Apoptotic Effects of Anthocyanins from Vitis coignetiae Pulliat Are Enhanced by Augmented Enhancer of the Rudimentary Homolog (ERH) in Human Gastric Carcinoma MKN28 Cells

• Published in: International journal of molecular sciences 2021-03, Vol.22 (6), p.3030
• Main Authors: Park, Cheol, Lee, Won Sup, Go, Se-Il, Jeong, Sang-Ho, Yoo, Jiyun, Cha, Hee-Jae, Lee, Young-Joon, Kim, Heui-Soo, Leem, Sun-Hee, Kim, Hye Jung, Kim, Gon Sup, Hong, Soon-Chan, Choi, Yung Hyun
• Format: Article
• Language: English
• Subjects: Anthocyanins; Anthocyanins - pharmacology; Antibodies; anticancer effects; Apoptosis; Apoptosis - drug effects; Bcl-2 protein; Cancer therapies; Caspase-3; Caspases - metabolism; Cell cycle; Cell Cycle Proteins - metabolism; Cell Line, Tumor; Cell Proliferation - drug effects; Depolarization; enhancer of the rudimentary homolog; Enzyme Activation - drug effects; Flow cytometry; Gastric cancer; Gene expression; Growth factors; Homology; Humans; Medical prognosis; Membrane Potential, Mitochondrial - drug effects; Metastasis; Mitochondria; MKN28 human gastric carcinoma cells; Ovaries; Plasmids; Proteins; Proto-Oncogene Proteins c-bcl-2 - metabolism; Reactive oxygen species; Reactive Oxygen Species - metabolism; Stomach Neoplasms - metabolism; Stomach Neoplasms - pathology; Transcription Factors - metabolism; Vitis - chemistry; Vitis coignetiae Pulliat; X-Linked Inhibitor of Apoptosis Protein - metabolism; XIAP protein
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms22063030

Evidence suggests that augmented expression of a certain gene can influence the efficacy of targeted and conventional chemotherapies. Here, we tested whether the high expression of enhancer of the rudimentary homolog (ERH), which serves as a prognostic factor in some cancers, can influence the efficacy of anthocyanins isolated from fruits of , Meoru in Korea (AIMs) on human gastric cancer cells. The anticancer efficacy of AIMs was augmented in ERH-transfected MKN28 cells (E-MKN28 cells). Molecularly, ERH augmented AIM-induced caspase-dependent apoptosis by activating caspase-3 and -9. The ERH-augmented apoptotic effect was related to mitochondrial depolarization and inhibition of antiapoptotic proteins, XIAP, and Bcl-2. In addition, reactive oxygen species (ROS) generation was augmented in AIMs-treated E-MKN28 cells compared to AIMs-treated naïve MKN28 cells. In conclusion, ERH augmented AIM-induced caspase-dependent mitochondrial-related apoptosis in MKN28 cells. A decrease in expression of Bcl-2 and subsequent excessive ROS generation would be the mechanism for ERH-augmented mitochondrial-related apoptosis in AIMs-treated MKN28 cells. A decrease in expression of XIAP would be another mechanism for ERH-augmented caspase-dependent apoptosis in AIMs-treated MKN28 cells.