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首页> 外文期刊>Biochimica et biophysica acta. Molecular basis of disease: BBA >Fenofibrate exhibits a high potential to suppress the formation of squamous cell carcinoma in an oral-specific 4-nitroquinoline 1-oxide/arecoline mouse model.
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Fenofibrate exhibits a high potential to suppress the formation of squamous cell carcinoma in an oral-specific 4-nitroquinoline 1-oxide/arecoline mouse model.

机译：非诺贝特在口服特异性4-硝基喹啉1-氧化物/槟榔碱小鼠模型中具有抑制鳞状细胞癌形成的高潜力。

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The excessive use of areca nut and/or tobacco may induce the production of free radicals and reactive oxygen species, which affect the lipid contents of the cell membrane and are possibly involved in tumorigenic processes in the oral cavity. The aim of this study was to investigate the therapeutic efficacy of fenofibrate (0.1% or 0.3%, w/w), a ligand of the peroxisome proliferator-activated receptor alpha (PPARalpha), in a 4-nitroquinoline 1-oxide (4-NQO)/arecoline-induced oral cancer mouse model. The carcinogen, 4-NQO/arecoline, was administrated to C57BL/6JNarl mice for 8weeks followed by fenofibrate treatment for 12 or 20weeks. After 28weeks, changes in serum lipids, the multiplicity of tumor lesions, and tumor sizes were determined together with changes in the immunohistochemical expressions of PPARalpha, acetyl-coenzyme A carboxylase (ACC), the epidermal growth factor receptor (EGFR), and cyclooxygenase-2 (COX2). The results showed that when compared to the 4-NQO/arecoline only group, 0.3% fenofibrate treatment increased serum total cholesterol, low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) levels. 0.3% fenofibrate treatment suppressed the incidence rate of tongue lesions, reduced the multiplicity of squamous cell carcinoma (SCC), decreased the tumor size, and increased the immunoreactivity of EGFR and COX2 in oral dysplasia but decreased EGFR and COX2 expressions in SCC. These findings indicated that fenofibrate reduced the tumor incidence rate and suppressed the tumor progression into SCC and that these molecular events might be linked to the EGFR and COX2 regulatory pathways. We suggest that fenofibrate provides a new strategy for preventing oral tumor progression.
机译：过量使用槟榔和/或烟草可能会导致自由基和活性氧的产生，从而影响细胞膜的脂质含量，并可能参与口腔的致瘤过程。这项研究的目的是研究过氧化物酶体增殖物激活受体α（PPARalpha）的配体非诺贝特（0.1％或0.3％，w / w）在4-硝基喹啉1-氧化物（4- NQO）/槟榔碱诱导的口腔癌小鼠模型。对C57BL / 6JNarl小鼠给药8周，然后对非诺贝特治疗12或20周，将致癌物4-NQO /槟榔碱。 28周后，测定血脂变化，肿瘤病变的多样性和肿瘤大小，以及PPARalpha，乙酰辅酶A羧化酶（ACC），表皮生长因子受体（EGFR）和环氧合酶- 2（COX2）。结果显示，与仅4-NQO /槟榔碱组相比，非诺贝特0.3％治疗可增加血清总胆固醇，低密度脂蛋白胆固醇（LDL-C）和高密度脂蛋白胆固醇（HDL-C）水平。 0.3％非诺贝特治疗可抑制舌癌的发生率，减少鳞状细胞癌（SCC）的多样性，减小肿瘤的大小，并增加EGFR和COX2在口腔异型增生中的免疫反应性，但会降低SCC中EGFR和COX2的表达。这些发现表明非诺贝特降低了肿瘤的发生率并抑制了肿瘤向SCC的发展，这些分子事件可能与EGFR和COX2调控途径有关。我们建议非诺贝特提供了预防口腔肿瘤进展的新策略。

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