Characterization of apoptosis induced by transforming growth factor beta 1 in human hepatoma cells.
Apoptotic cell death plays a major role in the regulation of cell growth and this process may be activated by different agents through various pathways. The present study aimed to elucidated the mechanism of apoptosis caused by transforming growth factor beta 1 (TGF-beta 1) in human hepatoma cells. Several biological parameters which were reported to be crucial in the induction of programmed cell death in other experimental systems were measured. We found that TGF-beta 1-induced cell death is independent of cytosolic calcium and protein kinase C. Insulin and tumor promotor can rescue hepatoma cells from apoptosis, but the effect is time-dependent. Our results highlight that different apoptotic signal transduction pathways exist in different cell types. Apoptosis induced by TGF-beta 1 provides a good model for the understanding of cell death and the development of new anti-cancer drugs. Apoptotic cell death (apoptosis or programmed cell death) in normal tissue is a biological phenomenon that maintains hemostasis of systems of the body under physiological conditions. The features of apoptosis include condensation of chromatin, blebbing of the cell surface, transient increase in buoyant density and fragmentation of chromatin by a specific endonuclease.
Chuang
L Y
LY
Department of Biochemistry, Kaohsiung Medical College, Kaohsiung City, Taiwan, R.O.C.
Hung
W C
WC
Chang
C C
CC
Tsai
J H
JH
D000818:Animals; D017209:Apoptosis / Q000187:drug effects* / Q000502:physiology; D002118:Calcium / Q000502:physiology; D016923:Cell Death / Q000187:drug effects / Q000502:physiology; D003432:Cross-Linking Reagents / Q000494:pharmacology; D004273:DNA, Neoplasm / Q000096:biosynthesis; D006801:Humans; D007328:Insulin / Q000494:pharmacology; D007329:Insulin Antagonists / Q000494:pharmacology; D007424:Intracellular Fluid / Q000378:metabolism; D007457:Iodine Radioisotopes; D007700:Kinetics; D008114:Liver Neoplasms, Experimental / Q000188:drug therapy* / Q000473:pathology*; D011493:Protein Kinase C / Q000494:pharmacology; D011956:Receptors, Cell Surface / Q000378:metabolism; D018125:Receptors, Transforming Growth Factor beta / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D016212:Transforming Growth Factor beta / Q000037:antagonists & inhibitors / Q000378:metabolism / Q000494:pharmacology*; D014407:Tumor Cells, Cultured
D003432:Cross-Linking Reagents; D004273:DNA, Neoplasm; D007328:Insulin; D007329:Insulin Antagonists; D007457:Iodine Radioisotopes; D011956:Receptors, Cell Surface; D018125:Receptors, Transforming Growth Factor beta; D016212:Transforming Growth Factor beta; D011493:Protein Kinase C; D013755:Tetradecanoylphorbol Acetate; D002118:Calcium