口腔扁平苔藓的恶性转化及相关遗传因素

E. C. Hwang, Se-Young Choi, Jeong Hee Kim
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引用次数: 1

摘要

口腔扁平苔藓(OLP)是一种慢性炎症性疾病,约占人口的0.5-2.2%,被认为是一种可进展为口腔鳞状细胞癌(OSCC)的癌前病变。恶性转化率约为1.09-2.3%,发生恶性转化的危险因素有年龄、女性、糜烂类型、舌部部位等。OLP的恶性转化可能与细胞凋亡现象的低频率有关。因此,本文对凋亡相关的遗传因子如p53、BCL-2、BAX等进行综述。OLP患者中p53表达升高,BCL-2、BAX表达改变,其恶性转化率较高。本文也对microRNA在OLP恶性转化中的作用进行了综述。由于自噬通过调节多种细胞过程参与细胞的生存和死亡,自噬相关的遗传因素可能作为恶性转化的因素发挥作用。在OLP中,观察到ATG9B mRNA水平降低,IGF1表达升高,表明细胞死亡和自噬反应减少。激活的IGF1-PI3K/AKT/mTor级联可能在OLP向OSCC恶性转化的信号通路中发挥重要作用。最近的研究表明,miR-199和miR-122等mirna可激活该级联,增加促生存和促增殖信号。
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Malignant transformation of oral lichen planus and related genetic factors
Oral lichen planus (OLP) is a chronic inflammatory disease observed in approximately 0.5–2.2% of the population, and it is recognized as a premalignant lesion that can progress into oral squamous cell carcinoma (OSCC). The rate of malignant transformation is approximately 1.09–2.3%, and the risk factors for malignant transformation are age, female, erosive type, and tongue site location. Malignant transformation of OLP is likely related to the low frequency of apoptotic phenomena. Therefore, apoptosis-related genetic factors, like p53, BCL-2, and BAX are reviewed. Increased p53 expression and altered expression of BCL-2 and BAX were observed in OLP patients, and the malignant transformation rate in these patients was relatively higher. The involvement of microRNA (miRNA) in the malignant transformation of OLP is also reviewed. Because autophagy is involved in cell survival and death through the regulation of various cellular processes, autophagy-related genetic factors may function as factors for malignant transformation. In OLP, decreased levels of ATG9B mRNA and a higher expression of IGF1 were observed, suggesting a reduction in cell death and autophagic response. Activated IGF1-PI3K/AKT/mTor cascade may play an important role in a signaling pathway related to the malignant transformation of OLP to OSCC. Recent research has shown that miRNAs, such as miR-199 and miR-122, activate the cascade, increasing the prosurvival and proproliferative signals.
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