1. N-trans-Feruloyloctopamine Wakes Up BBC3, DDIT3, CDKN1A, and NOXA Signals to Accelerate HCC Cell Apoptosis
- Author
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Zhong-Tian Bai, Mei-Gui Zhang, Bin Ma, Xiaodong Xie, Jing Li, and Wen-Ke Yang
- Subjects
0301 basic medicine ,Cancer Research ,Article Subject ,Pathology and Forensic Medicine ,Flow cytometry ,03 medical and health sciences ,0302 clinical medicine ,Downregulation and upregulation ,medicine ,KEGG ,Gene ,Protein kinase B ,RC254-282 ,QH573-671 ,medicine.diagnostic_test ,Chemistry ,Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,N-trans-feruloyloctopamine ,Cell Biology ,General Medicine ,medicine.disease ,030104 developmental biology ,Apoptosis ,030220 oncology & carcinogenesis ,Cancer research ,Molecular Medicine ,Cytology ,Liver cancer - 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.
- Published
- 2021
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