Interferon-α induces G1 cell-cycle arrest in renal cell carcinoma cells via activation of Jak-Stat signaling.

Abstract

The purpose of this study was to clarify the mechanism of IFN-α resistance in RCC. The effects of IFN-α on induction of apoptosis and cell-cycle arrest were analyzed by flow cytometric analysis. Jak-Stat pathway components induced by IFN-α was evaluated using Western blotting. The results suggested that IFN-α caused growth inhibition of RCC cell lines via arrest in the G1 phase without inducing apoptosis. The resistance of RCC to IFN-α was associated with the low expression of Stat1. This study indicated that the Jak-Stat pathway should be considered a primary target for improving the response of RCC to IFN-α treatment.

• Authors: Donghao Shang, Peiqian Yang, Yuting Liu, Jian Song, Fengbo Zhang, Ye Tian
• Journal: Cancer investigation (Cancer Invest) Vol. 29 Issue 5 Pg. 347-52 (Jun 2011) ISSN: 1532-4192 [Electronic] England
• PMID: 21599510 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Antineoplastic Agents
• Interferon alpha-2
• Interferon-alpha
• Proliferating Cell Nuclear Antigen
• Recombinant Proteins
• STAT1 Transcription Factor
• STAT1 protein, human
• Janus Kinases
• Caspases

Topics

• Antineoplastic Agents (pharmacology)
• Apoptosis (drug effects)
• Blotting, Western
• Carcinoma, Renal Cell (enzymology, genetics, pathology)
• Caspases (metabolism)
• Cell Cycle (drug effects)
• Cell Line, Tumor
• Cell Proliferation (drug effects)
• Dose-Response Relationship, Drug
• Down-Regulation
• Drug Resistance, Neoplasm
• Enzyme Activation
• Flow Cytometry
• Humans
• Interferon alpha-2
• Interferon-alpha (pharmacology)
• Janus Kinases (metabolism)
• Kidney Neoplasms (enzymology, genetics, pathology)
• Phosphorylation
• Proliferating Cell Nuclear Antigen (metabolism)
• Recombinant Proteins
• STAT1 Transcription Factor (genetics, metabolism)
• Signal Transduction (drug effects)
• Transfection