human
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.
INPUT: ['To investigate the role of Bcl-X(L) on the growth and survival of human ovarian carcinoma cells.', 'In this study, we enforced down-regulation of Bcl-X(L) by RNA interference in ovarian carcinoma cell lines CaOV3, SKOV3ip1 and OVCAR3 cell lines expressing various levels of Bcl-X(L). We also established stable transfectants of OVCAR3 cells overexpressing Bcl-X(L). We recently showed that Bcl-2 regulates cell cycle progression in ovarian cancer cells. Thus, the effect of Bcl-X(L) modulation on the rate of cell growth was determined by XTT assay. To evaluate the role of Bcl-X(L) in drug-induced apoptosis, cisplatin- and paclitaxel-induced apoptosis were determined in vitro for each of the three cell lines. Ovarian tumor cells must acquire the ability to survive in non-adherent conditions to grow in ascetic fluids. To mimic loss of anchorage and investigate the role of Bcl-X(L) in this process, cells were cultured on Hydrogel-coated plates and nuclear fragmentation, caspase-3 activation and nuclear propidium iodide staining were used to determine apoptosis.', 'We show that enforced down-regulation of Bcl-X(L) protein significantly affected the growth rates of CaOV3 whereas it had only minimal effect on the other two cell lines. Down-regulation of Bcl-X(L) enhanced the sensitivity of CaOV3, OVCAR3 and SKOV3ip1 to cisplatin and paclitaxel. The susceptibility to apoptosis induced by loss of anchorage was also increased but in a cell line-dependent manner. Overexpression of Bcl-X(L) slowed the growth of OVCAR3 cells and conferred resistance to drug-induced apoptosis and apoptosis induced by loss of anchorage.'] Is bcl-X ( L ) functionally non-equivalent for the regulation of growth and survival in human ovarian cancer cells?
OUTPUT:

agent
yes
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.
INPUT: ['To investigate the role of Bcl-X(L) on the growth and survival of human ovarian carcinoma cells.', 'In this study, we enforced down-regulation of Bcl-X(L) by RNA interference in ovarian carcinoma cell lines CaOV3, SKOV3ip1 and OVCAR3 cell lines expressing various levels of Bcl-X(L). We also established stable transfectants of OVCAR3 cells overexpressing Bcl-X(L). We recently showed that Bcl-2 regulates cell cycle progression in ovarian cancer cells. Thus, the effect of Bcl-X(L) modulation on the rate of cell growth was determined by XTT assay. To evaluate the role of Bcl-X(L) in drug-induced apoptosis, cisplatin- and paclitaxel-induced apoptosis were determined in vitro for each of the three cell lines. Ovarian tumor cells must acquire the ability to survive in non-adherent conditions to grow in ascetic fluids. To mimic loss of anchorage and investigate the role of Bcl-X(L) in this process, cells were cultured on Hydrogel-coated plates and nuclear fragmentation, caspase-3 activation and nuclear propidium iodide staining were used to determine apoptosis.', 'We show that enforced down-regulation of Bcl-X(L) protein significantly affected the growth rates of CaOV3 whereas it had only minimal effect on the other two cell lines. Down-regulation of Bcl-X(L) enhanced the sensitivity of CaOV3, OVCAR3 and SKOV3ip1 to cisplatin and paclitaxel. The susceptibility to apoptosis induced by loss of anchorage was also increased but in a cell line-dependent manner. Overexpression of Bcl-X(L) slowed the growth of OVCAR3 cells and conferred resistance to drug-induced apoptosis and apoptosis induced by loss of anchorage.'] Is bcl-X ( L ) functionally non-equivalent for the regulation of growth and survival in human ovarian cancer cells?
OUTPUT:
