DICER1-AS1 Promotes the Malignant Behaviors of Colorectal Cancer Cells by Regulating miR-296-5p/STAT3 Axis.

BACKGROUND: Long non-coding RNA (lncRNA) exerts a regulatory role in the occurrence and progression of tumors. This study aimed at probing into the function and mechanism of lncRNA DICER1 antisense RNA 1 (DICER1-AS1) in colorectal cancer (CRC). METHODS: The expressions of DICER1-AS1, miR-296-5p and STAT3 mRNA were tested by quantitative real-time polymerase chain reaction (qRT-PCR). Cell counting kit-8 (CCK-8) assay was employed to detect cell proliferation, and Transwell was used to detect cell migration and invasion. In addition, the expressions of apoptosis-related proteins Bax and Bcl2 were detected by Western blot. Interactions between DICER1-AS1 and miR-296-5p, and miR-296-5p and STAT3 were predicted and determined by bioinformatics analysis, luciferase reporter assay and RNA binding protein immunoprecipitation (RIP) assay. RESULTS: The expressions of DICER1-AS1 and STAT3 mRNA were significantly up-regulated while miR-296-5p expression was remarkably down-regulated in CRC tissues and cell lines. Over-expression of DICER1-AS1 or transfection of miR-296-5p inhibitors could promote the proliferation, migration and invasion and inhibit apoptosis of CRC cells, whereas knockdown of DICER1-AS1 or transfection of miR-296-5p mimics had the opposite effects. Additionally, DICER1-AS1 could down-regulate miR-296-5p expression via sponging it. DICER1-AS1 also enhanced the expression of STAT3, which was identified as a target gene of miR-296-5p. CONCLUSION: DICER1-AS1 acts as an oncogenic lncRNA in CRC via modulating miR-296-5p/STAT3 axis. Our results provide a new direction for the diagnosis and treatment of CRC.

PELP1 is a novel oncogene in gastric tumorigenesis and negatively regulated by miR-15 family microRNAs.

BACKGROUD: Gastric cancer (GC) is one of the leading causes of cancer-related death in East Asia and some South American countries, but its mechanism has not been clarified clearly. Proline-, glutamic acid-, and leucine-rich protein-1 (PELP1), a co-regulatory molecule of estrogen receptor α (ER α), is up-regulated in series of cancers such as endometrial carcinoma, ovarian cancer, colorectal cancer, breast cancer, and non-small cell lung cancer. However, PELP1's role in GC is still obscure, and its aberrant expression in cancers also remains to be explained. METHODS: Immunohistochemical staining and Real-time PCR were used to compare the expression level of PELP1 in GC tissues and adjacent tissues. Western blot was used to detect the expression of PELP1 in cell lines. Kaplan-meier analysis and chi-square test were applied to evaluate the potential of PELP1 to function as a cancer biomarker. RNA interference was used to inhibit PELP1 expression in GC cells, followed by detecting cell proliferation, apoptosis, migration and invasion. Luciferase assay was conducted to validate whether miR-15 family members can directly target PELP1. RESULTS: In this study, we validated that PELP1 was significantly up-regulated in GC samples and cell lines. It was also demonstrated that the up-regulation of PELP1 was associated with several clinicopathologic features such as tumor diameter (P< 0.001), serum CEA level (P= 0.034), and lymphatic metastasis (P= 0.0009) of GC patients, and its high expression was correlated with shorter disease-free survival and overall survival of the patients. Knockdown of PELP1 remarkably arrested the proliferationï» migration and invasion, while promoted apoptosis. We also confirmed that miR-15 family microRNAs, most of which were down-regulated and tumor suppressor in cancers, were posttranscriptional regulators of PELP1. CONCLUSION: In conclusion, we demonstrated that PELP1 was an oncogene of GC associated with patients' prognosis and miR-15 family members contributed to its aberrant expression in cancers.

Development of ionic liquid assisted-synthesized nano­silver combined with vascular endothelial growth factor as wound healing in the care of femoral fracture in the children after surgery.

This investigation aimed to develop the silver (Ag) nanoparticles incorporated vascular endothelial growth factor (VEGF) for the improvement wound healing and reduce Aseptic necrosis in treatment of femoral fracture healing. The spherical shaped Ag nanoparticles with improved morphology have been effectively synthesized via microwave assisted method using ionic liquids 1-dodecyl-3-methylimidazolium chloride. The morphological structure and crystalline properties of Ag nanoparticles are analyzed by using UV, XRD and TEM-EDX analytical methods. The average grain size of the Ag nanoparticles is 20 nm, which was observed by defining the width of the (111) Bragg reflection with the Debye-Scherer formula and TEM results. The biological analyses confirmed that the Ag nanoparticles with VEGF molecules are promoted the cell adhesion and proliferation of Human mesenchymal stem cells (MSCs) cells. Ag NPs at appropriate concentrations have favorable biocompatibility to encourage cell activation properties like cell proliferation, cytokines release and chemotaxis. In the present study, our experimental results indicated that Ag NPs incorporated VEGF material are highly favorable to fracture healing and mainly as blood vessel repair. The surface morphology improved synthetic Ag NPs using ionic liquids has shown advantageous for cell activity and also improve the materials performances with VEGF for the regeneration of femoral fractures.