BACKGROUND: The retinoid-inducible gene I (RIG1), belonging to the family of type II tumor suppressor genes, was isolated from human gastric cancer cells treated with all-trans retinoic acid. The activity of the RIG1 gene was investigated in this study. MATERIALS AND METHODS: HtTA cervical and TSGH9201 gastric cancer cells were transiently transfected with expression vectors that synthesized RIG1-myc or RIG1-EGFP fusion protein. Cell growth was analyzed by measuring the incorporation of bromodeoxyuridine. Apoptosis was evaluated by the formation of in situ DNA breakage. The activities of mitogen-activated kinase signal pathways were analyzed using signal pathway trans-reporting systems. RESULTS: Expression of the RIG1-myc fusion protein resulted in decreased cell growth. Both RIG1-EGFP and RIG1-myc fusion proteins induced cellular apoptosis that was characterized by the presence of apoptotic bodies and in situ DNA breakage. The transactivation activities of Elk1, c-Jun and CHOP proteins were suppressed by 80, 50 and 88%, respectively, in HtTA cells expressing the RIG1-myc fusion protein for two days. Similarly, the transactivation activities of the CHOP protein was suppressed in TSGH9201 and HtTA cells transiently expressing RIG1-myc and RIG1-EGFP, respectively. CONCLUSION: The RIG1 fusion proteins exhibited growth suppressive and apoptosis-inducing activity. The protein negatively-regulated signal pathways of extracellular signal-regulated kinase, c-Jun N-terminal kinase and p38 mitogen-activated kinase.
BACKGROUND: The retinoid-inducible gene I (RIG1), belonging to the family of type II tumor suppressor genes, was isolated from humangastric cancer cells treated with all-trans retinoic acid. The activity of the RIG1 gene was investigated in this study. MATERIALS AND METHODS: HtTA cervical and TSGH9201 gastric cancer cells were transiently transfected with expression vectors that synthesized RIG1-myc or RIG1-EGFP fusion protein. Cell growth was analyzed by measuring the incorporation of bromodeoxyuridine. Apoptosis was evaluated by the formation of in situ DNA breakage. The activities of mitogen-activated kinase signal pathways were analyzed using signal pathway trans-reporting systems. RESULTS:Expression of the RIG1-myc fusion protein resulted in decreased cell growth. Both RIG1-EGFP and RIG1-myc fusion proteins induced cellular apoptosis that was characterized by the presence of apoptotic bodies and in situ DNA breakage. The transactivation activities of Elk1, c-Jun and CHOP proteins were suppressed by 80, 50 and 88%, respectively, in HtTA cells expressing the RIG1-myc fusion protein for two days. Similarly, the transactivation activities of the CHOP protein was suppressed in TSGH9201 and HtTA cells transiently expressing RIG1-myc and RIG1-EGFP, respectively. CONCLUSION: The RIG1 fusion proteins exhibited growth suppressive and apoptosis-inducing activity. The protein negatively-regulated signal pathways of extracellular signal-regulated kinase, c-Jun N-terminal kinase and p38 mitogen-activated kinase.
Authors: Zhengting Wang; Liying Wang; Jiajia Hu; Rong Fan; Jie Zhou; Lei Wang; Jie Zhong Journal: Am J Cancer Res Date: 2015-05-15 Impact factor: 6.166