Serine/threonine/tyrosine kinase 1 (STYK1) has been previously shown to have oncogenic properties, and emerging evidence suggests that STYK1 expression correlates with epithelial-mesenchymal transition (EMT). However, the mechanism of STYK1 involvement in oncogenesis remains unknown. The present study aimed to elucidate how STYK1 expression level relates to the metastasis, migration, invasion, and EMT in non-small cell lung cancer (NSCLC) and to determine the molecular mechanism of STYK1 effects.Serine/threonine/tyrosine kinase 1 (STYK1) expression level and its relationship with the prognosis of NSCLC were determined using the ONCOMINE database and clinical cases. Non-small cell lung cancer cell lines with the overexpression or knockdown of STYK1 were established to determine whether STYK1 promotes cell migration, invasion, and EMT in vitro and in vivo. In addition, a constitutively active FoxO1 mutant (FoxO1AAA) was used to examine the role of FoxO1 in the STYK1-mediated upregulation of metastasis and EMT in NSCLC.Serine/threonine/tyrosine kinase 1 (STYK1) was upregulated in NSCLC tissues and cell lines, and its overexpression correlated with poor prognosis in patients with NSCLC after surgery. Enhanced expression of STYK1 potentiated the migration, invasion, and EMT in SW900 cells, thereby promoting metastasis, whereas knockdown of STYK1 inhibited these cellular phenomena in Calu-1 cells. Furthermore, STYK1 expression was positively related to the level of phosphorylated-FoxO1, whereas the constitutively active FoxO1 mutant protected against the positive effect of STYK1 overexpression on cell migration, invasion, and EMT.Serine/threonine/tyrosine kinase 1 (STYK1) was upregulated in NSCLC and correlated with poor clinical outcomes. In addition, STYK1 suppressed FoxO1 functions, thereby promoting metastasis and EMT in NSCLC.
Abstract The long noncoding RNA called MIR22 host gene (MIR22HG) was previously identified as a tumor suppressor in several cancers. However, the biological function of MIR22HG in breast cancer remains unknown. In this study, we aimed to determine the function and molecular mechanism of MIR22HG in breast cancer progression using transcriptomics and biotechnological techniques. Our results showed that MIR22HG expression was lower in the cancerous tissues than in the paired adjacent normal breast tissues. Additionally, MIR22HG was found to be mainly located in the cytoplasm and acted as a miR-629-5p sponge. Notably, MIR22HG stabilized the expression of large tumor suppressor 2 (LATS2), which promoted the LATS2-dependent phosphorylation of YAP1 and suppressed the expression of its downstream target oncogenes, thereby inhibiting the proliferation and migration of breast cancer cells. Therefore, our findings reveal the MIR22HG-dependent inhibition of breast cancer cell proliferation and migration via the miR-629-5p/LATS2 pathway, providing new insights and identifying novel therapeutic targets for breast cancer treatment.
As an advanced material with wide application, carbon fiber reinforced epoxy resin matrix composites (CF/EP) are flammable, but the traditional flame retardant methods negatively affect its molding process, heat resistance, mechanical properties, and how to solve this problem has been a challenge. This paper adopts a novel flame retardant method of inserting nanofiber film of flame retardant into the interlayer of the composite laminate to achieve fire resistance, higher strength, and toughness of the composite. In this work, pentaerythritol phosphate (PEPA) nanofiber films with phenoxy resin (PKHH) as a carrier was prepared by electrospinning and placed between the layers of CF/EP laminates. The results show that a dense charring layer with isolation and protection functions can be formed between the layers of the CF/EP intercalated by the nanofiber films during combustion. Accordingly, the nanofiber film containing 50 wt% PEPA with the thickness of only 30 μm increased the LOI value of CF/EP from 27.8% to 34.7%, while reducing the THR and TSR by 12.3% and 9.6% respectively. What’s more, due to the Ex-situ toughening effect of the nanofibers, the flexural strength, interlaminar shear strength, and compression strength after the impact of the modified CF/EP were increased by a maximum of 11.2%, 11.3%, and 12.2% compared to unmodified CF/EP. This work proves the feasibility of interlayer flame retardant fiber reinforced resin composites, and provides a new method to prepare high-performance flame-retardant composites.
MicroRNAs play crucial roles in the pathogenesis of cancers. MiRNA-218-5p may act as either an oncogene or a tumor suppressor, but its role in the pathogenesis of Breast Cancer (BC) remains unclear. Infiltrative breast ductal carcinoma as well as corresponding adjacent normal samples were collected from 30 patients. Mimics and inhibitors of miRNA-218-5p or corresponding negative controls were transfected into BC cells. miRNA-218-5p expression was detected by quantitative PCR. The effects of miRNA-218-5p on the malignant behaviors of BC were assessed. Dual-luciferase reporter assay was employed to evaluate the binding of miRNA-218-5p to LRIG1. BC tissues showed higher miRNA-218-5p expression as compared to the adjacent normal tissues. Ectopic miRNA-218-5p expression accelerated the cell cycle, cell growth and migration of BC, while repressed cell apoptosis. Interestingly, ectopic miRNA-218-5p expression down-regulated LRIG1 expression, and miRNA-218-5p could bind to LRIG1. Also, our study indicated that miRNA-218-5p up-regulated ErbB2 and EGFR expression by targeting LRIG1, suggesting that the LRIG1-mediated signaling pathway contributed to the pro-tumor effects of miRNA-218-5p on BC. MiRNA-218-5p up-regulates ErbB2 and EGFR expression by suppressing LRIG1 expression, thus promoting the malignant behaviors of BC. miRNA-218-5p may exert a pro-tumor effect on BC and serve as a therapeutic target for BC treatment.
