title: Indole-3-carbinol inhibits nasopharyngeal carcinoma cell growthin vivoandin vitrothrough inhibition of the PI3K/Akt pathway.
abstract: Indole-3-carbinol (I3C) is an active component of cruciferous vegetables and has been shown to markedly inhibit the growth of a variety of tumors. However, the role of I3C in nasopharyngeal carcinoma (NPC) remains unclear. Thus, the aim of the present study was to investigate the inhibition of NPC cells by I3Cin vitroandin vivo. The human CNE2 NPC cell line was treated with various concentrations (0, 100, 200 and 300 μM) of I3C and analysis of cell proliferation after 0, 24, 48 and 72 h, apoptosis after 48 h and expression levels of phosphatidylinositol 3-kinase (PI3K)/Akt pathway-associated proteinsin vitrowas performed. BALB/c nude mice were divided into the following groups: Prevention, treatment and control.In vivo, all the nude mice were inoculated with CNE2 NPC cells and the mice in the prevention and treatment groups were administered a diet containing 0.5% I3C prior to and following inoculation, respectively. The tumoricidal effect of I3C was investigated in the nude mice. After eight weeks, the expression levels of PI3K/Akt pathway-associated proteins were analyzed in the tumors from the nude mice in each group. The results demonstrated that with increasing I3C concentrations, cell proliferation decreased and apoptosis increased significantly. In addition, the expression levels of PI3K/Akt pathway-associated proteins decreased. In the animal experiments, the prevention and treatment groups developed smaller tumors and the expression levels of PI3K/Akt pathway-associated proteins were reduced when compared with those in the control group. In addition, very few changes to the heart, liver and kidney tissues were observed with hematoxylin and eosin staining in all the groups. Therefore, the results of the present study indicated that I3C inhibited the growth of NPC cells and induced apoptosis effectivelyin vivoandin vitro. The underlying mechanism may be that I3C suppresses the PI3K/Akt pathway.
authors.affiliation: Department of Otolaryngology-Head and Neck Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.
authors.forename: Cheng-Gang
authors.initials: CG
authors.lastname: Mao
authors.affiliation: Department of Otolaryngology-Head and Neck Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.
authors.forename: Ze-Zhang
authors.initials: ZZ
authors.lastname: Tao
authors.affiliation: Department of Otolaryngology-Head and Neck Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.
authors.forename: Zhe
authors.initials: Z
authors.lastname: Chen
authors.affiliation: Department of Otolaryngology-Head and Neck Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.
authors.forename: Chen
authors.initials: C
authors.lastname: Chen
authors.affiliation: Department of Otolaryngology-Head and Neck Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.
authors.forename: Shi-Ming
authors.initials: SM
authors.lastname: Chen
authors.affiliation: Department of Otolaryngology-Head and Neck Surgery, The Affiliated Jingzhou Central Hospital of Tongji Medical College, Huazhong University of Science & Technology, Jingzhou, Hubei 434020, P.R. China.
authors.forename: Li-Jia
authors.initials: LJ
authors.lastname: Wan
keywords: apoptosis; indole-3-carbinol; nasopharyngeal carcinoma; phosphatidylinositol 3-kinase/Akt pathway