K. Ahn, P. N. Khoi, Young‐Suk Cho, Shinan Li, Dhiraj Kumar Sah, Yong Xia, Y. Jung
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Specific inhibitor studies have shown that the transcription factors, activator protein-1 (AP-1) and nuclear factor-kappa B (NF- κ B), are involved in PMA-induced ICAM-1 expression. We found that sulforaphane inhibited the activation of both AP-1 and NF- κ B induced by PMA in bladder cancer cells. Interestingly, we also found that sulforaphane abrogated PMA-induced THP-1 monocyte adhesion to bladder cancer cells. Collectively, our results provide experimental evidence that sulforaphane could serve as a new therapeutic candidate against bladder cancer. bladder cancer, the mechanism of action is still unclear. This study suggests that sulforaphane inhibits the activation of the transcription factors, activator protein-1 (AP-1) and nuclear factor-kappa B (NF- κ B), and consequently sup presses ICAM-1 expression, thereby inhibiting bladder cancer progression and recurrence.","PeriodicalId":356245,"journal":{"name":"Anatomy & Biological Anthropology","volume":"1 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"1900-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Sulforaphane Inhibits ICAM-1 Expression and Monocyte Adhesion in Human Bladder Cancer T24 Cells\",\"authors\":\"K. Ahn, P. N. Khoi, Young‐Suk Cho, Shinan Li, Dhiraj Kumar Sah, Yong Xia, Y. 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引用次数: 0
摘要
:细胞内粘附分子-1 (Intracellular adhesion molecule-1, ICAM-1)属于介导细胞与其他细胞粘附的免疫球蛋白样粘附分子超家族,ICAM-1参与了癌症的进展和复发。由于ICAM-1被认为是膀胱癌的治疗靶点之一,我们研究了脂肪族异硫氰酸盐萝卜硫素是否可以抑制膀胱癌T24细胞中ICAM-1的表达。逆转录酶聚合酶链反应和western blot结果显示,萝卜硫素抑制PMA诱导的人膀胱癌细胞中ICAM-1 mRNA和蛋白水平的表达。特异性抑制剂研究表明,转录因子,激活蛋白1 (AP-1)和核因子κ B (NF- κ B)参与了pma诱导的ICAM-1表达。我们发现萝卜硫素抑制PMA诱导的膀胱癌细胞AP-1和NF- κ B的激活。有趣的是,我们还发现萝卜硫素可以消除pma诱导的THP-1单核细胞对膀胱癌细胞的粘附。总之,我们的研究结果提供了实验证据,表明萝卜硫素可以作为一种新的治疗膀胱癌的候选药物。膀胱癌的作用机制尚不清楚。本研究提示,萝卜硫素可抑制转录因子、激活因子蛋白-1 (AP-1)和核因子κ B (NF- κ B)的激活,从而抑制ICAM-1的表达,从而抑制膀胱癌的进展和复发。
Sulforaphane Inhibits ICAM-1 Expression and Monocyte Adhesion in Human Bladder Cancer T24 Cells
: Intracellular adhesion molecule-1 (ICAM-1) belongs to the immunoglobulin-like superfamily of adhesion molecules that mediate cell adhesion to other cells, and ICAM-1 is involved in cancer progression and recurrence. Since the ICAM-1 is considered as one of the therapeutic target against bladder cancer, we examined whether sulforaphane, an aliphatic isothiocyanate, could inhibit ICAM-1 expression in bladder cancer T24 cells. Sulforaphane inhibited phorbol 12-myristate 13-acetate (PMA)-induced ICAM-1 expression at the mRNA and protein levels in human bladder cancer cells, as revealed by reverse transcriptase polymerase chain reaction and western blot analyses, respectively. Specific inhibitor studies have shown that the transcription factors, activator protein-1 (AP-1) and nuclear factor-kappa B (NF- κ B), are involved in PMA-induced ICAM-1 expression. We found that sulforaphane inhibited the activation of both AP-1 and NF- κ B induced by PMA in bladder cancer cells. Interestingly, we also found that sulforaphane abrogated PMA-induced THP-1 monocyte adhesion to bladder cancer cells. Collectively, our results provide experimental evidence that sulforaphane could serve as a new therapeutic candidate against bladder cancer. bladder cancer, the mechanism of action is still unclear. This study suggests that sulforaphane inhibits the activation of the transcription factors, activator protein-1 (AP-1) and nuclear factor-kappa B (NF- κ B), and consequently sup presses ICAM-1 expression, thereby inhibiting bladder cancer progression and recurrence.