scholarly journals Ectopic Expression of miRNA-21 and miRNA-205 in Non-Small Cell Lung Cancer

2019 ◽  
Vol In Press (In Press) ◽  
Author(s):  
Abdolreza Mohamadnia ◽  
Seyedeh Afrooz Azimi ◽  
Hamid Reza Sadegh Nia ◽  
Hamid Reza Jamaati ◽  
Hossein Dargahi ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Ectopic Expression ◽  
Small Cell ◽  
Small Cell Lung

Ectopic expression of c-kit in small-cell lung cancer

1994 ◽  
Vol 57 (S8) ◽  
pp. 108-109 ◽  
Author(s):  
Toyoaki Hida ◽  
Ryuzo Ueda ◽  
Yoshitaka Sekido ◽  
Kenji Hibi ◽  
Ryohei Matsuda ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Ectopic Expression ◽  
Small Cell ◽  
Small Cell Lung

scholarly journals Neuroepithelial Cell Transforming Gene 1 Acts as an Oncogene and Is Mediated by miR-22 in Human Non-Small-Cell Lung Cancer

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Shengguang Ding ◽  
Haitao Huang ◽  
Yiming Xu ◽  
Liang Shen ◽  
Chongjun Zhong ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Ectopic Expression ◽  
Small Cell ◽  
Neuroepithelial Cell ◽  
Small Cell Lung ◽  
And Migration ◽  
Cell Transforming ◽  
Transforming Gene

Abnormal expression of neuroepithelial cell transforming gene 1 (NET1) has been authenticated in many human cancers, including lung cancer. We have previously reported that NET1 functioned as an oncogene and promoted human non-small-cell lung cancer (NSCLC) growth and migration. However, the correlation between NET1 and its upstream miRNAs needed further illustration. Our present work demonstrated that miR-22 had a relatively low expression, and NET1 had a relatively high expression in both NSCLC samples and lung adenocarcinoma cell lines compared with corresponding normal controls. Moreover, miR-22 directly regulated NET1 and was verified to weaken cancer cell proliferation and migration, as well as enhance cell apoptosis by suppressing NET1. Furthermore, the inhibitory effect of miR-22 can be reversed via overexpressing NET1 using an ectopic expression vector in NSCLC cells. Our findings showed that miR-22/NET-1 axis may contribute to the inhibition of NSCLC growth and migration and represents a promising therapeutic target for NSCLC.

Regulation of p27 by S-Phase Kinase-Associated Protein 2 Is Associated With Aggressiveness in Non–Small-Cell Lung Cancer

2004 ◽  
Vol 22 (20) ◽  
pp. 4165-4173 ◽  
Author(s):  
Atsushi Osoegawa ◽  
Ichiro Yoshino ◽  
Shinji Tanaka ◽  
Kenji Sugio ◽  
Toshifumi Kameyama ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Protein Level ◽  
Ectopic Expression ◽  
Small Cell ◽  
S Phase ◽  
Small Cell Lung ◽  
Skp2 Expression

PurposeThe F-box protein S-phase kinase-associated protein 2 (Skp2) is one of the positive regulators of the cell cycle that promote ubiquitin-mediated proteolysis of the cyclin-dependent kinase inhibitor p27. In this study, we investigated the significance of Skp2 expression in human non–small-cell lung cancer (NSCLC).Patients and MethodsClinicopathologic features and immunohistochemical expression of Skp2 and p27 proteins were studied in 138 patients with NSCLC. Survival analyses were performed using the Kaplan-Meier method and the Cox regression model. To analyze the role of Skp2 in vitro, NSCLC cells were transfected with an Skp2-expressing vector or small interfering RNA.ResultsSkp2 was overexpressed in males, smokers, patients with squamous cell carcinomas, and patients with poorly differentiated cancers (P = .034, < .0001, < .0001, and .002, respectively). The multivariant analysis revealed that Skp2 expression is an independent prognostic factor for survival in NSCLC. An inverse relationship of Skp2 with p27 expression was observed (P = .012), and patients with both a higher expression of Skp2 and a lower expression of p27 showed a significantly unfavorable prognosis (P = .0002). In vitro ectopic expression of Skp2 in NSCLC cells reduced the protein level of p27. Conversely, induction of Skp2 siRNA increased the protein level of p27, leading to growth inhibition in NSCLC cells.ConclusionSkp2 overexpression is closely associated with the suppression of p27 and the aggressiveness in NSCLC. It also could be a therapeutic target in NSCLC.

scholarly journals MT1DP loaded by folate-modified liposomes sensitizes erastin-induced ferroptosis via regulating miR-365a-3p/NRF2 axis in non-small cell lung cancer cells

2020 ◽  
Vol 11 (9) ◽  
Author(s):  
Chengcheng Gai ◽  
Chuanliang Liu ◽  
Xinghan Wu ◽  
Mengyu Yu ◽  
Jie Zheng ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Iron Concentration ◽  
Ectopic Expression ◽  
Small Cell ◽  
Luciferase Reporter ◽  
Related Factor ◽  
Small Cell Lung

Abstract Although ferroptosis has been recognized as a novel antitumoral treatment, high expression of nuclear factor erythroid 2-related factor 2 (NRF2) has been reported to be an antioxidant transcript factor that protects malignant cells from ferroptosis. Previous findings indicated that metallothionein 1D pseudogene (MT1DP), a long noncoding RNA (lncRNA), functioned to aggravate oxidative stress by repressing antioxidation. Here we aimed at assessing whether MT1DP could regulate erastin-induced ferroptosis on non-small cell lung cancer (NSCLC) and elucidating the mechanism. We found that ectopic expression of MT1DP sensitized A549 and H1299 cells to erastin-induced ferroptosis through downregulation of NRF2; in addition, ectopic MT1DP upregulated malondialdehyde (MDA) and reactive oxygen species (ROS) levels, increased intracellular ferrous iron concentration, and reduced glutathione (GSH) levels in cancer cells exposed to erastin, whereas downregulation of MT1DP showed the opposite effect. RNA pulldown assay and dual-luciferase reporter assay confirmed that MT1DP modulated the expression of NRF2 via stabilizing miR-365a-3p. As low solubility of erastin limits its efficient application, we further prepared folate (FA)-modified liposome (FA-LP) nanoparticles for targeted co-delivery of erastin and MT1DP to enhance the bioavailability and the efficiency of the drug/gene combination. Erastin/MT1DP@FA-LPs (E/M@FA-LPs) sensitized erastin-induced ferroptosis with decreased cellular GSH levels and elevated lipid ROS. In vivo analysis showed that E/M@FA-LPs had a favorable therapeutic effect on lung cancer xenografts. In short, our findings identify a novel strategy to elevate erastin-induced ferroptosis in NSCLCs acting through the MT1DP/miR-365a-3p/NRF2 axis.

Sign in / Sign up

Export Citation Format

Share Document