Department of Surgery, Mackay Memorial Hospital, Taipei, Taiwan, ROC.
Oncol Rep. 2011 Nov;26(5):1265-71. doi: 10.3892/or.2011.1388. Epub 2011 Jul 12.
The incidence of thyroid cancer has remarkably increased in recent years. Epidemiologic data suggest that obesity is associated with an increased incidence of several types of malignancies, including thyroid cancer. Leptin, an adipocyte-derived cytokine, has been shown to be involved in cancer development and progression. We previously demonstrated that papillary thyroid cancer expressing leptin receptor and/or leptin has a higher incidence of lymph node metastasis. In this study, we investigated the effects of leptin on cell migration in K1 and B-CPAP papillary thyroid cancer cells. Expression of leptin receptor was observed in both cell lines. Leptin enhanced the migratory activity significantly in a dose-dependent manner. We showed that leptin induced AKT and extracellular signal-regulated kinase (ERK) phosphorylation. Inhibition of phosphatidylinositol 3-kinase and ERK activation using pharmacological inhibitors effectively blocked leptin-induced migration of K1 and B-CPAP cells. Taken together, this study provides new mechanistic evidence for a role of leptin in the regulation of papillary thyroid cancer progression by stimulating tumor cell migration.
近年来，甲状腺癌的发病率显著增加。流行病学数据表明，肥胖与多种恶性肿瘤（包括甲状腺癌）的发病率增加有关。瘦素是一种脂肪细胞衍生的细胞因子，已被证明参与癌症的发生和发展。我们之前的研究表明，表达瘦素受体和/或瘦素的甲状腺乳头状癌淋巴结转移的发生率更高。在这项研究中，我们研究了瘦素对 K1 和 B-CPAP 甲状腺癌细胞迁移的影响。这两种细胞系均观察到瘦素受体的表达。瘦素呈剂量依赖性显著增强迁移活性。我们表明，瘦素诱导 AKT 和细胞外信号调节激酶（ERK）磷酸化。使用药理学抑制剂抑制磷脂酰肌醇 3-激酶和 ERK 激活可有效阻断 K1 和 B-CPAP 细胞中瘦素诱导的迁移。总之，这项研究为瘦素通过刺激肿瘤细胞迁移来调节甲状腺乳头状癌进展提供了新的机制证据。
