ABSTRACT
MicroRNAs (miRNAs) are related to the regulation of bone metabolism. Delayed fracture healing (DFH) is a common complication after fracture surgery. The study attempted to examine the role of miR-98-5p and bone morphogenetic protein (BMP)-2 with the onset of DFH. A total of 140 patients with femoral neck fracture were recruited, including 80 cases with normal fracture healing (NFH) and 60 cases with DFH. MC3T3-E1 cells were induced cell differentiation for cell function experiments. Real-time quantitative polymerase chain reaction (RT-qPCR) was carried out to test mRNA levels. Cell proliferation and apoptosis were determined via CCK-8 and flow cytometry assay. Luciferase reporter assay was done to verify the targeted regulatory relationship of miR-98-5p with BMP-2. In comparison with NFH cases, DFH patients owned high levels of serum miR-98-5p and low concentration of BMP-2, and the levels of the two indexes are significantly negatively correlated. Both miR-98-5p and BMP-2 had the ability to predict DFH, while their combined diagnostic value is the highest. BMP-2 was demonstrated to be the target gene of miR-98-5p. Overexpression of BMP-2 reversed the role of miR-98-5p in MC3T3-E1 cell proliferation, apoptosis and differentiation. Increased miR-98-5p and decreased BMP-2 serve as potential biomarkers for the diagnosis of DFH. MiR-98-5p overexpression inhibits osteoblast proliferation and differentiation via targeting BMP-2.
Subject(s)
Apoptosis , Bone Morphogenetic Protein 2 , Cell Proliferation , Fracture Healing , MicroRNAs , Aged , Animals , Female , Humans , Male , Mice , Middle Aged , Apoptosis/genetics , Base Sequence , Bone Morphogenetic Protein 2/metabolism , Bone Morphogenetic Protein 2/genetics , Cell Differentiation/genetics , Cell Line , Femoral Neck Fractures/metabolism , Femoral Neck Fractures/genetics , Fracture Healing/genetics , MicroRNAs/genetics , MicroRNAs/metabolismABSTRACT
The role of autophagy is known to be highly complex and context-dependent, and may be characterized as both tumor suppression and tumor promotion in some tumors, such as breast cancer and prostate cancer. This review outlines recent advances in the studies of the involvement of autophagy in the development, progression and treatment of prostate cancer, focusing on autophagy modulation during androgen deprivation, with a special discussion on the regulatory effect of androgens on the autophagy of prostate cancer cells. A critical evaluation and analysis of the studies suggests that autophagy inhibition combined with androgen deprivation therapy is a promising approach to the treatment of prostate cancer.
Subject(s)
Autophagy , Prostatic Neoplasms , Humans , MaleABSTRACT
Recent studies have demonstrated the importance of the non-protein coding part of human genome in carcinogenesis and metastasis of prostate cancer. Long non-coding RNAs (lncRNAs) play a key regulatory role in prostate cancer biology. LncRNAs are dysregulated in prostate cancer and the expression levels of certain lncRNAs are associated with the recurrence, metastasis and prognosis of cancer. It is also proved that lncRNAs, as oncogenes, can promote carcinogenesis and development of prostate cancer. This review focuses on the progress in the studies of lncRNAs in prostate cancer.
