Frequencies of cancer according to green tea polyphenol intake.

Frequencies of cancer according to green tea polyphenol intake.</p

HuR expression in non-cancer and cancer cells.

<p>IRS of nuclear HuR differed between cancer and non-cancer cells and between invasive and non-invasive cancer cells (A). Cytoplasmic HuR expression and the IRS of cytoplasmic HuR was higher in cancer than in non-cancer cells, and higher in invasive as compared to non-invasive cases (B).</p

Representative examples of HuR immunoreactivity in normal cells (A) and cancer cells (B) of chemical-induced bladder cancer mouse model.

<p>(Magnification, x400). Staining pattern was close to human tissues.</p

Effect of green tea polyphenol intake on cytoplasmic HuR expression.

<p>Effect of green tea polyphenol intake on cytoplasmic HuR expression.</p

Representative examples of HuR immunoreactivity in normal urothelial cells (A; magnification, ×200.) and cancer cells (B and C; magnification, ×400.).

<p>HuR was mainly detected in nuclei of both normal and cancer cells in bladder tissues. Moderate or strong cytoplasmic expression was evident in cancer cells (C), but was rare in normal urothelial cells (A). Some cancer cells are also showed weak cytoplasmic expression although nuclear expression was detected (B). In addition, we showed representative figures of HuR expression (C) and factors related thereto; (D) cyclooxygenase-2, (E) vascular endothelial growth factor-A, (F) vascular endothelial growth factor-C in same area. (all magnification, x400).</p

Correlation between pathological characteristics and cancer-related molecules.

<p>Correlation between pathological characteristics and cancer-related molecules.</p

Anti-cancer mechanisms of GTP.

<p>Schematic illustration of the role of GTP intake in the modulation of malignant characteristics in bladder cancer. GTP intake suppresses the expression of COX-2 and HO-1 directly and that of HO-1 and VEGF-A indirectly via regulation of cytoplasmic HuR expression. Downregulation of COX-2 and HO-1 or HO-1 and VEGF-A leads to inhibition of cancer cell proliferation and angiogenesis, respectively, thereby suppressing tumor growth.</p

Kaplan-Meier curves for recurrence-free survival rates with urinary tract cancer (A), recurrence-free survival rates with metastasis (B), and cause-specific survival rates (C).

<p>Kaplan-Meier curves for recurrence-free survival rates with urinary tract cancer (A), recurrence-free survival rates with metastasis (B), and cause-specific survival rates (C).</p

Schema of the relationships between cytoplasmic HuR expression and angiogenesis, lymphangiogenesis, and expressions of related molecules.

<p>MVD, microvessel density; LVD, lymphvessel density; VEGF, vascular endothelial growth factor; COX, cyclooxygenase.</p

Survival analyses for metastasis.

<p>Tx: therapy, HR: hazard ratio, CI: confidential interval.</p><p>Model A: including cytoplasmic HuR expression, grade, pT stage, and adjuvant therapy.</p><p>Model B: including cytoplasmic HUR expression, grade, and pT stage, but not adjuvant TX.</p