MPZL1 suppresses the cancer stem-like properties of lung cancer through ß-catenin/TCF4 signaling.

This study was designed to explore the influence of myelin protein zero-like protein 1 (MPZL1) on the stem-like properties of cancer cells and the underlying mechanism in lung adenocarcinoma. Real-time quantitative polymerase chain reaction (RT-qPCR) was utilized to evaluate mRNA expression level. CCK8, wound healing, and transwell assays were applied to assess cell proliferation, migration, and invasion. Tumorsphere-formation assay was utilized to assess cancer stem cell-like properties. LF3 was used to block the ß-catenin/Transcription factor 4 (TCF-4) signaling. Xenograft nude mouse model was conducted; tumor weight and volume were recorded. Western blot assay was utilized to detect the expression levels of CD44, CD133, ß-catenin, TCF-4, and MPZL1. Following MPZL1 knockdown, the mRNA expression levels of MPZL1, ß-catenin, and TCF-4 were inhibited, while the mRNA expression levels of the above genes were increased after the MPZL1 overexpression. MPZL1 knockdown suppressed cell proliferation, migration, and invasion, reduced the tumorsphere-formation capacity, and restrained the expression levels of CD44 and CD133. However, MPZL1 overexpression promoted the cell proliferation, migration, and invasion, enhanced the tumorsphere-formation capacity, and increased the expression levels of CD44 and CD133. Interestingly, LF3 treatment partially revised the effect of MPZL1 overexpression. These findings were further corroborated by in vivo experiments. We concluded that MPZL1 could suppress the lung adenocarcinoma cells' proliferation, migration, invasion, and lung cancer stem cells characteristics. The underlying mechanism is involved in the activation of ß-catenin/TCF-4 signaling.

Integrating Bulk-seq and Single-cell-seq Reveals Estrogen and MAPK Pathways Associating with Neuroblastoma Outcome.

INTRODUCTION: Neuroblastoma is the most common extracranial solid tumor in children. Patients with high-risk neuroblastoma have a 5-year survival rate less than 50% after extensive treatment. Signaling pathways control cell fate decisions that dictate the behavior of tumor cells. The deregulation of signaling pathways is etiological in cancer cells. Thus, we speculated that the pathway activity of neuroblastoma contains more prognostic information and therapeutic targets. METHODS: Using a footprint-based method, we calculated the activity of fourteen pathways in neuroblastoma. Through stepwise Cox regression analyses, we established a three-gene prognostic signature whose predictive performance was evaluated by external validation. Combining a single-cell sequencing dataset, the most active pathways in high-risk neuroblastoma were found. RESULTS: We found that several pathway activities were correlated with neuroblastoma outcomes. We built a three-gene model comprising DLK1, FLT3, and NTRK1, which exhibited superior internal and external performances. We created a nomogram that combines clinical characteristics to aid in the selection and visualization of high-risk neuroblastoma patients. Furthermore, by integrating a single-cell sequencing dataset, we found that estrogen and MAPK were the most active pathways in high-risk neuroblastoma. CONCLUSION: Our findings suggest that pathway-related therapies may hold promise for the treatment of high-risk neuroblastoma.

miR-134 inhibits osteosarcoma cell invasion and metastasis through targeting MMP1 and MMP3 in vitro and in vivo.

miR-134 has been shown to be associated with angiogenesis and the progression of osteosarcoma. This study further assessed the effects of miR-134 expression on osteosarcoma cell migration, invasion, and metastasis in vitro and in a nude mouse xenograft model, exploring the underlying molecular events. Luciferase reporter assays revealed that miR-134 directly targets the 3'-UTRs of MMP1 and MMP3 to reduce their expression in osteosarcoma cells. In conclusion, overexpression of miR-134 suppresses osteosarcoma cell invasion and metastasis through the inhibition of MMP1 and MMP3 expression. We propose miR-134 as an attractive novel therapeutic target for the treatment of osteosarcoma.

The effect of CYP2D6 *10 polymorphism on adjuvant tamoxifen in Asian breast cancer patients: a meta-analysis.

OBJECTIVE: To evaluate the effect of CYP2D6 *10 polymorphism (C 100C>T, rs1065852) on clinical outcomes of female Asian breast cancer patients with tamoxifen adjuvant treatment. METHODS: Meta-analysis of retrospective cohort studies published in July 2017 was performed. Fifteen studies with 1,794 Asian breast cancer patients were included, using strict eligibility requirements. Associations of disease-free survival (DFS), overall survival (OS) and recurrence rate after tamoxifen intake, with CYP2D6 *10 polymorphism were investigated through random effects models. RESULTS: CYP2D6 *10 polymorphism was found to have effect on DFS and recurrence rate in various comparison models, but not on overall survival in the female Asian breast cancer patients. CONCLUSION: In conclusion, our meta-analysis suggests that significant association of *10/*10 (TT) genotype with poorer DFS and recurrence exists in female Asian breast cancer patients with tamoxifen 20 mg/day adjuvant treatment. In the future, large and well-designed studies are required to illustrate the interactions of CYP2D6 genetic variants, including *10 polymorphism and tamoxifen response on female breast cancer patients.

Facile Preparation and Self-Assembly of Monodisperse Polystyrene Nanospheres for Photonic Crystals.

We have developed boiling emulsifier-free emulsion polymerization recipes for the synthesis of monodisperse polystyrene (PS) nanospheres with diameters between ca. 100 and 300 nm. The morphologies of the nanospheres during growth were characterized and the results showed that the PS nanospheres with uniform structures could be synthesized rapidly by modifying the reaction conditions. These nanospheres readily self-assemble into three-dimensionally colloidal photonic crystal film and whose photonic band-stop could be tuned over the entire visible spectral region by altering the sphere diameters.