Chen Yuanyuan, Wang Gang, Wang Yingmei, Gao Xiaoli, Wang Kan, Li Jie, Xue Fengxia
Department of Gynecology and Obstetrics, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China.
Oncol Lett. 2019 Jan;17(1):564-570. doi: 10.3892/ol.2018.9524. Epub 2018 Sep 28.
Previous studies have demonstrated that calpain small subunit 4 (Capn4) is able to regulate the viability and metastasis of cancer cells. However, the regulatory effects and underlying molecular mechanism of Capn4 in ovarian carcinoma cells are not well understood. The purpose of the present study was to investigate the role of Capn4 in ovarian carcinoma cells and analyze the possible mechanism mediated by Capn4. The expression levels of Capn4 and osteopontin (OPN) were determined and the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway was analyzed in ovarian carcinoma cells. The results of the present study revealed that Capn4 and OPN were overexpressed in clinical ovarian carcinoma tissues and ovarian carcinoma cells. Capn4 silencing downregulated OPN expression, and suppressed ovarian carcinoma cell viability and migration. Capn4 silencing enhanced apoptosis of ovarian carcinoma cells by increasing activity of the capase-3 apoptosis signaling pathway. Capn4 promoted the metastasis of ovarian carcinoma cells by interacting with the PI3K/AKT signaling pathway via upregulation of OPN expression. In conclusion, the results of the present study indicate that Capn4 may be a potential therapeutic target for the treatment of ovarian carcinoma.
先前的研究表明，钙蛋白酶小亚基4（Capn4）能够调节癌细胞的活力和转移。然而，Capn4在卵巢癌细胞中的调节作用及潜在分子机制尚未完全明确。本研究的目的是探讨Capn4在卵巢癌细胞中的作用，并分析Capn4介导的可能机制。测定了卵巢癌细胞中Capn4和骨桥蛋白（OPN）的表达水平，并分析了磷酸肌醇3激酶（PI3K）/蛋白激酶B（AKT）信号通路。本研究结果显示，Capn4和OPN在临床卵巢癌组织和卵巢癌细胞中均过度表达。Capn4沉默下调了OPN表达，并抑制了卵巢癌细胞的活力和迁移。Capn4沉默通过增加半胱天冬酶-3凋亡信号通路的活性增强了卵巢癌细胞的凋亡。Capn4通过上调OPN表达与PI3K/AKT信号通路相互作用，促进了卵巢癌细胞的转移。总之，本研究结果表明，Capn4可能是治疗卵巢癌的潜在治疗靶点。
