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Yang, Yoolhee,Park, Hyunjeong,Yang, Young,Kim, Tae Sung,Bang, Sa Ik,Cho, Daeho Munksgaard 2007 Experimental Dermatology Vol.16 No.1
<P>Abstract: </P><P>Melanoma is a malignant skin cancer that displays a high rate of tumor cell migration and metastasis. This study examined how corticotropin-releasing hormone (CRH) affects the migration of melanoma cells in order to further understand the relationship between stress and tumor cell migration. The migration assay data showed that CRH treatment increased the level of B16F10 cell migration in a dose- and time-dependent manner. To determine whether the extracellular signal-regulated protein kinase 1/2 (ERK1/2) signaling pathway is involved in the upregulation of melanoma migration, cells were pretreated with an inhibitor of ERK1/2 (PD098059). The pretreatment of PD098059 blocked the increase in cell migration. Furthermore, CRH induced the phosphorylation of ERK1/2. The maximum activation of ERK1/2 by CRH was observed at 15 min. Taken together, these results suggest that CRH is an important mediator that regulates the migration of melanoma cells in the skin during stress through the ERK1/2 signaling pathway.</P>
Yoon, Sun Young,Lee, Ha Reum,Park, Yoorim,Kim, Joo Heon,Kim, Soo Young,Yoon, Suk Ran,Lee, Wang Jae,Cho, Byung Joo,Min, Hyeyoung,Bang, Jung-Wook,Park, Hyunjeong,Bang, Sa Ik,Cho, Daeho National Hellenic Research Foundation 2011 Oncology reports Vol.25 No.1
<P>Intratumoral hypoxia has been correlated with distant metastatic potential. Two hypoxia inducible factors (HIFs), HIF-1관 and HIF-2관, are induced by hypoxia, and high expression of these proteins has been correlated to angiogenesis and distant metastasis. Thymosin 관4 (T관4) is frequently highly expressed in cancer, and this overexpression correlates with malignant progression. The objective of this study was to investigate the clinical correlation of HIF-관 with T관4 and the intracellular functional roles of T관4 on HIF-관 activation. We examined HIF-1관, HIF-2관 and T관4 expressions in clinical human breast carcinoma (n=70) by immunohistochemistry. We show that high expression of HIF-1관 and HIF-2관 strongly correlates with T관4 expression (P??.0001) and overexpression of T관4 correlates significantly with patients with lymph node metastasis (P<0.05) of human breast cancer. Additionally, we demonstrate that hypoxia up-regulates intracellular T관4 protein, which then affects HIF-관 activity, which is the key in regulating VEGF expression. We confirmed that hypoxia-induced intracellular T관4 and HIF-관 activities were reduced by interference of T관4 expression using T관4 shRNA lentivirus. Vascular epidermal growth factor (VEGF)-A, a well-recognized lymphangiogenic cytokine, was also down-regulated, but VEGF-C and VEGF-D expressions were not affected. These findings suggest that the overexpression of T관4 is strongly associated with HIF-1관 and HIF-2관 expression and is also clinicopathologically involved with lymph node metastatic potential of breast cancer through the modulation of HIF-관activation and induction of VEGF-A. Ultimately, these results highlight T관4 as a potentially therapeutic target in malignant cancers.</P>
Lee, Ji H.,Park, Sunyoung,Cheon, Soyoung,Lee, Joo H.,Kim, Sunghan,Hur, Dae Y.,Kim, Tae S.,Yoon, Suk R.,Yang, Yoolhee,Bang, Sa I.,Park, Hyunjeong,Lee, Hoon T.,Cho, Daeho WILEY‐VCH Verlag 2011 European journal of immunology Vol.41 No.10
<P><B>Abstract</B></P><P>The active metabolite of vitamin D<SUB>3</SUB>, 1α,25(OH)<SUB>2</SUB>D<SUB>3</SUB>, displays anticancer effects by regulating cell cycle and apoptosis in many cancer cells. However, it has not been determined whether 1α,25(OH)<SUB>2</SUB>D<SUB>3</SUB> increases the susceptibility of cancer cells to NK cells. Here, we investigated the anticancer effect of 1α,25(OH)<SUB>2</SUB>D<SUB>3</SUB> in human melanoma cell lines by investigating enhancement of NK susceptibility and elucidating the mediator of NK cytotoxicity. 