Liu Shuai, Han Liping, Wang Xiaoqing, Liu Zheng, Ding Sentai, Lu Jiaju, Bi Dongbin, Mei Yikun, Niu Zhihong
Department of Urology, Shandong Provincial Hospital Affiliated to Shandong University Jinan 250021, P. R. China.
Department of neurology, Qianfoshan Hospital Affiliated to Shandong University Jinan, People's Republic of China.
Int J Clin Exp Pathol. 2015 Feb 1;8(2):1302-11. eCollection 2015.
Renal cell carcinoma (RCC) carries a high risk of malignancy and metastasis. The inducible isoform of prostaglandin synthase, cyclooxygenase (COX)-2, and ICAM-1 may be involved in tumor metastasis. CCN3, also called nephroblastoma overexpressed gene (NOV), has been found to regulate the proliferation and differentiation of cancer cells. The effects of NOV on RCC cell migration and expression of COX-2 and ICAM-1 have not described yet in detail. But here, NOV was found to promote the migration and expression of COX-2 and ICAM-1 in human RCC cells. Akt inhibitor was found to interfere with this NOV-induced migration and up-regulation of COX-2 and ICAM-1 in RCC cells. NOV stimulation was here found to promote the phosphorylation of Akt. RCC tissue chips were subjected to IHC staining, which showed COX-2 expression in RCC tissues to be a significantly closely correlated with NOV expression, with significance determined using Pearson correlation testing (P < 0.05). The results of the current work indicate that NOV activates COX-2 and ICAM-1 through Akt, promoting the migration of RCC cells.
肾细胞癌（RCC）具有较高的恶性和转移风险。前列腺素合成酶的诱导型同工酶环氧合酶（COX）-2和细胞间黏附分子-1（ICAM-1）可能参与肿瘤转移。CCN3，也称为肾母细胞瘤过度表达基因（NOV），已被发现可调节癌细胞的增殖和分化。NOV对RCC细胞迁移以及COX-2和ICAM-1表达的影响尚未详细描述。但在此研究中，发现NOV可促进人RCC细胞中COX-2和ICAM-1的迁移及表达。发现Akt抑制剂可干扰RCC细胞中这种由NOV诱导的迁移以及COX-2和ICAM-1的上调。在此研究中发现NOV刺激可促进Akt的磷酸化。对RCC组织芯片进行免疫组化染色，结果显示RCC组织中COX-2的表达与NOV的表达显著密切相关，采用Pearson相关性检验确定其显著性（P < 0.05）。当前研究结果表明，NOV通过Akt激活COX-2和ICAM-1，促进RCC细胞的迁移。
