Department of Dentistry, Universidade Estadual de Montes Claros, Minas Gerais, Brazil; Instituto Federal do Norte de Minas Gerais - Campus Araçuaí, Minas Gerais, Brazil.
Department of Dentistry, Universidade Estadual de Montes Claros, Minas Gerais, Brazil.
Pathol Res Pract. 2018 Jan;214(1):30-37. doi: 10.1016/j.prp.2017.11.022. Epub 2017 Dec 10.
Gallic acid is a polyphenolic compost appointed to interfere with neoplastic cells behavior. Evidence suggests an important role of leptin in carcinogenesis pathways, inducing a proliferative phenotype. We investigated the potential of gallic acid to modulate leptin-induced cell proliferation and migration of oral squamous cell carcinoma cell lines. The gallic acid effect on leptin secretion by oral squamous cell carcinoma cells, as well as the underlying molecular mechanisms, was also assessed. For this, we performed proliferation, migration, immunocytochemical and qPCR assays. The expression levels of cell migration-related genes (MMP2, MMP9, Col1A1, and E-cadherin), angiogenesis (HIF-1α, mir210), leptin signaling (LepR, p44/42 MAPK), apoptosis (casp-3), and secreted leptin levels by oral squamous cell carcinoma cells were also measured. Gallic acid decreased proliferation and migration of leptin-treated oral squamous cell carcinoma cells, and reduced mRNA expression of MMP2, MMP9, Col1A1, mir210, but did not change HIF-1α. Gallic acid decreased levels of leptin secreted by oral squamous cell carcinoma cells, accordingly with downregulation of p44/42 MAPK expression. Thus, gallic acid appears to break down neoplastic phenotype of oral squamous cell carcinoma cells by interfering with leptin pathway.
没食子酸是一种多酚化合物，被指派来干扰肿瘤细胞的行为。有证据表明瘦素在致癌途径中起着重要作用，诱导增殖表型。我们研究了没食子酸调节口腔鳞状细胞癌细胞系中瘦素诱导的细胞增殖和迁移的潜力。还评估了没食子酸对口腔鳞状细胞癌细胞分泌瘦素的影响及其潜在的分子机制。为此，我们进行了增殖、迁移、免疫细胞化学和 qPCR 分析。还测量了与细胞迁移相关的基因（MMP2、MMP9、Col1A1 和 E-cadherin）、血管生成（HIF-1α、mir210）、瘦素信号（LepR、p44/42 MAPK）、细胞凋亡（casp-3）和口腔鳞状细胞癌细胞分泌的瘦素水平的表达。没食子酸降低了瘦素处理的口腔鳞状细胞癌细胞的增殖和迁移，并降低了 MMP2、MMP9、Col1A1、mir210 的 mRNA 表达，但未改变 HIF-1α。没食子酸降低了口腔鳞状细胞癌细胞分泌的瘦素水平，相应地下调了 p44/42 MAPK 的表达。因此，没食子酸似乎通过干扰瘦素途径破坏了口腔鳞状细胞癌细胞的肿瘤表型。
