Résumé
Objective @#To explore the etiology, clinical manifestations, diagnosis and treatment of multiple idiopathic root resorption to provide a reference for clinical diagnosis and treatment. @*Methods@# The clinical data of a case of multiple idiopathic root resorption were analyzed retrospectively, and the related literature was reviewed.@*Results@#The patient had no history of orthodontic correction, occlusal trauma, trauma history or other causes of root resorption. Clinical examination revealed full-mouth gingival congestion, redness, a loose texture, and variable degrees of destruction of the alveolar bone. Imaging examination showed that teeth 13, 16, 26, 36, 46 had idiopathic root resorption. The diagnoses were multiple idiopathic root resorption and periodontitis. The pathology tests showed that a large number of osteoclasts were present in the soft tissue surrounding the teeth. Whole-exome sequencing showed that there was a strong correlation between gene mutations (WNT7a and HSPG2) and the present phenotype. Root resorption of teeth without periodontitis was stopped after periodontal treatment during the 19-month follow-up. Tooth 13 was removed, and extraction socket preservation was performed. The etiology of idiopathic root resorption may be related to gene mutations, but it is not clear. At present, there is no effective treatment. @* Conclusion @#Multiple idiopathic root resorption has an unknown etiology, but it may be related to WNT7A and HSPG2 gene mutations. The rate of root resorption can be slowed by controlling periodontal inflammation.
Résumé
Objective:To observe the expression of microRNA (miRNA, miR)-5787 in breast cancer tissues and various cell lines, analyze the effect of overexpression of miR-5787 on breast cancer cell invasion and proliferation, and explore its possible molecular mechanism.Methods:Real-time fluorescence quantitative polymerase chain reaction (qRT-PCR) method was used to detect the expression of miR-5787 in 47 breast cancer tissues and adjacent tissues, 4 breast cancer cell lines and normal breast epithelial cells. Breast cancer cell lines with the lowest miR-5787 expression were selected and transfected with miR-5787 mimics (experimental group) and control NC mimics (control group), respectively. qRT-PCR was used to detect the expression of miR-5787 in cells of the two groups. Transwell invasion experiment and cell counting kit-8 (CCK-8) were used to detect the effect of miR-5787 overexpression on breast cancer cell invasion and proliferation. Bioinformatics software and dual luciferase reporter gene experiments were used to predict and verify the target genes that miR-5787 could complementally bind. qRT-PCR and Western blot were used to detect the expression of target gene mRNA and protein.Results:Compared with adjacent tissues (5.05±0.82), the expression of miR-5787 in breast cancer tissues (1.32±0.33) was significantly reduced ( P<0.01). Compared with normal breast epithelial cells, the expression of miR-5787 in the four breast cancer cell lines was reduced ( P<0.05), and the expression in HCC1937 cells was the lowest ( P<0.01). After transfection of miR-5787 mimics, the expression of miR-5787 in HCC1937 cells in the experimental group was significantly higher than that in the control group ( P<0.01). Overexpression of miR-5787 could inhibit the invasion ( P<0.05) and proliferation ( P<0.05) of breast cancer HCC1937 cells. Bioinformatics software showed that the target gene of miR-5787 might be heparan sulfate proteoglycan 2 (HSPG2), and miR-5787 could complement HSPG2 mRNA ( P<0.01). qRT-PCR and Western blot indicated that overexpression of miR-5787 could significantly inhibit the expression of HSPG2 gene ( P<0.01), with the decreased expression of Vimentin, N-cadherin, Ki67 and PCNA. Conclusions:miR-5787 expression was low in breast cancer tissues and cell lines. Overexpression of miR-5787 could inhibit the invasion and proliferation of breast cancer HCC1937 cells by interfering with the expression of HSPG2 gene.