1α,25(OH)<SUB>2</SUB>D<SUB>3</SUB>‐resistant melanoma cells (G‐361 and SK‐MEL‐5) treated with 1α,25(OH)<SUB>2</SUB>D<SUB>3</SUB> showed higher susceptibility to NK cells with up‐regulation of Fas expression. Furthermore, G‐361 cells treated with 1α,25(OH)<SUB>2</SUB>D<SUB>3</SUB> showed significantly increased caspase activity. In addition to Fas up‐regulation, expression of heat shock protein 60 (Hsp60) was elevated by 1α,25(OH)<SUB>2</SUB>D<SUB>3</SUB>. Increased expression of Hsp60 by 1α,25(OH)<SUB>2</SUB>D<SUB>3</SUB> was related to not only up‐regulation of Fas expression but also to NK susceptibility of G‐361 cells. Taken together, our data suggest that 1α,25(OH)<SUB>2</SUB>D<SUB>3</SUB> acts as an anticancer agent by increasing expression of Fas on the surface of melanoma cells through Hsp60 induction and strengthens caspase sensitivity to Fas‐mediated apoptotic pathway by NK cells. 1α,25(OH)<SUB>2</SUB>D<SUB>3</SUB> treatment may therefore have a preventive role in melanoma occurrence or potentiate the anticancer effects of NK‐cell immune therapy.</P>
YOON, SUN YOUNG;LEE, HA REUM;PARK, YOORIM;KIM, JOO HEON;KIM, SOO YOUNG;YOON, SUK RAN;LEE, WANG JAE;CHO, BYUNG JOO;MIN, HYEYOUNG;BANG, JUNG-WOOK;PARK, HYUNJEONG;BANG, SA IK;CHO, DAEHO Sookmyung Women's University Research Institute of 2011 여성과 건강 Vol.6 No.2
Intratumoral hypoxia has been correlated with distant metastatic potential. Two hypoxia inducible factors (HIFs). HIF-1α and HIF-2α, are induced by hypoxia, and high expression of these proteins has been correlated to angiogenesis and distant metastasis. Thymosin β4 (Tβ4) is frequently highly expressed in cancer, and this overexpression correlates with malignant progression. The objective of this study was to investigate the clinical correlation of HIF-α with Tβ4 and the intracellular functional roles of Tβ4 on HIF-α activation. We examined HIF-1α, HlF-2α and Tβ4 expressions in clinical human breast carcinoma (n=70) by immunohisto-chemistry. We show that high expression of HIF-1α and HIF-2α strongly correlates with Tβ4 expression (P≤0.0001) and overexpression of Tβ4 correlates significantly with patients with lymph node metastasis (P<0.05) of human breast cancer. Additionally, we demonstrate that hypoxia up-regulates intracellular Tβ4 protein, which then affects HIF-α activity, which is the key in regulating VEGF expression. We confirmed that hypoxia-induced intracellular Tβ4 and HIF-α activities were reduced by interference of TIM expression using Tβ4 shRNA lentivirus. Vascular epidermal growth factor (VEGF)-A, a well-recognized lymphangiogenic cytokine, was also down-regulated, but VEGF-C and VEGF-D expressions were not affected. These findings suggest that the overexpression of Tβ4 is strongly associated with HIF-1α and HIF-2α expression and is also clinicopathologically involved with lymph node metastatic potential of breast cancer through the modulation of HIF-a activation and induction of VEGF-A. Ultimately, these results highlight Tβ4 as a potentially therapeutic target in malignant cancers.
Expression of ADAM33 is a novel regulatory mechanism in IL-18-secreted process in gastric cancer.
Kim, Kyung-Eun,Song, Hyunkeun,Hahm, Candace,Yoon, Sun Young,Park, Sunyoung,Lee, Ha-reum,Hur, Dae Young,Kim, Taesung,Kim, Cherl-hyun,Bang, Sa Ik,Bang, Jung-Wook,Park, Hyunjeong,Cho, Dae-Ho Williams Wilkins 2009 JOURNAL OF IMMUNOLOGY Vol.182 No.6
<P>IL-18 has recently been reported to play a critical role in tumor migration, invasion, and metastasis. Because IL-18 has various biological activities after its secretion as an 18 kDa mature form, the regulation of the IL-18 secretion process is an important step in tumor progression. This study investigated the implication of IL-18 in vascular endothelial growth factor (VEGF)-D-regulated migration, along with the role of the IL-18 secretion process. VEGF-D enhanced cell migration, which was then blocked by inhibiting IL-18. VEGF-D increased IL-18 expression and secretion, suggesting that IL-18 is a critical mediator for VEGF-D-enhanced migration. VEGF-D induced a disintegrin and metalloprotease 33 (ADAM33) expression, which has a metalloproteinase domain. VEGF-D-enhanced IL-18 secretion and cell migration were inhibited by ADAM33 knock-down. Moreover, cell proliferation was considerably reduced in ADAM33 small interfering RNA transfectants. In conclusion, ADAM33 has a key role in gastric cancer pathogenesis by up-regulating IL-18 secretion process, resulting in increased cell migration and proliferation.</P>