Biomaterial Database

[Effects of genistein on apoptosis in HCT-116 human colon cancer cells and its mechanism]. 2014

Jing Wu, and Jiaying Xu, and Shufen Han, and Liqiang Qin

Department of Nutrition and Food Hygiene, School of Public Health, Soochow University, Suzhou 215123, China.

OBJECTIVE To investigate the effects of genistein on cell proliferation and apoptosis in HCT-116 human colon cancer cells and its possible mechanism. METHODS After treatment with genistein, cell proliferation was determined by MTT assay. Cell cycle, cell apoptosis, intracellular reactive oxygen species ( ROS) and mitochondrial membrane potential were determined by flow cytometry. Furthermore, ultrastructural change was observed using transmission electron microscopy (TEM). RESULTS Genistein inhibited cell proliferation in a dose- and time-dependent manner. Genistein treatment in 0 - 100 micromol/L resulted in G2/M cell cycle arrest. The ratio of Sub-G1 increased from (1.63 +/- 0.44)% to (8.33 -1.51)% (P < 0.01). The ratio of early apoptosis increased from (1.93 +/- 0.32)% to (7.25 +/- 0.86)% (P < 0.01). Genistein caused characteristic apoptotic changes in TEM observation. Genistein treatment in 100 micromol/L increased intracellular ROS level to a peak at 2 h [2 h, (15.53 +/- 1.55)% vs. 0 h, (8.57 +/- 0.35)%, P < 0.01] and decreased mitochondrial membrane potential to a bottom at 1 h [1 h, (0.82 +/- 0.02)% vs. 0 h, (6.70 +/- 0.21)%, P < 0.01). CONCLUSIONS Our findings indicated that genistein inhibits cell proliferation, induces G2/M cell cycle arrest and apoptosis in colon cancer cell line HCT-116, with the increase of intracellular ROS level and decrease of mitochondrial membrane potential.

UI	MeSH Term	Description	Entries
D006801	Humans	Members of the species Homo sapiens.	Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D017209	Apoptosis	A regulated cell death mechanism characterized by distinctive morphologic changes in the nucleus and cytoplasm, including the endonucleolytic cleavage of genomic DNA, at regularly spaced, internucleosomal sites, i.e., DNA FRAGMENTATION. It is genetically programmed and serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.	Apoptosis, Extrinsic Pathway,Apoptosis, Intrinsic Pathway,Caspase-Dependent Apoptosis,Classic Apoptosis,Classical Apoptosis,Programmed Cell Death,Programmed Cell Death, Type I,Apoptoses, Extrinsic Pathway,Apoptoses, Intrinsic Pathway,Apoptosis, Caspase-Dependent,Apoptosis, Classic,Apoptosis, Classical,Caspase Dependent Apoptosis,Cell Death, Programmed,Classic Apoptoses,Extrinsic Pathway Apoptoses,Extrinsic Pathway Apoptosis,Intrinsic Pathway Apoptoses,Intrinsic Pathway Apoptosis
D017382	Reactive Oxygen Species	Molecules or ions formed by the incomplete one-electron reduction of oxygen. These reactive oxygen intermediates include SINGLET OXYGEN; SUPEROXIDES; PEROXIDES; HYDROXYL RADICAL; and HYPOCHLOROUS ACID. They contribute to the microbicidal activity of PHAGOCYTES, regulation of SIGNAL TRANSDUCTION and GENE EXPRESSION, and the oxidative damage to NUCLEIC ACIDS; PROTEINS; and LIPIDS.	Active Oxygen Species,Oxygen Radical,Oxygen Radicals,Pro-Oxidant,Reactive Oxygen Intermediates,Active Oxygen,Oxygen Species, Reactive,Pro-Oxidants,Oxygen, Active,Pro Oxidant,Pro Oxidants,Radical, Oxygen
D045325	HCT116 Cells	Human COLORECTAL CARCINOMA cell line.	HCT 116 Cells,HCT-116 Cells,Cell, HCT 116,Cell, HCT-116,Cell, HCT116,Cells, HCT 116,Cells, HCT-116,Cells, HCT116,HCT 116 Cell,HCT-116 Cell,HCT116 Cell
D049109	Cell Proliferation	All of the processes involved in increasing CELL NUMBER including CELL DIVISION.	Cell Growth in Number,Cellular Proliferation,Cell Multiplication,Cell Number Growth,Growth, Cell Number,Multiplication, Cell,Number Growth, Cell,Proliferation, Cell,Proliferation, Cellular
D053078	Membrane Potential, Mitochondrial	The voltage difference, normally maintained at approximately -180mV, across the INNER MITOCHONDRIAL MEMBRANE, by a net movement of positive charge across the membrane. It is a major component of the PROTON MOTIVE FORCE in MITOCHONDRIA used to drive the synthesis of ATP.	Delta Psi M,DeltaPsi M,DeltapsiM,Mitochondrial Membrane Potential,Mitochondrial Transmembrane Potential,M, DeltaPsi,Membrane Potentials, Mitochondrial,Mitochondrial Membrane Potentials,Mitochondrial Transmembrane Potentials,Transmembrane Potential, Mitochondrial,Transmembrane Potentials, Mitochondrial
D059447	Cell Cycle Checkpoints	Regulatory signaling systems that control the progression through the CELL CYCLE. They ensure that the cell has completed, in the correct order and without mistakes, all the processes required to replicate the GENOME and CYTOPLASM, and divide them equally between two daughter cells. If cells sense they have not completed these processes or that the environment does not have the nutrients and growth hormones in place to proceed, then the cells are restrained (or "arrested") until the processes are completed and growth conditions are suitable.	Cell Cycle Arrest,Cell Cycle Control,Cell Cycle Transition Points,Cell Cycle-Transition Points,Arrest, Cell Cycle,Arrests, Cell Cycle,Cell Cycle Arrests,Cell Cycle Checkpoint,Cell Cycle Controls,Cell Cycle-Transition Point,Checkpoint, Cell Cycle,Checkpoints, Cell Cycle,Control, Cell Cycle,Controls, Cell Cycle,Cycle-Transition Point, Cell,Point, Cell Cycle-Transition
D019833	Genistein	An isoflavonoid derived from soy products. It inhibits PROTEIN-TYROSINE KINASE and topoisomerase-II (DNA TOPOISOMERASES, TYPE II); activity and is used as an antineoplastic and antitumor agent. Experimentally, it has been shown to induce G2 PHASE arrest in human and murine cell lines and inhibits PROTEIN-TYROSINE KINASE.	Genestein