Mol. Cells 2010; 30(1): 89-92
Published online July 14, 2010
https://doi.org/10.1007/s10059-010-0092-1
© The Korean Society for Molecular and Cellular Biology
Correspondence to : *Correspondence: doskim@knu.ac.kr (DSK); jaeyong@knu.ac.kr (JYP)
The growth arrest DNA-damage-inducible protein 45 (GADD45) can serve as a key coordinator of the stress response by regulating cell cycle progression, genomic stability, DNA repair, and other stress-related responses. Although deregulation of GADD45 expression has been reported in several types of human tumors, its role in lung cancer is still unknown. DNA hypermethylation of promoter CpG islands is known to be a major mechanism for epigenetic inactivation of tumor suppressor genes. We investigated the methylation status of GADD45 family genes (GADD45A, B, and G) in 139 patients with non-small cell lung cancer (NSCLC) using methylation-specific PCR (MSP) and correlated the results with clinicopathologic features of the patients. Methylation frequencies in tumors were 1.4% for GADD45A, 7.2% for GADD45B, and 31.6% for GADD45G. RT-PCR and MSP analysis showed that promoter methylation of the GADD45G gene resulted in down-regulation of its mRNA expression. GADD45G me-thylation was significantly more frequent in female pa-tients than male patients (P = 0.035). This finding suggests that methylation-associated down-regulation of the GADD45G gene may be involved in lung tumorigenesis.
Keywords GADD45 genes, methylation, non-small cell lung cancer
Mol. Cells 2010; 30(1): 89-92
Published online July 31, 2010 https://doi.org/10.1007/s10059-010-0092-1
Copyright © The Korean Society for Molecular and Cellular Biology.
Yeon Kyung Na, Su Man Lee, Hae Sook Hong1, Jae Bum Kim2, Jae Yong Park3,*, and Dong Sun Kim*
Department of Anatomy, School of Medicine, Kyungpook National University, Daegu 702-422, Korea, 1Colleage of Nursing, Kyungpook National University, Daegu 702-422, Korea, 2School of Biological Sciences, Seoul National University, Seoul 151-742, Korea, 3Internal Medicine, Kyungpook National University, Daegu 702-422, Korea
Correspondence to:*Correspondence: doskim@knu.ac.kr (DSK); jaeyong@knu.ac.kr (JYP)
The growth arrest DNA-damage-inducible protein 45 (GADD45) can serve as a key coordinator of the stress response by regulating cell cycle progression, genomic stability, DNA repair, and other stress-related responses. Although deregulation of GADD45 expression has been reported in several types of human tumors, its role in lung cancer is still unknown. DNA hypermethylation of promoter CpG islands is known to be a major mechanism for epigenetic inactivation of tumor suppressor genes. We investigated the methylation status of GADD45 family genes (GADD45A, B, and G) in 139 patients with non-small cell lung cancer (NSCLC) using methylation-specific PCR (MSP) and correlated the results with clinicopathologic features of the patients. Methylation frequencies in tumors were 1.4% for GADD45A, 7.2% for GADD45B, and 31.6% for GADD45G. RT-PCR and MSP analysis showed that promoter methylation of the GADD45G gene resulted in down-regulation of its mRNA expression. GADD45G me-thylation was significantly more frequent in female pa-tients than male patients (P = 0.035). This finding suggests that methylation-associated down-regulation of the GADD45G gene may be involved in lung tumorigenesis.
Keywords: GADD45 genes, methylation, non-small cell lung cancer
Su Man Lee, Jae Yong Park*, and Dong Sun Kim*
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