[Experimental study on transplantation of MIRB labeled human deciduous dental pulp stem cells to repair periodontal bone defects in rats].

PURPOSE: To trace the fate of transplanted stem cells from human exfoliated deciduous teeth (SHED) in the repair of periodontal bone defects, Molday ION rhodamine B (MIRB) was used to label SHED and explore the mechanism of SHED in the repair of periodontal bone defects. METHODS: In vitro cultured SHED were labeled by MIRB. The labeling efficiency, cell survival, proliferation and osteogenic differentiation of MIRB-labelled SHED were detected. The labeled cells were transplanted into the rat model with periodontal bone defect. The survival, differentiation and improvement of host periodontal bone healing of MIRB labeled SHED in vivo were analyzed by immunohistochemistry and fluorescence co-staining, nuclear magnetic imaging dual-mode tracking and H-E staining. The data were statistically analyzed with SPSS 24.0 software package. RESULTS: MIRB labeled SHED did not affect its growth and osteogenic differentiation. The optimal labeling concentration was 25 µg/mL, the labeling efficiency of SHED reached 100%. The transplantation of MIRB labeled SHED in vivo can survive for more than 8 weeks. It was found that MIRB labeled SHED could differentiate into osteoblasts in vivo and significantly promote the repair of alveolar bone defects. CONCLUSIONS: MIRB labeled SHED can be traced in vivo, and the effect of labeled SHED on the repair of defective alveolar bone was observed.

Circular RNA circ-ABCB10 promotes breast cancer proliferation and progression through sponging miR-1271.

Circular RNA (circRNA) is a key regulator in the development and progression of human cancers, however its role in breast cancer tumorigenesis is not well understood. The present study aims to investigate the expression profiles and potential modulation of circRNA on breast cancer carcinogenesis. Human circRNA microarray was performed to screen for abnormally expressed circRNA in breast cancer tissue. Results found circ-ABCB10, was significantly up-regulated in breast cancer tissue. And results were replicated in a larger sample size. In vitro, loss-of-function experiments showed circ-ABCB10 knockdown suppressed the proliferation and increased apoptosis of breast cancer cells. Bioinformatics prediction program predicted the complementary sequence within circ-ABCB10 and miR-1271, which was validated by luciferase reporter assay. Finally, miR-1271 rescued the function of circ-ABCB10 on breast cancer cells, confirming the sponge effect of circ-ABCB10 on miR-1271. Overall, results identified a new functional circ-ABCB10 in breast cancer tumorigenesis, and reveal the important regulatory role of circ-ABCB10 through sponging miR-1271, providing a novel insight for breast cancer pathogenesis.

Absence of gamma-interferon-inducible lysosomal thiol reductase (GILT) is associated with poor disease-free survival in breast cancer patients.

Tumor immunosurveillance is known to be of critical importance in controlling tumorigenesis and progression in various cancers. The role of gamma-interferon-inducible lysosomal thiol reductase (GILT) in tumor immunosurveillance has recently been studied in several malignant diseases, but its role in breast cancer remains to be elucidated. In the present study, we found GILT as a significant different expressed gene by cDNA microarray analysis. To further determine the role of GILT in breast cancer, we examined GILT expression in breast cancers as well as noncancerous breast tissues by immunohistochemistry and real-time PCR, and assessed its association with clinicopathologic characteristics and patient outcome. The absence of GILT expression increased significantly from 2.02% (2/99) in noncancerous breast tissues to 15.6% (34/218) in breast cancer tissues (P<0.001). In accordance with its proliferation inhibiting function, GILT expression was inversely correlated with Ki67 index (P<0.05). In addition, absence of GILT was positively correlated with adverse characteristics of breast cancers, such as histological type, tumor size, lymph nodes status, and pTNM stage (P<0.05). Consistently, breast cancers with reduced GILT expression had poorer disease-free survival (P<0.005). Moreover, significantly decreased expression of GILT was found in both primary and metastatic breast cancer cells, in contrast to normal epithelial cells. These findings indicate that GILT may act as a tumor suppressor in breast cancer, in line with its previously suggested role in anti-tumor immunity. Thus, GILT has the potential to be a novel independent prognostic factor in breast cancer and further studies are needed to illustrate the underlying mechanism of this relationship.