Hypermethylation of RASSF1A and BLU tumor suppressor genes in non‐small cell lung cancer: Implications for tobacco smoking during adolescence

2004 ◽  
Vol 114 (2) ◽  
pp. 219-223 ◽  
Author(s):  
Carmen J. Marsit ◽  
Duk‐Hwan Kim ◽  
Mei Liu ◽  
Philip W. Hinds ◽  
John K. Wiencke ◽  
...  
2019 ◽  
Vol 117 (1) ◽  
pp. 513-521 ◽  
Author(s):  
Sheng Rong Ng ◽  
William M. Rideout ◽  
Elliot H. Akama-Garren ◽  
Arjun Bhutkar ◽  
Kim L. Mercer ◽  
...  

Small cell lung cancer (SCLC) is a highly aggressive subtype of lung cancer that remains among the most lethal of solid tumor malignancies. Recent genomic sequencing studies have identified many recurrently mutated genes in human SCLC tumors. However, the functional roles of most of these genes remain to be validated. Here, we have adapted the CRISPR-Cas9 system to a well-established murine model of SCLC to rapidly model loss-of-function mutations in candidate genes identified from SCLC sequencing studies. We show that loss of the genep107significantly accelerates tumor progression. Notably, compared with loss of the closely related genep130, loss ofp107results in fewer but larger tumors as well as earlier metastatic spread. In addition, we observe differences in proliferation and apoptosis as well as altered distribution of initiated tumors in the lung, resulting from loss ofp107orp130. Collectively, these data demonstrate the feasibility of using the CRISPR-Cas9 system to model loss of candidate tumor suppressor genes in SCLC, and we anticipate that this approach will facilitate efforts to investigate mechanisms driving tumor progression in this deadly disease.


2003 ◽  
Vol 37 (6) ◽  
pp. 836-840 ◽  
Author(s):  
V. V. Zemlyakova ◽  
A. I. Zhevlova ◽  
I. B. Zborovskaya ◽  
V. V. Strelnikov ◽  
K. K. Laktionov ◽  
...  

BMC Cancer ◽  
2010 ◽  
Vol 10 (1) ◽  
Author(s):  
Vera N Senchenko ◽  
Ekaterina A Anedchenko ◽  
Tatiana T Kondratieva ◽  
George S Krasnov ◽  
Alexei A Dmitriev ◽  
...  

2020 ◽  
Author(s):  
Federica Lo Sardo ◽  
Claudio Pulito ◽  
Andrea Sacconi ◽  
Etleva Korita ◽  
Marius Sudol ◽  
...  

AbstractLung cancer is the leading cause of cancer-related deaths, worldwide. Non–small cell lung cancer (NSCLC) is the most prevalent lung cancer subtype. YAP and TAZ have been implicated in lung cancer by acting as transcriptional co-activators of oncogenes or as transcriptional co-repressors of tumor suppressor genes. Previously we reported that YAP and TAZ regulate microRNAs expression in NSCLC. Among the set of regulated miRNAs, the oncogenic miR-25, 93, and 106b, clustering within the MCM7 gene were selected for further studies. We firstly identified Transforming Growth Factor-β (TGF-β) Receptor 2 (TGFBR2), a member of the TGF-β signaling, as a target of the miRNA cluster, which exhibited prognostic value because of its tumor suppressor activity. We found that YAP/TAZ-mediated repression of TGFBR2 occurs both: post-transcriptionally through the miR-106b-25 cluster and transcriptionally by engaging the EZH2 epigenetic repressor that we reported here as a novel target gene of YAP/TAZ. Furthermore, we document that YAP/TAZ and EZH2 cooperate in lung tumorigenesis by transcriptionally repressing a specific subset of tumor suppressor genes, including TGFBR2. Our findings point to YAP/TAZ and EZH2 as potential therapeutic targets for NSCLC treatment.


2016 ◽  
Vol 33 (7) ◽  
Author(s):  
Dorota Pastuszak-Lewandoska ◽  
Jacek Kordiak ◽  
Adam Antczak ◽  
Monika Migdalska-Sęk ◽  
Karolina H. Czarnecka ◽  
...  

2002 ◽  
Vol 184 (2) ◽  
pp. 189-195 ◽  
Author(s):  
Qian An ◽  
Yong Liu ◽  
Yanning Gao ◽  
Jinfeng Huang ◽  
Xiaoli Fong ◽  
...  

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