Subject(s)
Carcinoma, Transitional Cell , Kidney Neoplasms , Cell Differentiation , Female , Humans , Kidney Neoplasms/surgery , Kidney Pelvis , MaleABSTRACT
Wnt5a is a representative Wnt ligand that regulates multiple cellular functions through the Wnt5a non-classical pathway. Although Wnt5a has been implicated in various pathological conditions, its role in cancer is ambiguous and might involve methyl modifications, distinct mRNA isoforms, as well as different downstream pathways. Therefore, it is an essential factor in cancers' progression (invasion, migration, proliferation, and epithelial-mesenchymal transition), and a potential biomarker for prognosis and treatment.
Subject(s)
Disease Progression , Neoplasms/metabolism , Neoplasms/pathology , Wnt-5a Protein/metabolism , Animals , Humans , Models, Biological , Receptors, Wnt/metabolism , Wnt Signaling PathwayABSTRACT
PURPOSE: To study the expression of insulin-like growth factor binding proteins (IGFBPs) in paclitaxel-treated gastric cancer SGC-7901 cells, and to further investigate underlying mechanisms. MATERIALS AND METHODS: Real time PCR and Western blot assays were applied to detect the mRNA and protein expression of IGFBP-2, -3 and -5 after paclitaxel (10 nM) treatment of SGC-7901 cells. In addition IGFBP-3 expression was silenced by RNA interference to determine effects. Cell viability was determined by MTT assay. Cell cycling and apoptosis were assessed by flow cytometry. RESULTS: Compared to the control group, only IGFBP-3 expression was elevated significantly after paclitaxel (10 nM) treatment (p<0.05). Paclitaxel treatment caused cell cycle arrest and apoptosis via downregulating Bcl-2 expression. However, the effect could be abrogated by IGFBP-3 silencing. CONCLUSIONS: IGFBP-3 exhibits anti-apoptotic effects on paclitaxel-treated SGC-7901 cells via elevating Bcl-2 expression.
Subject(s)
Antineoplastic Agents, Phytogenic/pharmacology , Apoptosis/genetics , Insulin-Like Growth Factor Binding Protein 3/genetics , Paclitaxel/pharmacology , Stomach Neoplasms/drug therapy , Apoptosis/drug effects , Cell Cycle Checkpoints/drug effects , Cell Line, Tumor , Cell Proliferation , Cell Survival , Down-Regulation , Gene Expression Regulation, Neoplastic , Humans , Insulin-Like Growth Factor Binding Protein 2/metabolism , Insulin-Like Growth Factor Binding Protein 3/biosynthesis , Insulin-Like Growth Factor Binding Protein 5/metabolism , Proto-Oncogene Proteins c-bcl-2/biosynthesis , RNA Interference , RNA, Messenger/biosynthesis , RNA, Small Interfering , Stomach Neoplasms/pathology , Tubulin Modulators/pharmacologyABSTRACT
AIM: To investigate effects of sulforaphane on the BIU87 cell line and underlying mechanisms involving IGFBP-3. METHODS: Both BIU87 and IGFBP-3-silenced BIU87 cells were treated with sulforaphane. Cell proliferation was detected by MTT assay. Cell cycle and apoptosis were determined via flow cytometry. Quantitative polymerase chain reaction and Western blotting were applied to analyze the expression of IGFBP-3 and NF-κB at both mRNA and protein levels. RESULTS: Sulforaphane (80 µM) treatment could inhibit cell proliferation, inducing apoptosis and cell cycle arrest at G2/M phase. All these effects could be antagonized by IGFBP-3 silencing. Furthermore, sulforaphane (80 µM) could down-regulate NF-κB expression while elevating that of IGFBP-3. CONCLUSIONS: Sulforaphane could suppress the proliferation of BIU87 cells via enhancing IGFBP-3 expression, which negatively regulating the NF-κB signaling pathway.
