scholarly journals miR-744-5p Inhibits Non-Small Cell Lung Cancer Proliferation and Invasion by Directly Targeting PAX2

2019 ◽  
Vol 18 ◽  
pp. 153303381987691 ◽  
Author(s):  
Shaolin Chen ◽  
Fei Shi ◽  
Weixing Zhang ◽  
Yuqi Zhou ◽  
Jing Huang

Non-small cell lung cancer is one of the leading causes of cancer-related death worldwide. MicroRNAs have been characterized as critical regulators for cancer progression including non-small cell lung cancer. This work explored microRNA-744-5p expression in non-small cell lung cancer cell lines and normal cell line using quantitative real-time polymerase chain reaction. Connection of microRNA-744-5p and paired box 2 was analyzed with bioinformatic analysis, luciferase activity reporter assay, and Western blot. Effects of microRNA-744-5p or paired box 2 expression on non-small cell lung cancer cell behaviors were analyzed using a series of in vitro experiments. MicroRNA-744-5p was found to have decreased expression in non-small cell lung cancer cell lines compared with normal cell line. Paired box 2 was identified as a direct target for microRNA-744-5p in non-small cell lung cancer. Overexpression of microRNA-744-5p inhibits non-small cell lung cancer cell proliferation, colony formation, and cell invasion in vitro through targeting paired box 2. The present study provided novel insights into the biological functions of microRNA-744-5p in non-small cell lung cancer.

2010 ◽  
Vol 28 (15_suppl) ◽  
pp. e21016-e21016 ◽  
Author(s):  
P. M. Marconi ◽  
K. Patel ◽  
L. Thimothy ◽  
S. Buchanan ◽  
M. J. Liptay ◽  
...  

Blood ◽  
1993 ◽  
Vol 82 (9) ◽  
pp. 2837-2844 ◽  
Author(s):  
MS Topp ◽  
M Koenigsmann ◽  
A Mire-Sluis ◽  
D Oberberg ◽  
F Eitelbach ◽  
...  

Abstract Cytokines play an important role in activating the immune system against malignant cells. One of these cytokines, interleukin-4 (IL-4) has entered clinical phase I trials because of its immunoregulatory potency. In the present study we report that recombinant human (rh) IL- 4 has major direct antiproliferative effects on one human lung cancer cell line (CCL 185) in vitro as measured by a human tumor cloning assay (HTCA), tritiated thymidine uptake, and counting cell numbers and marginal activity in a second cell line (HTB 56) in the HTCA. This activity could be abolished by neutralizing antibody against rhIL-4. The biological response of the tumor cells to the cytokine is correlated with expression of receptors for human IL-4 on both the mRNA level and the protein level. The responsive cell line, CCL 185, secretes IL-6 after being incubated with rhIL-4. On the other hand, neutralizing antibodies against IL-6 showed no influence on the growth modulatory efficacy of rhIL-4 in this cell line. Furthermore, CCL 185 does not show detectable production of IL-1, tumor necrosis factor alpha or interferon gamma after incubation with rhIL-4. Thus, the response to rhIL-4 is not mediated through autocrine production of these cytokines triggered by rhIL-4. In a next series of experiments some of the cell lines were xenotransplanted to BALB/c nu/nu mice. Subsequently, the mice were treated for 12 days with two doses of 0.5 mg/m2 rhIL-4 or control vehicle subcutaneously per day. Treatment with rhIL-4 yielded a significant inhibition of tumor growth versus control in two of the non-small cell lung cancer cell lines being responsive in vitro (CCL 185, HTB 56). Histology of the tumors in both groups showed no marked infiltration of the tumors with murine hematopoietic and lymphocytic cells consistent with the species specificity of IL-4. In contrast, no tumor growth inhibition was found in the small cell lung cancer cell lines (HTB 119, HTB 120) being nonresponsive in vitro. We conclude that rhIL-4 has direct antiproliferative effects on the growth of some human non-small cell lung cancer cell lines in vitro and in vivo, which together with its regulatory effects on various effector cell populations makes this cytokine an interesting candidate for further investigation in experimental cancer treatment.


2004 ◽  
Vol 3 (7) ◽  
pp. 624-631 ◽  
Author(s):  
Alan S. Lader ◽  
Marco F. Ramoni ◽  
Bruce R. Zetter ◽  
Isaac S. Kohane ◽  
David J. Kwiatkowski

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