Involvement of cyclin B1 in progesterone-mediated cell growth inhibition, G2/M cell cycle arrest, and apoptosis in human endometrial cell

Abstract

BackgroundProgesterone plays an important role in the proliferation and differentiation of human endometrial cells (hECs). Large-dose treatment with progesterone has been used for treatment of endometrial proliferative disorders. However, the mechanisms behind remain unknown.MethodsTo investigate the role of cyclin B1 in proliferation and differentiation of hECs in menstrual cycle, the expression of cyclin B1 throughout the menstrual cycle was evaluated in hECs. To determine the effects of progesterone on the proliferation, cell cycle progression and apoptosis of hECs and to test if cyclin B1 is involved in these effects, progesterone and/or Alsterpaullone (Alp, a specific inhibitor of Cyclin B1/Cdc2) were added to primary hECs. Cellular proliferation was evaluated with MTT test, cell cycle with propidium iodide (PI) staining and flow cytometry, apoptosis with FITC-Annexin V and the expression of cyclin B1 with Western blotting.ResultsThe expression level of cyclin B1 in secretory endometria was significantly lower than in proliferative endometria (p < 0.01). Progesterone significantly inhibited the growth of hECs in a concentration-dependent manner (P < 0.01). The treatment with progesterone significantly decreased the expression of cyclin B1, increased the proportions of cell in G2/M phase, and apoptotic cells (P < 0.05 for all). The presence of Alp significantly enhanced the effects of progesterone on cyclin B1 down-regulation, G2/M cell cycle arrest and induction of apoptosis (P < 0.01 for all).ConclusionOur findings suggest that cyclin B1 is a critical factor in proliferation and differentiation of hECs. Progesterone may inhibit cell proliferation, mediate G2/M cell cycle arrest and induce apoptosis in hECs via down-regulating Cyclin B1.

Effects of SASH1 on melanoma cell proliferation and apoptosis in vitro

“…Our results demonstrated that the mRNA expression of cyclin B (CCNB1) and Cdc2 (CDK1) increased by 4-and 2.5-fold, respectively in the A-375 (SASH1) cells compared with the A-375 (EGFP) cells. The G2/M arrest mostly resulted from the inhibition of the expression of cyclin B or Cdc2 (20,21). However, our findings suggested that SASH1 enhanced G2/M arrest via the upregulation of cyclin B and Cdc2.…”

Galangin Induces Apoptosis in MCF-7 Human Breast Cancer Cells Through Mitochondrial Pathway and Phosphatidylinositol 3-Kinase/Akt Inhibition

“…The downregulation of cyclin D3-CDK 4 complexes contribute to limiting in transition of cells from the G1 to S phase of cell growth [45]. It is different from the function of D-type cyclins, cyclin B1 mainly control the G2 to M transition through associated with CDK 1 [46]. It is reported that cyclin B1 antagonized chemotherapeutic-induced apoptosis in human ESCC cells via PTEN/Akt signaling pathway [47].…”

LncRNA16 is a potential biomarker for diagnosis of early-stage lung cancer that promotes cell proliferation by regulating the cell cycle

“…One of the cyclins, cyclin B1, controls the transition from the G2 to M phase of the cell cycle, and abnormal expression of this protein is widely reported in cancers [33–35]. Our results indicated that lncRNA16 affected the G2/M phase by regulating the expression of cyclin B1 at the mRNA level in PC9 cells.…”