Title of article :
N-trans-Feruloyloctopamine Wakes Up BBC3, DDIT3, CDKN1A, and NOXA Signals to Accelerate HCC Cell Apoptosis
Author/Authors :
Ma, Bin Key Laboratory of Preclinical Study for New Drug of Gansu Province - School of Basic Medical Science - Lanzhou University, Lanzhou, China , Li, Jing General Surgery Department - The First Hospital of Lanzhou University, The First Clinical Medical College - Lanzhou University, Lanzhou, Gansu Province, China , Yang, Wen-Ke Key Laboratory of Preclinical Study for New Drug of Gansu Province - School of Basic Medical Science - Lanzhou University, Lanzhou, China , Zhang, Mei-Gui General Surgery Department - The First Hospital of Lanzhou University, The First Clinical Medical College - Lanzhou University, Lanzhou, Gansu Province, China , Xie, Xiao-Dong Key Laboratory of Preclinical Study for New Drug of Gansu Province - School of Basic Medical Science - Lanzhou University, Lanzhou, China , Bai, Zhong-Tian Key Laboratory of Preclinical Study for New Drug of Gansu Province - School of Basic Medical Science - Lanzhou University, Lanzhou, China
Abstract :
N-trans-Feruloyloctopamine (FO), a natural compound, was reported in our previous study to inhibit a tumor cell malignant phenotype by AKT- and EMT-related signals and might be used as a promising drug for HCC treatment. However, the specific targets and detailed mechanisms still need to be clarified. Screening with RNA-Seq in Huh7 cells treated with FO revealed that 317 genes were modulated, of which 188 genes were upregulated and 129 genes were downregulated. Real-time cell analyzer and flow cytometry data reveal that tumor cell proliferation and apoptosis were impacted by FO. DAVID bioinformatic data showed that most of the biological process GO terms are related to proliferation and apoptosis. KEGG enrichment analysis showed that FO mainly regulates PI3K-AKT- and apoptosis-related signals, in which BBC3, DDIT3, NOXA, and CDKN1A on the surface serve as the novel targets of FO inducing HCC cell apoptosis. The result implied that FO might exacerbate HCC cell apoptosis by regulating BBC3, DDIT3, CDKN1A, and NOXA signals. The obstacle effect of FO can provide new targets and new credibility for the treatment of liver cancer.
