[Application of miR-182 for Determination of Glucocorticoid-Resistant Patients with Lymphoid Malignancy].

OBJECTIVE: To validate the clinical relationship between miR-182 and glucocorticoid-resistance in patients with lymphoid malignancy. METHODS: Real-time quantitative PCR(qRT-PCR) was employed to detect the expression of miR-182 in lymphoma patients (68 cases, the specimens indluded bone marrow of 20 cases, and plasma of 48 cases), multiple myeloma patients (24 cases, the specimens included bone marrow of 14 cases and plasma of 10 cases), ALL patients (3 cases, specimen was plasma of 3 cases) and non-lymphotic system disorder patients (18 cases, specimens included bone marrow of 8 cases and plasma of 10 cases). RESULTS: The expression of miR-182 in refractory lymphoblastic tumor patients was significantly higher than that in initial treatment group (P<0.05); the expression of miR-182 in initial treatment patients was not significantly different from the controls. The expression level of miR-182 in plasma of lymphoid malignancy patient significantly correlated with their used dosage of corticosteroids (P<0.05). When the expression level of miR-182 in bone marrow cells was 10.09, its sensitivity and specificity for diagnosis were 100% and 88.2% respectively; when the expression level of miR-182 in plasma was 1.393, its sensitivity and specificity for diagnosis of glucocorticoid resistance of lymphoblastic tumor cells were 90.9% and 51.3% respectively. CONCLUSION: The expression of miR-182 in lymphoblastic tumor with glucocorticoid resistance is significantly up-regulated, suggesting that the glucocorticoid resistance of lymphoblastic tumor is related with the over-expression of miR-182. The miR-182 is expected as a new biomarker for the diagnosis of glucocorticoid resistant lymphoblastic tumor.

Galectin-3 gene silencing inhibits migration and invasion of human tongue cancer cells in vitro via downregulating ß-catenin.

AIM: Galectin-3 (Gal-3) is a member of the carbohydrate-binding protein family that contributes to neoplastic transformation, tumor survival, angiogenesis, and metastasis. The aim of this study is to investigate the role of Gal-3 in human tongue cancer progression. METHODS: Human tongue cancer cell lines (SCC-4 and CAL27) were transfected with a small-interfering RNA against Gal-3 (Gal-3-siRNA). The migration and invasion of the cells were examined using a scratch assay and BD BioCoat Matrigel Invasion Chamber, respectively. The mRNA and protein levels of ß-catenin, Akt/pAkt, GSK-3ß/pGSK-3ß, MMP-9 in the cells were measured using RT-PCR and Western blotting, respectively. RESULTS: Transient silencing of Gal-3 gene for 48 h significantly suppressed the migration and invasion of both SCC-4 and CAL27 cells. Silencing of Gal-3 gene significantly decreased the protein level of ß-catenin, leaving the mRNA level of ß-catenin unaffected. Furthermore, silencing Gal-3 gene significantly decreased the levels of phosphorylated Akt and GSK-3ß, and suppressed the mRNA and protein levels of MMP-9 in the cells. CONCLUSION: Our data suggest that Gal-3 mediates the migration and invasion of tongue cancer cells in vitro via regulating the Wnt/ß-catenin signaling pathway and Akt phosphorylation.

[Effects of high mobility group box 1 in activating periodontal ligament fibroblasts to express cytokine].

OBJECTIVE: To investigate the influence of high mobility group box 1 (HMGB1) on the expression of interleukin 6 (IL-6), receptor activator of nuclear factor-kappa B ligand (RANKL) and osteoprotegerin (OPG) on periodontal ligament fibroblasts. METHODS: Human periodontal ligament fibroblasts were stimulated with HMGB1 at concentrations of 10, 30, and 100 ng x mL(-1) for 24 h. RT-PCR and Western blot analysis were performed to check mRNA and protein expression of IL-6, RANKL and OPG on the cells. RESULTS: The ratio of RANKL/OPG was increased at both mRNA and protein level after HMGB1 stimulation at 10, 30, 100 ng x mL(-1). Inflammatory cytokine IL-6 was upregulated by HMGB1 at the concentration of 100 ng x mL(-1). CONCLUSION: Increased ratio of RANKL/OPG and IL-6 on periodontal ligament fibroblasts suggests that HMGB1 might play a role in the pathogenesis and progression of periodontal disease.