lncRNA NEF (Neighboring Enhancer of FoxA2) Inhibits Pancreatic Cancer via Regulation Wnt Pathway

2019 ◽  
Vol 9 (8) ◽  
pp. 1094-1099
Author(s):  
Zeqian Yu ◽  
Susu Zhao

Aim: The purpose of our work was to research the effects and mechanisms of lncRNA NEF in pancreatic cancer treatment. Methods: Gathering the 35 pairs of clinical sample from pancreatic cancer patients. Evaluating the histopathology by HE staining and lncRNA NEF expression by ISH assay. The PANC-1 and Hs766T cells were respectively divided into NC, pIRSE2 and pIRSE2-NEF. Measuring cell viability, invasion cell number and wound healing rate by CCK8, transwell and wound healing assay. Evaluating Wnt and β-catenin protein expression by WB assay. Results: The lncRNA NEF level were significantly down-regulation in pancreatic cancer (P < 0.01). The cell viabilities of pIRSE2-NEF groups were significantly suppressed (P < 0.01); with lncRNA NEF supplement, the invasion cell number and wound healing rate of pIRSE2-NEF groups were significantly depressed compared with those of NC groups (P < 0.01). Meanwhile, the Wnt and β-catenin proteins levels of pIRSE2-NEF groups were significantly down-regulation (P < 0.01). Conclusion: lncRNA NEF inhibits pancreatic cancer cell biological activities via regulation Wnt/β-catenin pathway.

2019 ◽  
Vol 9 (8) ◽  
pp. 1073-1080
Author(s):  
Wei Liu ◽  
Bin Wang ◽  
Shaojing Ju

Background: Osteosarcoma is a type of primary bone tumor that usually occurs in the metaphyseal region of long bones. It has been unclear lncRNA MT1JP in osteosarcoma development. Material and Methods: The MG63 cell were respectively MT1JP, miRNA-383 and miRNA-383 inhibitor. Measuring the cell proliferation, apoptosis and cell cycle by MTT and flow cytometry and evaluation the MG63 cell invasion and migration by transwell and wound healing assay in difference groups. The relative proteins (Wnt, β-catenin, Cyclin D1, MMP-2 and MMP-9) were measured by Western blot (WB) assay. By luciferase target assay, analysis the correlation between miRNA-383 and Wnt in MG63 cell. Results: Compared with WT group, the cell proliferation rate of pcDNAMT1JP and miRNA-383 groups were significantly down-regulation with cell apoptosis rates and G1 phase rates were significantly increased (P < 0.01, respectively). By transwell and wound healing assay, the invasion cell number and wound healing rate of pcDNA-MT1JP and miRNA-383 groups were significantly depressed (P < 0.01, respectively). By WB assay, Wnt, β-catenin, c-Myc, MMP-2 and MMP-9 proteins expressions of pcDNA-MT1JP and miRNA-383 groups were significantly suppressed compared with those of WT group (P < 0.01, respectively). By luciferase target assay, Wnt was the targeted gene of miRNA-383 in MG63 cell. Conclusion: MT1JP could suppress osteosarcoma cell lines MG63 cell biological activities via stimulating miRNA-383 and depressing Wnt pathway.


2022 ◽  
Vol 12 (4) ◽  
pp. 701-710
Author(s):  
Ming Liu ◽  
Shenghu Guo ◽  
Jing Cao ◽  
Zheng Wu ◽  
Lei Zhang ◽  
...  

Objective: Our research was to discuss effects and mechanism of lncRNA TUG1 in NSCLC by vitro study. Methods: A549 and H1299 cells were divided into NC, pcDNA 3.1 and lncRNA TUG1 groups. Measuring cell proliferation using CCK-8 assay, cell apoptosis by flow cytometry, invasion cell number by transwell and wound healing rate by wound healing assay. Relative gene and protein expressions by RT-qPCR and WB assay. Results: Compared with NC group, the cell proliferation rate, invasion cell number and wound healing rate were significantly depressed in A549 and H1299 cell lines (P < 0.001, respectively). By RT-qPCR and WB assay, lncRNA TUG1 gene expression were significantly increased (P < 0.001, respectively); E-cadherin gene and protein expression were significantly up-regulation, and N-cadherin and Vimentin gene and protein expressions were significantly depressed compared with those of NC group in A549 and H1299 cell lines (P < 0.001, respectively). Conclusion: lncRNA TUG1 had effects to suppress NSCLC cell biological activities by regulation EMT relative gene and proteins expression in vivo study.


2019 ◽  
Vol 9 (11) ◽  
pp. 1512-1519
Author(s):  
Caiyan Xu ◽  
Jianjun Zhai ◽  
Yujing Fu

Objection: The purpose of this work was to discuss the effects and relative mechanisms of F11-AS1 in cervical cancer treatment by vitro study. Methods: 20 pairs of cervical carcinoma and adjacent normal tissue were collected and measured pathology and F11-AS1 expression by HE and HIS staining. Measuring F11-AS1 expression in difference cell lines and cell groups by RT-qPCR assay. Transfection F11-AS1 in Hela cells, evaluating hela cell biological including proliferation, apoptosis, invasion and migration by MTT, flow cytometry, transwell and wound healing assay. PTEN, p-PI3K and AKT proteins expression were evaluated by WB assay, and p-PI3K nuclear volume were measured by cellular immunofluorescence assay. Results: F11-AS1 level of cancer tissues were significantly down-regulation with state increasing by ISH assay (P < 0.01, respectively). After transfection with F11-AS1, the Hela cell proliferation rate was significantly down-regulation with apoptosis significantly increasing (P < 0.05); The invasion Hela cell number and wound healing rate were significantly depressed with F11-AS1 transfection (P < 0.05). By WB assay, PTEN protein expression was significantly increasing, and p-PI3K and AKT proteins expression were significantly inhibited (P < 0.05). By cellular immunofluorescence assay, p-PI3K nuclear volume of pcDNA3.1/F11-AS1 group was significantly depressed (P < 0.05). Conclusion: lncRNA F11-AS1 suppressed cervical cancer biological activities by regulation PTEN/p-PI3K/AKT pathway in vitro study.


