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.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Antineoplastic Agents / pharmacology*
-
Apoptosis / drug effects
-
Blotting, Western
-
Carcinoma, Renal Cell / enzymology*
-
Carcinoma, Renal Cell / genetics
-
Carcinoma, Renal Cell / 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*
-
Kidney Neoplasms / genetics
-
Kidney Neoplasms / pathology
-
Phosphorylation
-
Proliferating Cell Nuclear Antigen / metabolism
-
Recombinant Proteins
-
STAT1 Transcription Factor / genetics
-
STAT1 Transcription Factor / metabolism*
-
Signal Transduction / drug effects*
-
Transfection
Substances
-
Antineoplastic Agents
-
Interferon alpha-2
-
Interferon-alpha
-
Proliferating Cell Nuclear Antigen
-
Recombinant Proteins
-
STAT1 Transcription Factor
-
STAT1 protein, human
-
Janus Kinases
-
Caspases