Background：Bisdemethoxycurcumin （BDMC） is an active component of curcumin and a chemotherapeutic agent,which has been suggested to inhibit tumor growth,invasion and metastasis in multiple cancers.But its contributi...Background：Bisdemethoxycurcumin （BDMC） is an active component of curcumin and a chemotherapeutic agent,which has been suggested to inhibit tumor growth,invasion and metastasis in multiple cancers.But its contribution and mechanism of action in invasion and metastasis of non-small cell lung cancer （NSCLC） are not very clear.Therefore,we tried to study the effects of BDMC on regulation of epithelial-to-mesenchymal transition （EMT）,which is closely linked to tumor cell invasion and metastasis.Methods：In this study,we first induced transforming growth factor-βl （TGF-β1） mediated EMT in highly metastatic lung cancer 95D cells.Thereafter,we studied the effects of BDMC on invasion and migration of 95D cells.In addition,EMT markers expressions were also analyzed by western blot and immunofluorescence assays.The contribution of Wnt inhibitory factor-1 （WIF-1） in regulating BDMC effects on TGF-β1 induced EMT were further analyzed by its overexpression and small interfering RNA knockdown studies.Results：It was observed that BDMC inhibited the TGF-β1 induced EMT in 95D cells.Furthermore,it also inhibited the Wnt signaling pathway by upregulating WIF-1 protein expression.In addition,WIF-1 manipulation studies further revealed that WIF-1 is a central molecule mediating BDMC response towards TGF-β1 induced EMT by regulating cell invasion and migration.Conclusions：Our study concluded that BDMC effects on TGF-β1 induced EMT in NSCLC are mediated through WIF-1 and elucidated a novel mechanism of EMT regulation by BDMC.展开更多
The present study investigated the influence of anti-estrogen treatment （fulvestrant） on pituitary adenoma cell line GH3 biological activity, the estrogen receptor a pathway, the WnT pathway, and mechanisms of decre...The present study investigated the influence of anti-estrogen treatment （fulvestrant） on pituitary adenoma cell line GH3 biological activity, the estrogen receptor a pathway, the WnT pathway, and mechanisms of decreased Wnt inhibitory factor-1 expression in GH3 cells. Results showed that fulvestrant suppressed GH3 cell proliferation and reduced hormone secretion in a dose-dependent manner. Estrogen receptor a and Wnt4 expression decreased, but Wnt inhibitory factor-1 expression increased in a dose-dependent manner following fulvestrant treatment, and β-catenin expression remained unchanged. Inhibitors of DNA methylation and histone modification upregulated Wnt inhibitory factor-1 expression. Results suggested that fulvestrant suppressed biological activity of GH3 cells via the estrogen receptor a and Wnt pathways. These results suggested that decreased Wnt inhibitory factor-1 expression in GH3 cells played a role in epigenetic mechanisms. Anti-estrogen therapies could provide novel treatments for growth hormone adenomas.展开更多
文摘Background：Bisdemethoxycurcumin （BDMC） is an active component of curcumin and a chemotherapeutic agent,which has been suggested to inhibit tumor growth,invasion and metastasis in multiple cancers.But its contribution and mechanism of action in invasion and metastasis of non-small cell lung cancer （NSCLC） are not very clear.Therefore,we tried to study the effects of BDMC on regulation of epithelial-to-mesenchymal transition （EMT）,which is closely linked to tumor cell invasion and metastasis.Methods：In this study,we first induced transforming growth factor-βl （TGF-β1） mediated EMT in highly metastatic lung cancer 95D cells.Thereafter,we studied the effects of BDMC on invasion and migration of 95D cells.In addition,EMT markers expressions were also analyzed by western blot and immunofluorescence assays.The contribution of Wnt inhibitory factor-1 （WIF-1） in regulating BDMC effects on TGF-β1 induced EMT were further analyzed by its overexpression and small interfering RNA knockdown studies.Results：It was observed that BDMC inhibited the TGF-β1 induced EMT in 95D cells.Furthermore,it also inhibited the Wnt signaling pathway by upregulating WIF-1 protein expression.In addition,WIF-1 manipulation studies further revealed that WIF-1 is a central molecule mediating BDMC response towards TGF-β1 induced EMT by regulating cell invasion and migration.Conclusions：Our study concluded that BDMC effects on TGF-β1 induced EMT in NSCLC are mediated through WIF-1 and elucidated a novel mechanism of EMT regulation by BDMC.
基金supported by the National Natural Science Foundation of China, No. 81072075
文摘The present study investigated the influence of anti-estrogen treatment （fulvestrant） on pituitary adenoma cell line GH3 biological activity, the estrogen receptor a pathway, the WnT pathway, and mechanisms of decreased Wnt inhibitory factor-1 expression in GH3 cells. Results showed that fulvestrant suppressed GH3 cell proliferation and reduced hormone secretion in a dose-dependent manner. Estrogen receptor a and Wnt4 expression decreased, but Wnt inhibitory factor-1 expression increased in a dose-dependent manner following fulvestrant treatment, and β-catenin expression remained unchanged. Inhibitors of DNA methylation and histone modification upregulated Wnt inhibitory factor-1 expression. Results suggested that fulvestrant suppressed biological activity of GH3 cells via the estrogen receptor a and Wnt pathways. These results suggested that decreased Wnt inhibitory factor-1 expression in GH3 cells played a role in epigenetic mechanisms. Anti-estrogen therapies could provide novel treatments for growth hormone adenomas.
