BACKGROUND & OBJECTIVE: There has always been a significant morbidity difference of renal cell carcinoma between the Oriental and Occidental countries. The high soybean consumption in Oriental countries may be one of the reasons. We investigated the effect of a tyrosine protein kinase inhibitor extracted from soybean, namely genistein, on the proliferation of a renal cell carcinoma cell line, GRC-1; and analyzed the correlation between this effect and a well-known anti-oncogene, p27. METHODS: Inverted microscopy, MTT method, and flow cytometry (FCM) were used to examine the changes in proliferation of GRC-1 cells after treatment with genistein; and the intracellular p27 protein expression was determined by Western blot analysis. RESULTS: (1)After treatment with genistein, changed morphology of the GRC-1 cells was observed. Cell junctions decreased. In the presence of 20 micromol/L genistein, GRC-1 cells showed shuttle-shaped, and fewer pseudopodia, mitoses and cell junctions were observed. In the 40 micromol/L genistein group, many cells broke into debris, and became extremely irregular in shape. Meanwhile, mitoses and cell junctions were rarely seen. (2)Treated with 20 micromol/L genistein, 73.8% GRC-1 cells were in G(1) phase, 26.2% in G2 phase 72 hours after treatment; while in control group, 31.6% in G(1) phase and 3.8% in G2 phase, respectively. (3)After exposure to 20 micromol/L genistein for 72 hours, Western blot suggested that the band of p27 was 65.4+/-4.7 in gray scale value, while the control group was 52.3+/-6.3. CONCLUSION: Genistein can inhibit the proliferation of renal cell carcinoma cells, and cause cell cycle arrest at G(1)/M, G(2)/S phase. The possible underlying mechanism may involve its upregulation of p27 expression in the renal cancer cells.
BACKGROUND & OBJECTIVE: There has always been a significant morbidity difference of renal cell carcinoma between the Oriental and Occidental countries. The high soybean consumption in Oriental countries may be one of the reasons. We investigated the effect of a tyrosine protein kinase inhibitor extracted from soybean, namely genistein, on the proliferation of a renal cell carcinoma cell line, GRC-1; and analyzed the correlation between this effect and a well-known anti-oncogene, p27. METHODS: Inverted microscopy, MTT method, and flow cytometry (FCM) were used to examine the changes in proliferation of GRC-1 cells after treatment with genistein; and the intracellular p27 protein expression was determined by Western blot analysis. RESULTS: (1)After treatment with genistein, changed morphology of the GRC-1 cells was observed. Cell junctions decreased. In the presence of 20 micromol/L genistein, GRC-1 cells showed shuttle-shaped, and fewer pseudopodia, mitoses and cell junctions were observed. In the 40 micromol/L genistein group, many cells broke into debris, and became extremely irregular in shape. Meanwhile, mitoses and cell junctions were rarely seen. (2)Treated with 20 micromol/L genistein, 73.8% GRC-1 cells were in G(1) phase, 26.2% in G2 phase 72 hours after treatment; while in control group, 31.6% in G(1) phase and 3.8% in G2 phase, respectively. (3)After exposure to 20 micromol/L genistein for 72 hours, Western blot suggested that the band of p27 was 65.4+/-4.7 in gray scale value, while the control group was 52.3+/-6.3. CONCLUSION:Genistein can inhibit the proliferation of renal cell carcinoma cells, and cause cell cycle arrest at G(1)/M, G(2)/S phase. The possible underlying mechanism may involve its upregulation of p27 expression in the renal cancer cells.