2020 ◽  
Vol 2 (3) ◽  
pp. 01-03
Author(s):  
Ravi Chittoria

Pressure ulcer or pressure sore is one of the complications seen in bedridden patients. Management of these ulcers is often challenging. But there is no well-established method that accelerates the wound healing rate. Various adjunctive methods are used for wound bed preparation before definitive reconstruction plan is made. Here we describe our experience in the role of insulin therapy as an adjunct in the management of pressure sores.


2013 ◽  
Vol 61 (10) ◽  
pp. E2105
Author(s):  
Norihiro Kobayashi ◽  
Muramatsu Toshiya ◽  
Tsukahara Reiko ◽  
Ito Yoshiaki ◽  
Hirano Keisuke

2018 ◽  
Vol 47 (1) ◽  
pp. 201-211 ◽  
Author(s):  
Takahiro Mizoguchi ◽  
Koji Ueno ◽  
Yuriko Takeuchi ◽  
Makoto Samura ◽  
Ryo Suzuki ◽  
...  

Background/Aims: We have developed a mixed-cell sheet consisting of autologous fibroblasts and peripheral blood mononuclear cells with a high potency for angiogenesis and wound healing against refractory cutaneous ulcers in mouse and rabbit models. To increase the effectiveness of the mixed sheet, we developed a multilayered mixed sheet. Methods: We assessed the therapeutic effects of multilayered sheets on cutaneous ulcers in mice. Growth factors and chemokines were assessed by enzyme-linked immunosorbent assay. Angiogenesis and fibroblast migration were measured by using tube formation and migration assays. Wound healing rate of cutaneous ulcers was evaluated in mice with diabetes mellitus. Results: The concentration of secreted vascular endothelial growth factor, hepatocyte growth factor, transforming growth factor, C-X-C motif chemokine ligand (CXCL)-1, and CXCL-2 in multilayered sheets was much higher than that in single-layered mixed-cell sheets (single-layered sheets) and multilayered sheets of fibroblasts alone (fibroblast sheets). The supernatant in multilayered sheets enhanced angiogenic potency and fibroblast migration compared with single-layered and fibroblast sheets in an in vitro experiment. The wound healing rate in the multilayered sheet-treated group was higher compared with the no-treatment group (control) at the early stage of healing. Moreover, both vessel lumen area and microvessel density in tissues treated with multilayered sheets were significantly increased compared with tissues in the control group. Conclusion: Multilayered sheets promoted wound healing and microvascular angiogenesis in the skin by supplying growth factors and cytokines. Accordingly, our data suggest that multilayered sheets may be a promising therapeutic material for refractory cutaneous ulcers.


Author(s):  
Jie Zhang ◽  
Xiaolin Feng ◽  
Yuxia Wang ◽  
Dakang Chen ◽  
Bo Zhang

Research purposes: Autologous platelet-rich plasma gel (Platelet-Rich Plasma, PRP) was prepared and used for transplantation for the treatment of traumatic trauma wounds of extremities. Explore platelet-rich plasma gel (PRP) to promote the healing of exposed bone and tendon wounds. Methods: Fifteen patients with extremity bone and tendon exposed wounds were treated with autologous platelet-rich plasma gel (PRP) transplantation to observe the wound healing rate and wound healing time. Results: Among the 15 patients, 8 cases healed directly, 7 cases had active granulation growth, and second-stage skin graft wound healing; the wound healing rate was 100%, and the average wound healing time was 36 days. Conclusion: Autologous platelet-rich plasma gel (PRP) transplantation for the treatment of traumatic trauma hard wounds of the extremities, can inhibit the bacterial growth of the wounds, effectively promote the repair of soft tissue defects and accelerate the healing of bone and tendon wounds of the extremities.


2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 15146-15146
Author(s):  
L. Maute ◽  
W. Glienke ◽  
E. Milz ◽  
N. Bauer ◽  
L. Bergmann

15146 The rapamycin derived mTOR inhibitor RAD001 (everolimus) is cytotoxic to a number of cell lines. Because survivin, an important mediator of apoptosis and cell survival, is one of the targets down-regulated by RAD001, we tested the ability of a combination of RAD001 and siRNA mediated inhibition of survivin to enhance the cytotoxic effects. We have used four pancreatic cancer cell lines, MiaPaCa-2, BxPC-3, AsPC-1 and Panc-1. We found that the cytotoxic effect was enhanced in all cell lines after treatment with RAD001 and survivin siRNA. An efficient way of treatment was the initial down-regulation of survivin with RAD001 and a subsequent incubation with survivin siRNA. We conclude, that the transformation efficiency of siRNA, still a limiting factor in using this method, is more sufficiently combining both ways to down-regulate survivin. Our data indicate that a combination of mTOR inhibitors like RAD001 and survivin-targeted down-regulation with siRNA may improve the efficacy of therapy in pancreatic cancer. No significant financial relationships to disclose.


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