The most frequent cause of death for cancer patients is metastasis. The precise molecular events leading to the acquisition of malignant phenotypes remain largely unknown. During the past 10 years, we have focused our...The most frequent cause of death for cancer patients is metastasis. The precise molecular events leading to the acquisition of malignant phenotypes remain largely unknown. During the past 10 years, we have focused our efforts on exploring signaling mechanisms underlying malignant progression of human prostate carcinoma. We found that activation of P2Y purinoceptor on androgen independent prostate carcinoma cell lines resulted in significant growth inhibition. This growth inhibitory effect was accompanied by activation of phospholipase C and calcium mobilization, and proved receptor specific. We also demonstrated that the G protein coupled P2Y purinoceptor was linked to Erk1/2 and p38 MAPK pathway, and there existed cross talk between phospholipase C and MAPK pathways. We found Erk1/2 and p38 MAPK pathways were differentially activated between metastatic and non metastatic prostate carcinoma cell subclones, providing valuable clue to further study molecular mechanism of tumor metastasis.展开更多
文摘The most frequent cause of death for cancer patients is metastasis. The precise molecular events leading to the acquisition of malignant phenotypes remain largely unknown. During the past 10 years, we have focused our efforts on exploring signaling mechanisms underlying malignant progression of human prostate carcinoma. We found that activation of P2Y purinoceptor on androgen independent prostate carcinoma cell lines resulted in significant growth inhibition. This growth inhibitory effect was accompanied by activation of phospholipase C and calcium mobilization, and proved receptor specific. We also demonstrated that the G protein coupled P2Y purinoceptor was linked to Erk1/2 and p38 MAPK pathway, and there existed cross talk between phospholipase C and MAPK pathways. We found Erk1/2 and p38 MAPK pathways were differentially activated between metastatic and non metastatic prostate carcinoma cell subclones, providing valuable clue to further study molecular mechanism of tumor metastasis.