The starch xanthate/natural rubber (SX/NR) composite was prepared by directly mixing and co-coagulating NR latex and the modified starch paste with carbon bisulfide. The vulcanization kinetics of NR and SX/NR composite were investigated by using a rubber process analysis (RPA). The mechanism of SX/NR composite vulcanization was similar to that of pure NR. The values t 0 and t dis of XS/NR composite were shorter than that of NR, and the activation energy E 1 for the induction period was smaller. The activation energies E 2 and E 3 for the curing period were smaller than that of NR.
CDK8 is a cyclin-dependent kinase (CDK) member of the mediator complex that couples transcriptional regulators to the basal transcriptional machinery, and it has been investigated for possible tumor promoting functions. However, it is unclear whether CDK8 is involved in breast tumor cells growth. The aim of this study was to determine whether the suppression of CDK8 by small interfering RNA (siRNA) inhibits the growth of human breast cancer cell.CDK8-siRNA transfection was used to silencing the CDK8 gene in established breast cancer cell line, MDA-MB-231 and MCF-7, successful transfection being confirmed by Real-time PCR and could be shown by Western Blotting. CDK8 deletion caused significant decline in cell proliferation was observed in breast cancer cell lines as investigated by MTS assay, the number and size of the colonies formed were also significantly reduced in the absence of CDK8. Furthermore, transwell test were conducted to explore the migration of breast cancer cells. Moreover CDK8 gene knockdown arrested cell cycle.CDK8 mRNA expression was reduced after transfection with CDK8-siRNA, and protein expression had a similar trend. Transfection of CDK8-siRNA suppressed breast cancer cells proliferation and migration; meanwhile the cells were arrested at G0/G1 phase.CDK8 plays an essential role in breast cancer progression, which might inhibit the proliferation and migration in breast cancer cells.
MicroRNAs (MiRNAs) constitute 19-25 nulceotide, non-coding RNA that regulate the expression of target genes, mainly at the post-transcriptional level. Breast cancer (BC) is most common cause of death in women accounting for 522,000 in 2012.It has got poor prognosis. In this review, we aim to provide a comprehensive story on miRNA signatures of cancers specially breast cancer.
Abstract PI3K/AKT signaling pathway plays an important role in regulating the tumorigenesis, recurrence, and metastasis of breast cancer (BC). In this study, we discovered a circRNA with protein-coding potential, which we named circSEMA4B. CircSEMA4B could encode a novel protein, SEMA4B-211aa. Both circSEMA4B and SEMA4B-211aa were remarkably downregulated in BC tissues and cell lines. Low expression of circSEMA4B was positively associated with TNM stage, tumor size, lymph node metastasis, and distant metastasis of BC patients. The functional investigation showed that circSEMA4B and SEMA4B-211aa could significantly inhibit the proliferation and migration of BC in vivo and in vitro. Of note, SEMA4B-211aa inhibited the generation of PIP3 by binding to p85, thereby inhibiting the phosphorylation of AKT (Thr308). CircSEMA4B inhibited the phosphorylation of AKT (Ser473) through miR-330-3p/PDCD4 axis. Taken together, circSEMA4B is a novel negative regulator of PI3K/AKT signaling pathway, providing novel mechanistic insights into the underlying mechanisms of BC.
Even though colon cancer ranks among the leading causes of cancer mortality, early detection dramatically increases survival rates. Many studies have been conducted to determine whether altered metabolite levels may serve as a potential biomarker of cancer that affects key metabolic pathways. The goal of the study was to detect metabolic biomarkers in patients with colon cancer using liquid chromatography-mass spectrometry (LC-MS). This study consisted of 30 patients with colon cancer. An analysis of the metabolomes of cancer samples and para-carcinoma tissues was conducted. We identified a series of important metabolic changes in colon cancer by analyzing metabolites in cancerous tissues compared to their normal counterparts. They are mainly involved in the pentose phosphate pathway, the TCA cycle, glycolysis, galactose metabolism, and butanoate metabolism. As well, we observed dysregulation of AMP, dTMP, fructose, and D-glucose in colon cancer. Additionally, the AUCs for AMP, dTMP, fructose, and D-glucose were greater than 0.7 for the diagnosis of colon cancer. In conclusion, AMP, dTMP, fructose, and D-glucose showed excellent diagnostic performance and could serve as novel disease biomarkers for colon cancer diagnosis.
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