HIF-1 对口腔扁平苔藓中 MMP-9 和 Galectin-3 的关键影响。
A critical influence of HIF-1 on MMP-9 and Galectin-3 in oral lichen planus.
发表日期:2024 Jun 29
作者:
Hala H Hazzaa, Marwa A M El Shiekh, Osama Elkashty, Eman Magdy, Dalia Riad, Eman Khalifa, Gasser M Elewa, Naglaa M Kamal
来源:
BMC Oral Health
摘要:
口腔扁平苔藓有患恶性肿瘤的风险。该疾病的发病机制是由多种炎症介质介导的。在某些情况下,多种介质可能导致致癌行为。缺氧诱导因子 1a (HIF-1) 及其与半乳糖素 3 (Gal-3) 和基质金属蛋白酶 9 (MMP-9) 过度表达的可能相关性是恶性转化的重要指标。对这些因素的研究可能会提供有关疾病恶性转化的循证信息。该研究调查了 OLP 组织样本中 HIF-1、Gla-3 和 MMP-9 的表达,与未发炎牙龈过度生长的对照受试者进行比较。每组分配20个生物样本。OLP的免疫组织化学结果显示大多数上皮细胞对Galectin 3、HIF1a和MMP-9具有免疫反应性。 HIF1α与MMP-9呈正相关,r = 0.9301(P值 < 0.00001)。 Galectin 3 和 MMP-9 之间呈正相关,r = 0.7292(P 值 = 0.000264) Galectin 3 和 HIF1α 之间,r = 0.5893(P 值 = 0.006252)。这些发现证实了以下假设:适应性途径Gal 3 和 MMP-9 表达及其 HIF-1 等缺氧可能在 OLP 的致癌过程中发挥关键作用。© 2024。作者。
Oral lichen planus carries a risk for malignancy. The pathogenesis of the disease is mediated by various inflammatory mediators. Several mediators could be responsible for the oncogenic behavior in certain cases. Hypoxia-inducible factor-1a (HIF-1), and its possible correlation to Galactin-3 (Gal-3) and matrix metalloproteinase-9 (MMP-9) over expression represents an important indicator for malignant transformation. The investigation of these factors may present evidence-based information on malignant transformation of the disease.The study investigated the expression of HIF-1, Gla-3 and MMP-9 in tissue samples of OLP compared to control subjects of un-inflamed gingival overgrowth. 20 biospecimen were allocated in each group.Immunohistochemical findings of OLP showed immunoreactivity for Galectin 3, HIF1a and MMP-9 by most of the epithelial cells. There was a positive correlation between HIF1α and MMP-9, r = 0.9301 (P-value < 0.00001). A positive correlation was detected between Galectin 3 and MMP-9, r = 0.7292 (P-value = 0.000264) between Galectin 3 and HIF1α, r = 0.5893 (P-value = 0.006252).These findings confirm the hypothesis that the adaptive pathways to hypoxia as Gal 3 and MMP-9 expressions and their HIF-1 may play a crucial role in carcinogenesis of OLP.© 2024. The Author(s).