Sulforaphane Inhibits ICAM-1 Expression and Monocyte Adhesion in Human Bladder Cancer T24 Cells
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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-κB), are involved in PMA-induced ICAM-1 expression. We found that sulforaphane inhibited the activation of both AP-1 and NF-κB 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.
Abstract
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-κB), are involved in PMA-induced ICAM-1 expression. We found that sulforaphane inhibited the activation of both AP-1 and NF-κB 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.
참고문헌 (45)
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