assays, hsa_circ_0018289 was observed to directly bind to miR-497. Taken together, the results indicate that hsa_circ_0018289 plays important role in cervical cancer proliferation, migration and invasion, suggesting the miRNA 'sponge' of hsa_circ_0018289 and its oncogenic role on cervical cancer tumorigenesis.

Long Noncoding RNA PVT1 Facilitates Cervical Cancer Progression via Negative Regulating of miR-424.

Emerging evidence suggests that the long noncoding RNA (lncRNA) plasmacytoma variant translocation 1 (PVT1) gene is involved in the pathogenesis of cervical cancer. However, the potential mechanism is rarely reported. Our study found that PVT1 was upregulated in cervical cancer tissue and cell lines. After transfecting PVT1 siRNA, the proliferation, migration, and invasion of cervical cancer cells were markedly decreased. miRNA expression profiles demonstrate that miR-424 was markedly downregulated in cervical cancer tissue. Bioinformatics analysis revealed that miR-424 was potentially targeted by PVT1, which was confirmed by dual-luciferase reporter assay. Pearson's correlation analysis showed that PVT1 expression was negatively related to miR-424 expression in glioma cancer tissues. Finally, lowered expression of miR-424 could recover the tumor-suppressive effects of PVT1 knockdown in cervical cancer cell lines. Our results reveal a tumor-promoting role for PVT1, acting as a competing endogenous RNA (ceRNA) or a molecular sponge in negatively modulating miR-424, which might provide a novel therapeutic target for cervical cancer.

Ectopic expression of miR-34a enhances radiosensitivity of non-small cell lung cancer cells, partly by suppressing the LyGDI signaling pathway.

miR-34a is transcriptionally induced by the tumor suppressor gene p53, which is often downregulated in non-small cell lung cancer (NSCLC). To address whether the downstream signal of miR-34a is sufficient to induce apoptosis and to alter cellular radiosensitivity, a chemical synthetic miR-34a mimic was delivered into A549 and H1299 cells, with or without co-treatment of γ-irradiation. Results showed that ectopic expression of miR-34a induced dose-dependent cell growth inhibition and apoptosis in a p53-independent manner in both NSCLC cell lines. Interestingly, LyGDI was discovered as a new target gene of miR-34a, and downregulation of LyGDI promoted Rac1 activation and membrane translocation, resulting in cell apoptosis. Furthermore, restoration of miR-34a indirectly reduced cyclooxygenase-2 (COX-2) expression. Taken together, these results demonstrate that restoration of miR-34a expression enhances radiation-induced apoptosis, partly by suppressing the LyGDI signaling pathway, and miR-34a could possibly be used as a radiosensitizer for non-small cell lung cancer therapy.