PDF(Pubmed)
Abstract：
UNASSIGNED: The progression and pathogenesis of oral cancer is greatly impacted by epigenetic modifications, such as DNA methylation. Autophagy, is an adaptive mechanism used to maintain the survival and integrity of cells. Oral squamous cell carcinoma is linked to a number of autophagy indicators, although it is yet unknown if DNA methylation of autophagy-related genes promotes the development of oral leukoplakia (OL), oral squamous cell carcinoma (OSCC).
UNASSIGNED: Our study was aimed to assess, compare and evaluate the DNA methylation of ATG5 and MAP1LC3Av1 genes in oral leukoplakia, oral squamous cell carcinoma.
UNASSIGNED: This cross-sectional study was designed with sample size of 48 tissues which was clinically and histopathologically diagnosed as OL, OSCC and normal tissue. The samples were divided into three groups (Group A, Group B, and Group C; (n = 16 each). Following histopathological confirmation, the tissue was stored in the RNA reagent, then subjected to DNA extraction, methylation-sensitive polymerase chain reaction (MS-PCR). DNA methylation of the ATG5 and MAP1LC3Av1 genes were assessed.
UNASSIGNED: Shapiro-Wilk and Kolmogorov-Smirnov tests showed that the values were normally distributed. Both the ATG5 and MAP1LC3Av1 genes were methylated in OSCC, OL tissues compared to normal tissues. A statistically significant results was seen among the three study groups.
UNASSIGNED: A significant difference was noted in the hypermethylation status of the promoter regions of the ATG5 and MAP1LC3Av1 genes. This provides some insight into their crucial role in the development of tumors. Future research with larger sample is needed to assess its potential clinical implications in oral carcinoma.
UNASSIGNED: Our study was aimed to assess, compare and evaluate the DNA methylation of ATG5 and MAP1LC3Av1 genes in oral leukoplakia, oral squamous cell carcinoma.
UNASSIGNED: This cross-sectional study was designed with sample size of 48 tissues which was clinically and histopathologically diagnosed as OL, OSCC and normal tissue. The samples were divided into three groups (Group A, Group B, and Group C; (n = 16 each). Following histopathological confirmation, the tissue was stored in the RNA reagent, then subjected to DNA extraction, methylation-sensitive polymerase chain reaction (MS-PCR). DNA methylation of the ATG5 and MAP1LC3Av1 genes were assessed.
UNASSIGNED: Shapiro-Wilk and Kolmogorov-Smirnov tests showed that the values were normally distributed. Both the ATG5 and MAP1LC3Av1 genes were methylated in OSCC, OL tissues compared to normal tissues. A statistically significant results was seen among the three study groups.
UNASSIGNED: A significant difference was noted in the hypermethylation status of the promoter regions of the ATG5 and MAP1LC3Av1 genes. This provides some insight into their crucial role in the development of tumors. Future research with larger sample is needed to assess its potential clinical implications in oral carcinoma.
摘要：
■口腔癌的进展和发病机制受到表观遗传修饰的极大影响，如DNA甲基化。自噬,是一种用于维持细胞存活和完整性的适应性机制。口腔鳞状细胞癌与许多自噬指标有关，尽管尚不清楚自噬相关基因的DNA甲基化是否促进口腔白斑（OL）的发展，口腔鳞状细胞癌（OSCC）。
■我们的研究旨在评估，比较和评估口腔白斑中ATG5和MAP1LC3Av1基因的DNA甲基化，口腔鳞状细胞癌。
■这项横断面研究设计了48个组织的样本大小，这些组织在临床和组织病理学上被诊断为OL，OSCC和正常组织。样本分为三组(A组,B组,和C组;(各n=16)。经过组织病理学确认,组织储存在RNA试剂中，然后进行DNA提取，甲基化敏感聚合酶链反应（MS-PCR）。评估ATG5和MAP1LC3Av1基因的DNA甲基化。
■Shapiro-Wilk和Kolmogorov-Smirnov测试表明值呈正态分布。ATG5和MAP1LC3Av1基因在OSCC中均被甲基化,OL组织与正常组织比较。在三个研究组中观察到统计学上显著的结果。
■注意到ATG5和MAP1LC3Av1基因的启动子区域的超甲基化状态存在显着差异。这为它们在肿瘤发展中的关键作用提供了一些见解。未来需要更大样本的研究来评估其在口腔癌中的潜在临床意义。
■我们的研究旨在评估，比较和评估口腔白斑中ATG5和MAP1LC3Av1基因的DNA甲基化，口腔鳞状细胞癌。
■这项横断面研究设计了48个组织的样本大小，这些组织在临床和组织病理学上被诊断为OL，OSCC和正常组织。样本分为三组(A组,B组,和C组;(各n=16)。经过组织病理学确认,组织储存在RNA试剂中，然后进行DNA提取，甲基化敏感聚合酶链反应（MS-PCR）。评估ATG5和MAP1LC3Av1基因的DNA甲基化。
■Shapiro-Wilk和Kolmogorov-Smirnov测试表明值呈正态分布。ATG5和MAP1LC3Av1基因在OSCC中均被甲基化,OL组织与正常组织比较。在三个研究组中观察到统计学上显著的结果。
■注意到ATG5和MAP1LC3Av1基因的启动子区域的超甲基化状态存在显着差异。这为它们在肿瘤发展中的关键作用提供了一些见解。未来需要更大样本的研究来评估其在口腔癌中的潜在临床意义。
