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Research Paper
Induction of the Interferon-Inducible RNA-Degrading Enzyme, RNase L by Stress-Inducing Agents in the Human Cervical Carcinoma Cells
Mitali Pandey, Gagan Deep Bajaj and Pramod C. Rath
volume 1 | issue 1
may/june 2004Pages: 21 - 27
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RNA-degradation is one of the fundamental mechanisms of interferon (IFN)-inducible antiviral response in mammalian cells. This is primarily brought about by the IFN-inducible 2',5'-oligoadenylate (2-5A)-cofactor dependent ribonuclease L (RNase L). RNase L also functions as a tumor suppressor gene in case of prostate cancer due to its role in apoptosis. We report that RNase L is induced by stress-inducing agents such as double-stranded RNA [poly(I:C)], chemotherapeutic drugs, hydrogen peroxide (H2O2), calcium chloride (CaCl2) and tumor necrosis factor-? (TNF) in the human cervical carcinoma (HeLa) cells. The level of RNase L was not detected in the untreated cells. Induction of RNase L by such stress-inducing agents correlated with degradation of cellular RNA, fragmentation of chromatin-DNA and induction of apoptosis. We checked the stress-inducible transcription factor, nuclear factor kappa B (NF-?B), which was persistently activated by cycloheximide but not by other agents after 24 hours indicating no role of NF-?B in the RNase L-induction. However, as expected, TNF-induced NF-?B activity was stimulated within 10-30 minutes through degradation of I?B-?. Our results strongly suggest that the IFN-inducible RNase L is induced by a broad range of stress-inducing signals such as double-stranded RNA (dsRNA) produced during viral infection, membrane- and osmotic shock caused by CaCl2 and oxidative stress induced by H2O2, inflammation stimulated by TNF-? and chemotherapy. Thus, in addition to its antiviral function, the IFN-inducible RNase L may play an important role during stress-response through RNA-degradation and apoptosis.
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