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HYPERMETHYLATION OF p14^(ARF) PROMOTER REGION AND EXPRESION OF p14^(ARF) GENE PRODUCT IN NON-SMALL CELL LUNG CANCER 被引量:1

HYPERMETHYLATION OF p14^(ARF) PROMOTER REGION AND EXPRESION OF p14^(ARF) GENE PRODUCT IN NON-SMALL CELL LUNG CANCER
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摘要 Objective: This study was designed to investigate promoter methylation status and protein expression of p14^ARF gene in non-small cell lung cancer, and value the role of p14^ARF promoter methylation in carcinogenesis of non-small cell lung cancer. Methods: Promoter methylation status and protein expression of p14^ARF gene in 40 cases of non-small cell lung cancer were analyzed by methylation specific polymerase china reaction (MSP), restriction enzyme-related polymerase chain reaction (RE-PCR) and immunohistochemistry (IHC). Results: The positive rates of p14^ARF promoter methylation in tumor tissues and normal tissues adjacent to cancer were 17.5% (7/40) and 2.5% (1/40) respectively. There were statistically significant differences between them, P〈0.05. The results of RE-PCR were consistent with that of MSP. The expression rate of p14^ARF protein in tumor tissues was significantly lower than that in normal tissues adjacent to cancer, p〈0.01. Promoter methylation status and protein expression of p14^ARF gene in non-small cell lung cancer showed significantly an inverse correlation (r=-0.56, P〈0.01), and both of them did not relate statistically with the clinicopathologic characteristics of patients such as histological classification, clinical stage, differentiation grade and lymph node involvement. Conclusion: Promoter methylation is a crucial mechanism of inactivation of p14^ARF gene. Promoter methylation of p14^ARF gene might he involved in carcinogenesis of non-small cell lung cancer, and is an early event in development process of non-small cell lung cancer. It might be used as a new target in gene treatments in the future. Objective: This study was designed to investigate promoter methylation status and protein expression of p14^ARF gene in non-small cell lung cancer, and value the role of p14^ARF promoter methylation in carcinogenesis of non-small cell lung cancer. Methods: Promoter methylation status and protein expression of p14^ARF gene in 40 cases of non-small cell lung cancer were analyzed by methylation specific polymerase china reaction (MSP), restriction enzyme-related polymerase chain reaction (RE-PCR) and immunohistochemistry (IHC). Results: The positive rates of p14^ARF promoter methylation in tumor tissues and normal tissues adjacent to cancer were 17.5% (7/40) and 2.5% (1/40) respectively. There were statistically significant differences between them, P〈0.05. The results of RE-PCR were consistent with that of MSP. The expression rate of p14^ARF protein in tumor tissues was significantly lower than that in normal tissues adjacent to cancer, p〈0.01. Promoter methylation status and protein expression of p14^ARF gene in non-small cell lung cancer showed significantly an inverse correlation (r=-0.56, P〈0.01), and both of them did not relate statistically with the clinicopathologic characteristics of patients such as histological classification, clinical stage, differentiation grade and lymph node involvement. Conclusion: Promoter methylation is a crucial mechanism of inactivation of p14^ARF gene. Promoter methylation of p14^ARF gene might he involved in carcinogenesis of non-small cell lung cancer, and is an early event in development process of non-small cell lung cancer. It might be used as a new target in gene treatments in the future.
出处 《Chinese Journal of Cancer Research》 SCIE CAS CSCD 2006年第4期276-281,共6页 中国癌症研究(英文版)
关键词 Lung neoplasms Non-small cell lung cancer Tumor suppressor gene P14^ARF METHYLATION HISTOPATHOLOGY Lung neoplasms Non-small cell lung cancer Tumor suppressor gene p14^ARF Methylation Histopathology
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  • 1Kaye FJ. RB and cyclin dependent kinase pathways:defining a distinction between Rb and p16 loss in lung cancer [J]. Oncogene 2002; 21:6908-14.
  • 2Divine KK, Pulling LC, Marron-Terada PG, et al.Multiplicity of abnormal promoter methylation in lung adenocarcinomas from smokers and never smokers[J]. Int J Cancer 2005; 114:400-5.
  • 3Park MJ, Shimizu K, Nakano T, et al. Pathogenetic and biologic significance o TP14ARF alterations in nonsmall cell lung carcinoma[J]. Cancer Genet Cytogenet 2003;141:5-13.
  • 4Serrano M. The INK4A/ARF locus in murine tumorigenesis[J]. Carcinogeenesis 2000; 21:865-9.
  • 5Quelle DE, Ashmun RA, Harmon GJ, et al. Cloning and characterization of murine p16INK4a and p15INK4b genes[J]. Oncogene 1995; 111:635-45.
  • 6Kamijo T, Zindy F, Roussel MF, et al. Tumor suppressionatt the mouse INK4a locus mediated by the alternative reading frame product p19ARF[J]. Cell 1997; 91:649-59.
  • 7Zhang Y, Xiong Y, Yarbrough WG ARF promocs MDM2 degradstion and stabilizes p53: ARF-INK4a locus deletion impairs both the Rb and p35 tumor suppression pathways[J]. 1998; 92:725-34.
  • 8Belinsky SA, Palmisano WA, Gilliland FD, et al. Aberrant promoter methylation in bronchial epithelium and sputum from current and former smokers[J]. Cancer Res 2002;21; 7421-34.
  • 9Osada H, Takahashi T. Genetic alterations of multiple tumor suppressors and oncogenes in the carcinogenesis and progression of lung cancer[J]. Oncogene 2002;21:7421-34.
  • 10Robertson KD, Jones PA. The human ARF cell cycle regulatory gene promoter is a CpG island which can be silenced by DNA methylation and downregulated by wild-type p53[J]. Mol Cell Biol 1998; 18:6457-73.

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