Mao C G, Wan L J, Zhou X C, Lu H T, Jiang Y D, Tao Z Z
Department of Otolaryngology, Jingzhou Central Hospital, the Second Clinical Medical College, Yangtze University, Jingzhou, 434020, China.
Department of Otolaryngology, Renmin Hospital of Wuhan University.
Lin Chuang Er Bi Yan Hou Tou Jing Wai Ke Za Zhi. 2016 Aug 5;30(15):1215-1218. doi: 10.13201/j.issn.1001-1781.2016.15.009.
The aim of this study is to investigate the inhibition of nasopharyngeal carcinoma cells by indole-3-carbinol in vitro and in vivo.The human nasopharyngeal carcinoma cell line CNE2 was treated in different concentrations 0,100,200,300 μmol/L of indole-3-carbinol. Then we detected cell proliferation after 0,24,48 and 72 h, apoptosis after 48 h and the levels of PI3K/Akt pathway-related proteins in vitro. The BALB/c nude mice were divided into three groups: prevention group, treatment group and control group. In vivo, the nude mice in every group were inoculated with nasopharyngeal carcinoma cells CNE2, and mice in prevention and treatment groups were given feed containing 0.5% indole-3-carbinol. We investigated the tumoricidal effect of I3C in nude mice , and eight weeks later, the PI3K/Akt pathway-related proteins expressions in tumors from nude mice of each group were detected.With the indole-3-carbinol concentration increased, cell proliferation decreased and apoptosis increased significantly.The levels of PI3K/Akt pathway-related proteins were decreased.In animal experiments, the prevention and treatment group developed smaller tumors, and the expression of PI3K/Akt pathway-related proteins in prevention and treatment groups PI3K/Akt pathway also reduced, compared to control group. Meanwhile, nearly no changes of heart, liver and kidney tissues in all groups were seen in HE staining.Indole-3-carbinol inhibited the growth of nasopharyngeal carcinoma cells and induced apoptosis effectively in vivo and in vitro. The mechanism might be that indole-3-carbinol could suppress PI3K/Akt pathway.
本研究旨在探讨吲哚 - 3 - 甲醇在体外和体内对鼻咽癌细胞的抑制作用。将人鼻咽癌细胞系CNE2用不同浓度（0、100、200、300 μmol/L）的吲哚 - 3 - 甲醇处理。然后检测0、24、48和72小时后的细胞增殖情况、48小时后的细胞凋亡情况以及体外PI3K/Akt通路相关蛋白的水平。将BALB/c裸鼠分为三组：预防组、治疗组和对照组。在体内，每组裸鼠接种鼻咽癌细胞CNE2，预防组和治疗组的小鼠给予含0.5%吲哚 - 3 - 甲醇的饲料。我们研究了吲哚 - 3 - 甲醇对裸鼠的杀瘤作用，八周后，检测每组裸鼠肿瘤中PI3K/Akt通路相关蛋白的表达。随着吲哚 - 3 - 甲醇浓度的增加，细胞增殖减少，凋亡显著增加。PI3K/Akt通路相关蛋白的水平降低。在动物实验中，预防组和治疗组的肿瘤较小，与对照组相比，预防组和治疗组PI3K/Akt通路相关蛋白的表达也降低。同时，在HE染色中，所有组的心脏、肝脏和肾脏组织几乎未见变化。吲哚 - 3 - 甲醇在体内和体外均能有效抑制鼻咽癌细胞的生长并诱导凋亡。其机制可能是吲哚 - 3 - 甲醇可抑制PI3K/Akt通路。
