Clinical curative effect observation of therapy of Chinese drug iontophoresis in treatment of degenerative osteoarthropathy.

Degenerative osteoarthropathy is a kind of arthrosis induced by various factors, with main pathological feature of articular cartilage and syndesmophyte formation. In recent years, its morbidity increases year by year and tend to appear more among young people. Its curative effect has yet to be improved. This paper mainly discussed the clinical curative effect of therapy of Chinese drug iontophoresis in degenerative osteoarthropathy. A total of 296 cases of degenerative osteoarthropathy was randomly divided into two groups (with no consideration on gender): Chinese drug iontophoresis group: joint was treated by therapy of Chinese drug iontophoresis and MTZ-F experiment; frequency electrotherapy group: joint was only treated by medium frequency electrotherapy. Two groups were both treated for 30 min for one time, 1 time for a day, total for 4 weeks. Result of the study found that, total effective rate of medium frequency electrotherapy group was 74.3%, Chinese medicine iontophoresis group was 93.2%; curative effect of Chinese medicine iontophoresis group was superior to electrotherapy group. It indicates that, Chinese medicine iontophoresis has good clinical effect in the treatment of osteoarthropathy and deserves to be popularized and applied.

Increased expression of lncRNA HULC indicates a poor prognosis and promotes cell metastasis in osteosarcoma.

INTRODUCTION: Long non-coding RNAs (lncRNAs) are aberrantly expressed in many diseases including cancer. LncRNA HULC (highly up-regulated in liver cancer) has recently been revealed to be involved in hepatocellular carcinoma development and progression. However, the role and function of HULC in human osteosarcoma remains unknown. METHODS: LncRNA HULC expression in osteosarcoma tissues and cell lines was detected by quantitative real-time PCR. Then, the association of HULC level with survival of osteosarcoma patients was performed by the Kaplan-Meier and Cox proportional regression analyses. Furthermore, the effects of HULC on tumorigenicity of osteosarcoma cells were evaluated by in vitro assays. RESULTS: In the present study, we demonstrated that HULC was significantly up-regulated in osteosarcoma tissues and cell lines compared with normal controls, and over-expression of HULC was correlated with clinical stage and distant metastasis. Moreover, higher HULC expression was associated with shorter overall survival of osteosarcoma patients. Furthermore, decreased expression of HULC markedly suppressed osteosarcoma cell proliferation, migration, and invasion. CONCLUSIONS: Our results indicated that HULC is a novel molecule involved in osteosarcoma progression, which may provide a new marker of poor prognosis and a potential therapeutic target for osteosarcoma intervention.

miRNA-646 suppresses osteosarcoma cell metastasis by downregulating fibroblast growth factor 2 (FGF2).

MicroRNAs are short regulatory RNAs that play crucial roles in cancer development and progression. MicroRNA-646 (miR-646) is downregulated in many human cancers, and increasing evidence indicates that it functions as a tumor suppressor. However, the role of miR-646 in osteosarcoma remains unclear. Expression levels of miR-646 in osteosarcoma cell lines and patient tissues were evaluated by quantitative real-time PCR (qRT-PCR), and the clinicopathological significance of the resultant data was later analyzed. Next, we investigated the role of miR-646 to determine its potential roles on osteosarcoma cell proliferation, migration, and invasion in vitro. A luciferase reporter assay was conducted to confirm the target gene of miR-646, and the results were validated in the osteosarcoma cell line. In this study, we found that miR-646 was downregulated in osteosarcoma cell lines and osteosarcoma tissues compared with normal osteoblast cell line NHOst and paired adjacent nontumor tissue. We found that a lower expression of miR-646 was associated with metastasis. In osteosarcoma cells, overexpression of miR-646 inhibited cell proliferation, migration, and invasion. In contrast, downregulation of miR-646 expression promoted osteosarcoma cell proliferation, migration, and invasion. Next, we identified that the FGF2 gene is a novel direct target of miR-646 in osteosarcoma cells. Moreover, enforced expression of FGF2 partially reversed the inhibition of cell proliferation, migration, and invasion that was caused by miR-646. Our study demonstrated that miR-646 might be a tumor suppressor in osteosarcoma via the regulation of FGF2, which provided a potential prognostic biomarker and therapeutic target.

The association of XPG and MMS19L polymorphisms response to chemotherapy in osteosarcoma.

OBJECTIVE: To assess the role of XPG, XPC, CCNH and MMS19L polymorphisms response to chemotherapy in osteosarcoma, and the clinical outcome of osteosarcoma. METHODS: One hundred and sixty eight osteosarcoma patients who were histologically confirmed were enrolled in our study between January 2007 and March 2009. Genotyping of XPG, XPC, CCNH and MMS19L was performed in a 384-well plate format on the MassARRAY® platform. RESULTS: Individuals with rs2296147 TT genotype showed a better response as compared with CC genotype, with the OR (95% CI) of 3.89(1.49-10.95). Those carrying rs29001322 TT genotype presented better response to chemotherapy, and the OR (95% CI) was as high as 12.25(2.63-121.84). Patients carrying TT genotype of XPG rs2296147 and MMS19L rs29001322 showed a significantly longer overall survival than CC genotype, they had 0.37 and 0.31-fold risk of death when compared with wide-type of this gene. CONCLUSIONS: XPG rs2296147 and MMS19L rs29001322 are correlated with response to chemotherapy and prognosis of osteosarcoma. Our findings would provide important evidence for prognostic and therapeutic implications in osteosarcoma.

[Correlation of the expression of NF-κB p65 and hepatic fibrosis in hepatitis patients].

OBJECTIVE: To explore the relationship between the expression of NF-κB p65 and hepatic fibrosis in chronic hepatitis B (CHB) patients. METHODS: Sixty CHB patients with hepatic fibrosis underwent liver biopsy to determine the stages of liver fibrosis (S0-S4). The distribution and expression of collagens I, III and NF-κB p65 in different stages of fibrosis in liver tissue were observed by immunohistochemistry and the results analyzed statistically. RESULTS: The expression of NF-κB p65 was positively correlated with the stage of hepatic fibrosis. That was S4 > S3 > S2 > S1 (S0) (P < 0.01). And it was also positively correlated with the expression of collagens I and III (P < 0.01). CONCLUSION: The elevated expression of NF-κB p65 is closely associated with the occurrence and development of hepatic fibrosis. Its mechanism is probably related with the increased secretion of collagens I and III after the activation of hepatic stellate cell.