ABSTRACT
OBJECTIVE: The aim of this study was to investigate the effects of microRNA-5195-3p (miR-5195-3p) on the proliferation of glioma cells and to explore its related mechanisms. PATIENTS AND METHODS: The expression level of miR-5195-3p in glioma tissues and cell lines was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Online prediction websites (TargetScan and miRanda) were used to screen the potential targets of miR-5195-3p. Luciferase reporter gene assay and Western blot were performed to confirm the targets of miR-5195-3p. Furthermore, the effects of miR-5195-3p on cell proliferation were detected by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide), colony formation assay, and flow cytometry, respectively. RESULTS: MiR-5195-3p was lowly expressed in both glioma tissues and cells. Baculoviral IAP repeat-containing 2 (BIRC2) was identified as a direct target of miR-5195-3p. Over-expression of miR-5195-3p in glioma cells significantly decreased the protein expression of BIRC2. Besides, the proliferative capacity and colony formation ability were significantly inhibited after transfection of miR-5195-3p in vitro. In addition, flow cytometry indicated that an evident G1 phase arrest occurred in miR-5195-3p over-expressed group. CONCLUSIONS: In this work, we emphasized the suppressor function of miR-5195-3p in the proliferation of glioma cells. Furthermore, our findings provided an experimental basis for the research and treatment of glioma.
Subject(s)
Central Nervous System Neoplasms/metabolism , Glioma/metabolism , Inhibitor of Apoptosis Proteins/metabolism , MicroRNAs/metabolism , Ubiquitin-Protein Ligases/metabolism , Cell Line , Cell Proliferation , Central Nervous System Neoplasms/pathology , Glioma/pathology , Humans , Inhibitor of Apoptosis Proteins/genetics , MicroRNAs/genetics , Ubiquitin-Protein Ligases/geneticsABSTRACT
Breast cancer is the most common cause of cancer among women in most countries (WHO). Ovarian hormone disorder is thought to be associated with breast tumorigenesis. The present study investigated the effects of estrogen and progesterone administration on cell proliferation and underlying mechanisms in breast cancer MCF-7 cells. It was found that a single administration of estradiol (E2) or progesterone increased MCF-7 cell viability in a dose-dependent manner and promoted cell cycle progression by increasing the percentage of cells in the G2/M phase. A combination of E2 and progesterone led to a stronger effect than single treatment. Moreover, cyclin G1 was up-regulated by E2 and/or progesterone in MCF-7 cells. After knockdown of cyclin G1 in MCF-7 cells using a specific shRNA, estradiol- and progesterone-mediated cell viability and clonogenic ability were significantly limited. Additionally, estradiol- and progesterone-promoted cell accumulation in the G2/M phase was reversed after knockdown of cyclin G1. These data indicated that estrogen and progesterone promoted breast cancer cell proliferation by inducing the expression of cyclin G1. Our data indicated that novel therapeutics against cyclin G1 are promising for the treatment of estrogen- and progesterone-mediated breast cancer progression.
Subject(s)
Breast Neoplasms/pathology , Cell Proliferation/drug effects , Cyclin G1/metabolism , Estrogens/pharmacology , Progesterone/pharmacology , Blotting, Western , Breast Neoplasms/metabolism , Cell Survival , Female , Humans , MCF-7 Cells/drug effects , Real-Time Polymerase Chain ReactionABSTRACT
Breast cancer is the most common cause of cancer among women in most countries (WHO). Ovarian hormone disorder is thought to be associated with breast tumorigenesis. The present study investigated the effects of estrogen and progesterone administration on cell proliferation and underlying mechanisms in breast cancer MCF-7 cells. It was found that a single administration of estradiol (E2) or progesterone increased MCF-7 cell viability in a dose-dependent manner and promoted cell cycle progression by increasing the percentage of cells in the G2/M phase. A combination of E2 and progesterone led to a stronger effect than single treatment. Moreover, cyclin G1 was up-regulated by E2 and/or progesterone in MCF-7 cells. After knockdown of cyclin G1 in MCF-7 cells using a specific shRNA, estradiol- and progesterone-mediated cell viability and clonogenic ability were significantly limited. Additionally, estradiol- and progesterone-promoted cell accumulation in the G2/M phase was reversed after knockdown of cyclin G1. These data indicated that estrogen and progesterone promoted breast cancer cell proliferation by inducing the expression of cyclin G1. Our data indicated that novel therapeutics against cyclin G1 are promising for the treatment of estrogen- and progesterone-mediated breast cancer progression.
