Mol. Cells 2011; 32(4): 343-348
Published online October 17, 2011
https://doi.org/10.1007/s10059-011-0073-z
© The Korean Society for Molecular and Cellular Biology
Su Man Lee1, Yeon Kyung Na2, Hae Sook Hong2, Eun Jeong Jang3, Ghil Suk Yoon3, Jae Yong Park4,*, and Dong Sun Kim1,*
Correspondence to : *Correspondence: doskim@knu.ac.kr (DSK); jaeyong@knu.ac.kr (JYP)
Lung cancer is the leading cause of cancer-related deaths worldwide and is usually associated with a late diagnosis and a poor prognosis. Thymosin beta10 (TMSB10) is a mono-meric actin sequestering protein that regulates actin cytoskeleton organization. The aberrant TMSB10 expression has been implicated in the pathogenesis of human cancers. However, its role in carcinogenesis is still controversial. To better understand the role of TMSB10 in lung tumorigenesis and its regulatory mechanism, we examined the methylation status and expression of the TMSB10 gene in non-small cell lung cancers (NSCLCs) using methylation-specific PCR (MSP) and immunohistochemistry (IHC), respectively. MSP analysis showed that the TMSB10 promoter was already unmethylated in most tumor tissues and became demethylated in 20 (14.4%) of the 139 NSCLCs. TMSB10 hypomethylation was not significantly correlated with the clinicopathological features. IHC showed that the TMSB10 protein was strongly expressed in the cytoplasm of malignant cells and its overexpression was detected in 50.0% of the tumor tissues compared to normal tissues. TMSB10 overexpression was frequently observed in sqau-mous cell carcinomas compared to adenocarcinomas with border line significance (P = 0.072). However, TMSB10 methylation status was not linked to its overexpression. Collectively, these results suggest that TMSB10 hypome-thylation may be a frequent event in NSCLCs, but it may not be a common mechanism underlying TMSB10 overexpression. However, further studies with large num-bers of patients are needed to confirm our findings.
Keywords hypomethylation, immunohistochemistry, methylation-specific PCR, non-small cell lung cancer, thymosin beta10
Mol. Cells 2011; 32(4): 343-348
Published online October 31, 2011 https://doi.org/10.1007/s10059-011-0073-z
Copyright © The Korean Society for Molecular and Cellular Biology.
Su Man Lee1, Yeon Kyung Na2, Hae Sook Hong2, Eun Jeong Jang3, Ghil Suk Yoon3, Jae Yong Park4,*, and Dong Sun Kim1,*
1Department of Anatomy, School of Medicine, Kyungpook National University, Daegu 702-422, Korea, 2College of Nursing, Kyungpook National University, Daegu 702-422, Korea, 3Department of Pathology, School of Medicine, Kyungpook National University, Daegu 702-422, Korea, 4Department of Internal Medicine, School of Medicine, Kyungpook National University, Daegu 702-422, Korea
Correspondence to:*Correspondence: doskim@knu.ac.kr (DSK); jaeyong@knu.ac.kr (JYP)
Lung cancer is the leading cause of cancer-related deaths worldwide and is usually associated with a late diagnosis and a poor prognosis. Thymosin beta10 (TMSB10) is a mono-meric actin sequestering protein that regulates actin cytoskeleton organization. The aberrant TMSB10 expression has been implicated in the pathogenesis of human cancers. However, its role in carcinogenesis is still controversial. To better understand the role of TMSB10 in lung tumorigenesis and its regulatory mechanism, we examined the methylation status and expression of the TMSB10 gene in non-small cell lung cancers (NSCLCs) using methylation-specific PCR (MSP) and immunohistochemistry (IHC), respectively. MSP analysis showed that the TMSB10 promoter was already unmethylated in most tumor tissues and became demethylated in 20 (14.4%) of the 139 NSCLCs. TMSB10 hypomethylation was not significantly correlated with the clinicopathological features. IHC showed that the TMSB10 protein was strongly expressed in the cytoplasm of malignant cells and its overexpression was detected in 50.0% of the tumor tissues compared to normal tissues. TMSB10 overexpression was frequently observed in sqau-mous cell carcinomas compared to adenocarcinomas with border line significance (P = 0.072). However, TMSB10 methylation status was not linked to its overexpression. Collectively, these results suggest that TMSB10 hypome-thylation may be a frequent event in NSCLCs, but it may not be a common mechanism underlying TMSB10 overexpression. However, further studies with large num-bers of patients are needed to confirm our findings.
Keywords: hypomethylation, immunohistochemistry, methylation-specific PCR, non-small cell lung cancer, thymosin beta10
Su Man Lee, Jae Yong Park*, and Dong Sun Kim*
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