Department of Pathology, the First Affiliated Hospital of China Medical University and Department of Pathology, College of Basic Medical Sciences, China Medical University, Shenyang, Liaoning, China.
PLoS One. 2012;7(5):e37657. doi: 10.1371/journal.pone.0037657. Epub 2012 May 30.
The objective of the current study was to investigate the expression pattern and clinicopathological significance of TRIM24 in patients with non-small cell lung cancer (NSCLC). The expression profile of TRIM24 in NSCLC tissues and adjacent noncancerous lung tissues was detected by immunohistochemistry. TRIM24 was found to be overexpressed in 81 of 113 (71.7%) human lung cancer samples and correlated with p-TNM stage (p = 0.0006), poor differentiation (p = 0.004), Ki67 index (p<0.0001), cyclin D1(p = 0.0096) and p-Rb expression (p = 0.0318). In addition, depleting TRIM24 expression by small interfering RNA inhibited growth and invasion in lung cell lines. Moreover, TRIM24 depletion induced cell cycle arrest at the G1/S boundary and induced apoptosis. Western blotting analysis revealed that knockdown of TRIM24 decreased the protein levels of Cyclin A, Cyclin B, Cyclin D1, cyclin E and p-Rb and increased P27 expression. These results indicate that TRIM24 plays an important role in NSCLC progression.
本研究旨在探讨 TRIM24 在非小细胞肺癌(NSCLC)患者中的表达模式及其与临床病理特征的关系。采用免疫组织化学法检测 NSCLC 组织及癌旁正常肺组织中 TRIM24 的表达水平。结果发现,在 113 例人类肺癌样本中,TRIM24 在 81 例(71.7%)中呈高表达,且与 p-TNM 分期(p = 0.0006)、低分化(p = 0.004)、Ki67 指数(p<0.0001)、cyclin D1(p = 0.0096)和 p-Rb 表达(p = 0.0318)相关。此外,通过小干扰 RNA 沉默 TRIM24 表达可抑制肺癌细胞系的生长和侵袭。进一步研究发现,TRIM24 敲低可诱导细胞周期阻滞于 G1/S 期,并诱导细胞凋亡。Western blot 分析显示,TRIM24 下调可降低 Cyclin A、Cyclin B、Cyclin D1、cyclin E 和 p-Rb 的蛋白水平,并增加 P27 的表达。这些结果表明,TRIM24 在 NSCLC 的进展中发挥重要作用。