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The molecular mechanisms of vitamin C on cell cycle regulation in B16F10 murine melanoma
Hahm, Eunsil,Jin, Dong-Hoon,Kang, Jae Seung,Kim, Young-In,Hong, Seung-Woo,Lee, Seung Koo,Kim, Ha Na,Jung, Da Jung,Kim, Jee Eun,Shin, Dong Hoon,Hwang, Young Il,Kim, Yeong Seok,Hur, Dae Young,Yang, Yool Wiley Subscription Services, Inc., A Wiley Company 2007 Journal of cellular biochemistry Vol.102 No.4
<P>Vitamin C has inconsistent effects on malignant tumor cells, which vary from growth stimulation to apoptosis induction. It is well known that melanoma cells are more susceptible to vitamin C than any other tumor cells, but the precise mechanism remains to be elucidated. In the present study, the proliferation of B16F10 melanoma cells was suppressed by vitamin C, which induced growth arrest in a dose-dependent manner without cytotoxic effects. Therefore, we investigated the changes in cell cycle distribution of B16F10 melanoma cells by staining DNAs with propidium iodide (PI). The growth inhibition of B16F10 melanoma by vitamin C was associated with an arrest of cell cycle distribution at G1 stage. In addition, the levels of p53-p21<SUP>Waf1/Cip1</SUP> increased during G1 arrest, which were essential for vitamin C-induced cell cycle arrest. The increased p21<SUP>Waf1/Cip1</SUP> inhibited CDK2. Moreover, the activity of p53-p21<SUP>Waf1/Cip1</SUP> pathway was closely related with the activation of checkpoint kinase 2 (Chk2). Inhibitor of the PI3K-family, LY294002 and the ATM/ATR inhibitor, caffeine, blocked vitamin C-induced growth arrest in B16F10 melanoma cells. These results suggest that vitamin C might be a potent agent to inhibit proliferative activity of melanoma cells via the regulation of Chk2-p53-p21<SUP>Waf1/Cip1</SUP> pathway. J. Cell. Biochem. 102: 1002–1010, 2007. © 2007 Wiley-Liss, Inc.</P>
Regulation of IL-18 expression by CRH in mouse microglial cells
Yang, Yoolhee,Hahm, Eunsil,Kim, Youngin,Kang, Jaeseung,Lee, Wangjae,Han, Innoc,Myung, Pyungkeun,Kang, Hyungsik,Park, Hyunjeong,Cho, Daeho 충남대학교 형질전환복제돼지연구센터 2007 논문집 Vol. No.10
Corticotropin releasing hormone (CRH) is a major regulator of the stress response. This study examined whether CRH regulates interleukin-18 expression on microglia, BV2. Our data show that CRH enhanced IL-18 expression and significantly induced the secretion of functional IL-18 protein. Furthermore, CRH induced IL-18 production could be blocked by N-acetyl-L-cystein (NAC), which suggests that reactive oxygen intermediates (ROI) may be involved in regulating IL-I8. Indeed, it was also found that CRH increased the generation of ROJ. Taken together, these results indicate that CRH is an important mediator that regulates IL-18 expression in the brain during stress.
Regulation of IL-18 expression by CRH in mouse microglial cells
Yang, Yoolhee,Hahm, Eunsil,Kim, Youngin,Kang, Jaeseung,Lee, Wangjae,Han, Innoc,Myung, Pyungkeun,Kang, Hyungsik,Park, Hyunjeong,Cho, Daeho 충남대학교 형질전환복제돼지연구센터 2004 논문집 Vol. No.8
Corticotropin Releasing Hormone (CRH) is a major regulator of the stress response. This study examined whether CRH regulates interleukin-18 expression on microglia, BV2. Our data show that CRH enhanced IL-18 expression and significantly induced the secretion of functional IL-18 protein. Furthermore, CRH induced IL-18 production could be blocked by N-acetyl-L-cystein (NAC), which suggests that reactive oxygen intermediates (ROI) may be involved in regulating IL-18. Indeed, it was also found that CRH increased the generation of ROI. Taken together, these results indicate that CRH is an important mediator that regulates IL-18 expression in the brain during stress.
Endogenous interleukin-l8 modulates immune escape of murine melanoma cells
Cho, Daeho,Kim, Youngin,Kang, Jaeseung,Hahm, Eunsil,Lee, Wangjae,Song, Hyunkeun,Pyun, Kwangho,Choi, Inpyo 이화여자대학교 세포신호전달연구센터 2001 고사리 세포신호전달 심포지움 Vol. No.3
It has been known that melanoma cells can suppress the immune system by the Fas ligand. The present study investigated whether interleukin(IL)-18, which can enhance Fas ligand expression, is produced by B16F10 melanoma cells and is involved in immune escape of tumor cells. Immunohistology, RT-PCR, intracellular FACS analysis, and immunoblotting demonstrated that melanoma cells express IL-18. In addition to IL-18, the IL-18 receptor was also detected in B16F10 melanoma cells, suggesting a role of this cytokine in regulating the functions of B16F10 melanoma cells. The functional effect of IL-18 on B16F10 melanoma cells was shown by reduction of Fas ligand expression in cells transfected with IL-18 antisense cDNA. In addition, the same treatments decreased intracellular reactive oxygen intermediate levels in B16F10 melanoma cells, indicating that IL-18 regulates reactive oxygen intermediate production. Furthermore, transfection of IL-18 antisense cDNA into melanoma cells increased the susceptibility of tumor cells to natural killer cells in vitro. When IL-18 antisense transfectants were implanted into syngeneic mice, severe reduction of tumor cell growth was observed. Taken together, these results demonstrate that IL-18 has a critical role as a survival factor for B16F10 melanoma cells.
Cho, Daeho,Kang, Jae Seung,Park, Jong Hoon,Kim, Young-In,Hahm, Eunsil,Lee, Junechul,Yang, Yoolhee,Jeon, Junho,Song, HyunKeun,Park, Hyunjeong,Kim, Taesung,Pang, Saic,Kim, Chul-Woo,Hwang, Young Il,Lee, 전남대학교 약품개발연구소 2002 약품개발연구지 Vol.11 No.-
Based on our recent observation that enhanced IL-18 expression positively correlates with malignant skin tumors, such as SCC and melanoma, we examined the possible role of UVB, known to be associated with skin cancer development, in the enhancement of IL-18 production using primary human epidermal keratinocytes and human cell line HaCaT. After cells were exposed to UVB irradiation in vitro, IL-18 production was examined by Northern blot analysis and ELISA, and it was found that IL-18 production is enhanced by UVB irradiation in a dose- and time-dependent manner. In addition, we confirmed that it is functionally active form of IL-18 using the inhibitor of caspase-1. The effect of UVB irradiation was blocked by antioxidant, N-acetyl-ι-cysteine (NAC), which suggested the involvement of reactive oxygen intermediates (ROI) in the signal transduction of UVB irradiation-enhanced IL-18 synthesis. We also found that UVB irradiation increased AP-1 binding activity by using EMSA with AP-1-specific oligonucleotide. Furthermore, inhibitors of UVB-induced AP-1 activity, such as PD98059, blocked enhanced IL-18 production, indicating that AP-1 activation is required for UVB-induced IL-18 production. Taken together, our results suggest that UVB irradiation-enhanced IL-18 production is selectively mediated through the generation of ROI and the activation of AP-1.