1.Biocompatibility of osteoblast and demineralized dental matrix
Xianxin LU ; Dong ZHANG ; Ying XIE ; Puliang ZHANG ; Zhige LI ; Bin LIU
Chinese Journal of Tissue Engineering Research 2009;13(47):9295-9298
BACKGROUND: Bone-induced protein and its carrier are widely used at present; however, the source is limited, and the preparation is complex. Demineralized dental matrix (DDM) is a natural compound containing many osteoinductional proteins and carriers, thus DDM is an ideal material as the substitute of allogenic bone transplantation.OBJECTIVE: By co-culture of MC-3T3 osteoblast and DDM, to evaluate the biocompatibility of DDM via measuring proliferation and alkaline phosphatase (ALP) activity of osteoblast.DESIGN, TIME AND SETTING: A randomized controlled experiment was performed in Stomatology Hospital of Lanzhou University and Stomatology Hospital of Liwan from November 2007 to May 2009.MATERIALS: DDM was supported by Shenzhen Chuangbo Biological Products Development Co., Ltd.; hydroxyapatite (HAP) was supported by Nanjing Emperor Nano Material Co., Ltd.METHODS: 0.1 g HAP and DDM were added in to a 24-well plate, three wells per samples, and the MC-3T3 osteoblasts were seeded onto the surface of samples. After culturing for 2, 4, and 6 days, the cell proliferation percentage was calculated according to MTT assay. ALP activity was evaluated by the quantitative ALP assay.MAIN OUTCOME MEASURES: The effect of DDM on the proliferation and ALP activity of osteoblasts.RESULTS: The proliferation of osteoblasts in DDM group was obviously higher than that in HAP group. With culture time increasing, the ALP activity of osteoblasts in two groups was all augmented, and DDM group was higher than HAP group. There was significant difference between the two groups (P < 0.05).CONCLUSION: DDM can promote adhesion and proliferation of osteoblasts, and promote osteoblastic growth, displaying a great biocompatibility.
2.circNHSL1 inhibits proliferation and promotes apoptosis of human breast cancer cell line through regulating miR-125b-5p/HMGB3 axis
Basic & Clinical Medicine 2024;44(12):1678-1684
Objective To investigate the regulation of miR-125b-5p/HMGB3 axis by circNHSL1 on the biological behavior of breast cancer cells.Methods The breast cancer cells T47D were divided into si-NC group,si-circNH-SL1 group,miR-NC group,and miR-125b-5p mimic group and si-circNHSL1+miR-125b-5p inhibitor group.The expression of circNHSL1 and miR-125b-5p in breast cancer tissues and adjacent tissues was determined using RT-qPCR.Western blot was conducted to detect the protein expression of high mobility group protein 3(HMGB3).Dual luciferase reporter gene assay was used to confirm the interaction between circNHSL1 and miR-125b-5p,miR-125b-5p and HMGB3.The proliferation rate was measured by CCK-8 method;the colony formation assay was applied to detect the colony formation numbers;flow cytometry was used to measure cell apoptosis rate;Transwell assay was used to detect the numbers of migratory and invasive cells.Results Compared with adjacent tissues,cir-cNHSL1 and HMGB3 expression in breast cancer tissues was significantly increased(P<0.05),while the expres-sion of miR-125b-5p was significantly decreased(P<0.05).miR-125b-5p directly bound to circNHSL1 and HMGB3,respectively.The circNHSL1 knockdown down regulated circNHSL1 and HMGB3 expression and upregu-lated miR-125b-5p expression in T47D cells(P<0.05).After transfection with miR-125b-5p mimic,miR-125b-5p expression was up-regulated and HMGB3 expression was down-regulated(P<0.05).Moreover,transfection of miR-125b-5p inhibitor reversed the effect of circNHSL1 silencing on the expression of miR-125b-5p and HMGB3.Low expression of circNHSL1 or high expression of miR-125b-5p increased the cell inhibition rate,colony formation and apoptosis rate of T47D and decreased the number of migratory and invasive cells(P<0.05).Moreover,trans-fection of miR-125b-5p inhibitor saved the effect of circNHSL1 silencing on cell phenotypes(P<0.05).Conclusions Interfering with circNHSL1 might promote cell apoptosis and inhibit cell proliferation,migration and invasion in breast cancer cell by up-regulating the miR-125b-5p/HMGB3 axis.