Dataset Information

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

ABSTRACT: 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.

SUBMITTER: Ding S

PROVIDER: S-EPMC7201585 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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

Ding Shengguang S Huang Haitao H Xu Yiming Y Shen Liang L Zhong Chongjun C Zheng Shiying S

BioMed research international 20200111

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 NSCL ...[more]

PMID: 32420320

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Project description:BackgroundFerroptosis is a newly generated regulatory cell death promoted by the accumulated lipid-based reactive oxygen species (ROS). Solute carrier family 7 member 11 (SLC7A11), the cystine/glutamate antiporter, is known as a ferroptosis executor that exhibits a positive correlation with carcinoma progression because of antioxidant function. Nonetheless, it is yet unclear on the understanding of ferroptosis regulation in lung cancer.MethodsDatabase, qRT-PCR, Western-blot (WB), and immunohistochemistry were utilized to determine SLC7A11 expression and function, as well as gene iron related to necrosis in clinical tissue specimens and cells; a ferroptosis inducer, inhibitors, and SLC7A11 lentivirus were used to confirm SLC7A11's biological activity in cell viability, oxidative stress, lipid peroxidation, and iron ion enrichment in non-small cell lung cancer (NSCLC) in different cells; lentivirus was used to infect lung adenocarcinoma cell lines to acquire miR-27a-3p overexpression and knockdown cell lines, and to detect SLC7A11 level through qRT-PCR and WB. The influence of upregulated/downregulated miR-27a-3p on ferroptosis and other related biological characteristics of lung adenocarcinoma cell lines was detected.ResultsUpregulated SLC7A11 was shown in NSCLC patients and cells, and increased SLC7A11 had a relation to the poorly prognostic status of NSCLC patients. Besides, a novel miRNA, miR-27a-3p, was an essential modulator of ferroptosis via directly targeting SLC7A11 in NSCLC cells. Overexpressing miR-27a-3p led to SLC7A11 suppression via directly binding to its 3'-UTR, followed by the reduction of erastin-caused ferroptosis. In contrast, inhibited miR-27a-3p resulted in an increase in NSCLC cells' sensitivity to erastin. Of importance, the accumulated lipid ROS and cell death of iron peptide mediated by anti-miR-27a-3p can be eliminated by impeding the glutamylation process. Our literature collectively uncovered that miR-27a-3p modulated ferroptosis by targeting SLC7A11 in NSCLC cells, illustrating the important role of miRNA in ferroptosis.ConclusionMiR-27a-3p modulates ferroptosis via targeting SLC7A11 in NSCLC cells, implying the significant role of miR-27a-3p/SLC7A11 in ferroptosis.

Dataset Information

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

Publications

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

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