scholarly journals Distinct expression pattern and prognostic values of pituitary tumor transforming gene family genes in non‑small cell lung cancer

2019 ◽  
Author(s):  
Shaolong Yang ◽  
Xiaodi Wang ◽  
Jingxing Liu ◽  
Bisha Ding ◽  
Kairi Shi ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Gene Family ◽  
Expression Pattern ◽  
Cell Lung Cancer ◽  
Pituitary Tumor ◽  
Small Cell ◽  
Small Cell Lung ◽  
Pituitary Tumor Transforming Gene ◽  
Transforming Gene

Redox regulation of matrix metalloproteinase gene family in small cell lung cancer cells

2005 ◽  
Vol 39 (4) ◽  
pp. 373-381 ◽  
Author(s):  
Niramol Savaraj ◽  
Yingjie Wei ◽  
Hitoshi Unate ◽  
Pei-Man Liu ◽  
C.J. Wu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Matrix Metalloproteinase ◽  
Small Cell Lung Cancer ◽  
Gene Family ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Redox Regulation ◽  
Small Cell ◽  
Lung Cancer Cells ◽  
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.

scholarly journals Neuroepithelial transforming gene 1 functions as a potential prognostic marker for patients with non-small cell lung cancer

2015 ◽  
Vol 12 (5) ◽  
pp. 7439-7446 ◽  
Author(s):  
LI FANG ◽  
JIALIANG ZHU ◽  
YUCHAO MA ◽  
CAO HONG ◽  
SHENG XIAO ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Prognostic Marker ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung ◽  
Transforming Gene

scholarly journals Multiple mechanisms for transcriptional regulation of the myc gene family in small-cell lung cancer.

1988 ◽  
Vol 8 (8) ◽  
pp. 3373-3381 ◽  
Author(s):  
G Krystal ◽  
M Birrer ◽  
J Way ◽  
M Nau ◽  
E Sausville ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Gene Family ◽  
Gene Amplification ◽  
Cell Lung Cancer ◽  
Promoter Activity ◽  
Small Cell ◽  
Mrna Levels ◽  
Small Cell Lung ◽  
Myc Gene

The molecular mechanisms reported to regulate the expression of myc family genes are multiple and complex and include gene amplification, transcriptional activation, transcriptional attenuation, and mRNA stability. We have investigated which of these mechanisms are responsible for the extreme variation in myc gene family mRNA levels observed in human small-cell lung cancer cell lines. In addition to gene amplification, a block to nascent mRNA chain elongation, causing attenuation of transcription, is an important regulatory mechanism controlling the steady-state levels of c-myc and L-myc mRNA. The loss of transcriptional attenuation is correlated with overexpression of these two genes in cell lines which do not show gene amplification. Expression of c-myc mRNA appears to be dependent on promoter activity and attenuator function. In contrast, regulation of expression of the N-myc gene does not involve transcriptional attenuation; steady-state mRNA levels are correlated with promoter activity as well as gene amplification. We conclude that transcriptional regulation of each member of the myc gene family is accomplished by a different assortment of complex mechanisms, including gene copy number, promoter activation, and transcriptional attenuation. Interference at multiple points in this complex regulatory process appears to be an important mechanism by which small-cell lung cancer and other human tumors evade growth control.

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