Prostate cancer is a leading cause of death among the aging men. Surgical or radio therapy is effective when the cancer is confined to the prostate gland but once the cancer spreads beyond the pelvis, even chemotherapy and hormonal ablation therapy fails in curing this disease. Our previous studies have shown that β-glucan induces apoptosis in prostate cancer cells. Cellular viability of these cells treated with β-glucan was measured by MTT assay. β-glucan induced dose- and time-dependent inhibition of cell viability in LNCaP cancer cells. In flow cytometry analysis, β-glucan induced dose- and timedependent apoptotic activities in LNCaP cancer cells. In addition, increased of expression caspase-3, caspase-9, Bax, and cytochrome C but decreased of expression Bcl-2 was observed in LNCaP cells treated with β-glucan. These results suggest that β-glucan induces apoptosis in LNCaP human prostate cancer cells mediated mainly through the increased of expression caspase-3, -9, Bax, cytochrome C and decreased of expression Bcl-2.

The trace element nutrient selenium discharges its well-known nutritional anti-tumor activity. Converging data from epidemiological, ecological and clinical studies have shown that selenium can decrease the risk for some types of human cancers, especially those of the prostate, lung, and colon. Mechanistic studies have indicated that selenium has many desirable attributes of chemoprevention targeting cancer cells through DNA single strand breaks, the induction of reactive oxygen species. However, there is no reports about the relationship between methylseleninic acid (MSeA), one of methylselenol metabolites and cell cycle arrest in LNCaP human prostate cancer cells. Our data showed that MSeA arrested G1/S pahse of cell cycle arrest and inhibited DNA synthesis in LNCaP cells and those cellular events by MSeA were due to the induction of p27 protein which is a well-known cyclin-dependent kinase inhibitor. Taken together, cell cycle arrest occurred by MSeA may contribute to the growth-inhibition of prostate cancer cells.

본 연구는 3,3'-diindolylmethane(DIM)이 인간전립선암 세포인 PC3 세포와 DU145 세포의 부착, 이동, 침윤에 미치 는 영향을 살펴보았다. DIM은 PC3와 DU145 세포의 부착을 농도 의존적으로 억제하였다. 24시간동안 DIM으로 PC3 세포를 전 처리한 후 부착실험을 한 결과 농도 의존적으로 억제하였다. 그러나 암세포가 부착 시 DIM의 암세포 부착 억제가 전처리에 의한 부착 억제보다 효과적이었다. DIM 은 인간 전립선암세포의 이동과 침윤도 억제하였으며 24시 간 동안 PC3 세포를 DIM으로 전처리를 했을 때도 침윤 억제효과를 나타내었다. 또한 DIM의 억제효과는 세포주에 따라 다소 다른 경향을 보여 PC3 세포에 대한 억제효과가 DU145 세포에 대한 억제효과보다 큰 것으로 관찰되었다. DIM은 150 μM 까지 세포 독성이 관찰되지 않은 것으로 보고되고 있으므로 본 연구결과 DIM은 세포 독성이 없는 수준에서 인간 전립선암 세포인 PC3와 DU145 세포의 부 착, 이동, 침윤을 효과적으로 억제하여 전립선암 전이 억제 제로 이용될 수 있을 것으로 사료된다.