cardamonin and Nasopharyngeal-Neoplasms

cardamonin has been researched along with Nasopharyngeal-Neoplasms* in 1 studies

Other Studies

1 other study(ies) available for cardamonin and Nasopharyngeal-Neoplasms

Article	Year
Cardamonin induces ROS-mediated G2/M phase arrest and apoptosis through inhibition of NF-κB pathway in nasopharyngeal carcinoma. Cell death & disease, 2017, 08-31, Volume: 8, Issue:8 Cardamonin has been demonstrated to have an inhibitory effect in many cancers, but its underlying mechanism remains elusive. Here, we studied, for the first time, the mechanism of cardamonin-induced nasopharyngeal carcinoma cell death both in vitro and in vivo. In our study, we showed that cardamonin inhibited cancer cell growth by inducing G2/M phase cell cycle arrest and apoptosis via accumulation of ROS. NF-κB activation was involved in breaking cellular redox homeostasis. Therefore, our results provided new insight into the mechanism of the antitumor effect of cardamonin, supporting cardamonin as a prospective therapeutic drug in nasopharyngeal carcinoma by modulating intracellular redox balance. Topics: Animals; Antineoplastic Agents, Phytogenic; Apoptosis; bcl-2-Associated X Protein; BH3 Interacting Domain Death Agonist Protein; Carcinoma; Cell Line, Tumor; Cell Proliferation; Chalcones; G2 Phase Cell Cycle Checkpoints; Gene Expression Regulation, Neoplastic; Humans; Mice; Mice, Nude; Nasopharyngeal Carcinoma; Nasopharyngeal Neoplasms; NF-kappa B; Reactive Oxygen Species; Signal Transduction; Tumor Suppressor Protein p53; Xenograft Model Antitumor Assays	2017

Article

Year

Cardamonin induces ROS-mediated G2/M phase arrest and apoptosis through inhibition of NF-κB pathway in nasopharyngeal carcinoma.

Cell death & disease, 2017, 08-31, Volume: 8, Issue:8

Cardamonin has been demonstrated to have an inhibitory effect in many cancers, but its underlying mechanism remains elusive. Here, we studied, for the first time, the mechanism of cardamonin-induced nasopharyngeal carcinoma cell death both in vitro and in vivo. In our study, we showed that cardamonin inhibited cancer cell growth by inducing G2/M phase cell cycle arrest and apoptosis via accumulation of ROS. NF-κB activation was involved in breaking cellular redox homeostasis. Therefore, our results provided new insight into the mechanism of the antitumor effect of cardamonin, supporting cardamonin as a prospective therapeutic drug in nasopharyngeal carcinoma by modulating intracellular redox balance.

Topics: Animals; Antineoplastic Agents, Phytogenic; Apoptosis; bcl-2-Associated X Protein; BH3 Interacting Domain Death Agonist Protein; Carcinoma; Cell Line, Tumor; Cell Proliferation; Chalcones; G2 Phase Cell Cycle Checkpoints; Gene Expression Regulation, Neoplastic; Humans; Mice; Mice, Nude; Nasopharyngeal Carcinoma; Nasopharyngeal Neoplasms; NF-kappa B; Reactive Oxygen Species; Signal Transduction; Tumor Suppressor Protein p53; Xenograft Model Antitumor Assays

2017