Given the loss of func tional PgR in MCF7 miR155 cells compared to vector

Others have shown that exogenous SPARC can be internalized by cells and, indeed, M cells in cubated with S CM as a source of SPARC INNO-406 価格 show enhanced cytoplasmic and nuclear staining for SPARC, suggesting active uptake. Thus, in order to further establish the origin of the observed stain ing for SPARC in prostate tumor samples, real time PCR was performed on RNA samples isolated from laser microdissected epithelial or stromal components of non metastatic or metastatic primary tumors. The epithelial components of tumors from the four non metastatic cases expressed lower levels of SPARC mRNA than the corre sponding stromal components. In contrast, the epi thelial components of tumors from all four metastatic cases expressed higher SPARC mRNA levels than the epi thelial components of non metastatic cases, surpassing in several cases the relative expression levels of the corre sponding stromal components.<br><br> This increased ex pression of SPARC in the epithelial tumor components of metastatic cases Lapatinib ic50 did not appear to associate with higher SPARC expression levels in the overall tumor sample, as tumors with low overall levels exhibited high epithelial stromal SPARC expression ratios and tumors from non metastatic cases with high overall SPARC expression levels showed low epithelialstromal SPARC expression ratios. These observations support the en dogenous neoplastic cell of origin of the SPARC staining observed in the epithelial tumoral components of primary prostate tumors associated with metastasis, although they do not formally rule out a stromal contribution of the SPARC protein detected in the neoplastic cells.<br><br> In contrast to the strong concordance between epithe lial tumor expression of SPARC and metastatic status, overall SPARC mRNA levels from non microdissected purchase LY2109761 samples did not show a significant correlation with meta static status, with the observation of a high variability among samples, in particular in non metastatic cases. To determine if elevated epithelial SPARC levels in metastasis associated primary tumors is reflected in levels of circulating SPARC, we quantified by ELISA the levels of SPARC in the plasma of prostate cancer patients with our without associated lymph node or distant metastases that were not under systemic therapy.<br><br> We found that plasma SPARC levels in metastatic prostate cancer pa tients tended to be lower than those in non metastatic cases or control individuals, and thus we conclude that plasma levels of SPARC in prostate can cer patients do not reflect tumoral SPARC expression levels. To summarize these observations, expression of SPARC is limited to the stroma of non metastatic primary tumors, whereas primary tumors from metastatic cases also ex press SPARC in the tumoral epithelium. Overall tumor SPARC mRNA levels or plasma SPARC protein levels show no significant correlation to metastatic status in prostate cancer. Discussion Neoplastic cellular subpopulations displaying distinct phenotypes can interact among them in different ways, including competition or cooperation. In a prostate cancer cell model previously characterized by us, two subpopulations interact in a cooperative manner, such that one subpopulation enhances the metastatic dissemination potential of the other.