Methylation Status of theSOCS3 Gene Promoter in H2228 Cells and EML4-ALK-positive Lung Cancer Tissues
10.3779/j.issn.1009-3419.2016.09.01
- VernacularTitle:H2228细胞和EML4-ALK阳性肺癌组织中SOCS3基因启动子区甲基化状态的研究
- Author:
LIU CHUNLAI
1
;
LI YONGWEN
;
DONG YUNLONG
;
ZHANG HONGBING
;
LI YING
;
LIU HONGYU
;
CHEN JUN
Author Information
1. 天津医科大学总医院肺部肿瘤外科
- Keywords:
Lung neoplasms;
Echinoderm microtubule-associated-protein-like 4 (EML4);
Anaplastic lymphoma kinase (ALK);
Suppressor of cytokine signaling 3 (SOCS3);
DNA methylation
- From:
Chinese Journal of Lung Cancer
2016;19(9):565-570
- CountryChina
- Language:Chinese
-
Abstract:
Background and objective TheEML4-ALK fusion gene is a newly discovered driver gene of non-small cell lung cancer and exhibits special clinical and pathological features. hTe JAK-STAT signaling pathway, an important downstream signaling pathway of EML4-ALK, is aberrantly sustained and activated in EML4-ALK-positive lung cancer cells fusion gene, but the underlying reason remains unknown. hTe suppressor of cytokine signaling (SOCS) is a negative regula-tory factor that mainly inhibits the proliferation, differentiation, and induction of apoptotic cells by inhibiting the JAK-STAT signaling pathway. hTe aberrant methylation of theSOCS gene leads to inactivation of tumors and abnormal activation of the JAK2-STAT signaling pathway. hTe aim of this study is to investigate the methylation status of the SOCS3 promoter in EML4-ALK-positive H2228 cells and lung cancer tissues.Methods hTe methylation status of the SOCS3 promoter in EML4-ALK-positive H2228 lung cancer cells and lung cancer tissues was detected by methylation-speciifc PCR (MSP) analysis and veri-ifed by DNA sequencing. hTe expression levels of SOCS3 in H2228 cells were detected by Western blot and Real-time PCR analyses atfer treatment with the DNA methyltransferase inhibitor 5'-Aza-dC.Results MSP and DNA sequencing assay results indicated the presence of SOCS3 promoter methylation in H2228 cells as well as in three cases of seven EML4-ALK-positive lung cancer tissues. hTe expression level of SOCS3 signiifcantly increased in H2228 cells atfer 5′-Aza-dC treatment.Conclu-sion hTe aerrant methylation of the SOCS3 promoter region in EML4-ALK (+) H2228 cells and lung cancer tissues may be signiifcantly involved in the pathogenesis of EML4-ALK-positive lung cancer.
