Objective To detect the different expression of Runx2 in dedifferentiated chondrosarcoma and conventional chondrosarcoma, and to investigate the role of Runx2 in the occurrence and development of dedifferentiated chondrosarcoma. Methods Dedifferentiated chondrosarcoma cell line NDCS-1 and normal chondrosarcoma cell line SW1353 were cultured, then mRNA and total cellular protein were extracted.RT-PCR Western blotting, and immunocytochemistry were used to detect the expression of Runx2.Immunohistochemistry was used to test Runx2's expression in the dedifferentiated chondrosarcoma specim ens that confirmed by pathology. Results Runx2 was high expression in dedifferentiated chondrosarcoma cell line and high-grade component of dedifferentiated chondrosarcoma tissues. Conclusion The high expression of Runx2 in dedifferentiated chondrosarcoma is involved in the occurrence and development of dedifferentiated chondrosarcoma.

Objective To study the effect and mechanism of arsenic trioxide on the motility, metastasis and invasion of osteosarcoma in vitro. Methods Wound healing assay, migration assay, invasion assay and Western-blot were performed to study the effect of arsenic trioxide on metastasis of osteosarcoma. Results Through screening MNNG cell was selected to perform the following research. After treatment of As_2O_3, the ability of MNNC cell flattening and spreading along the edges of the wound was inhibited, and the number of MNNG cells with migration and invasion in As_2O_3 - treated group was significantly less than in control group. Arsenic trioxide treatment also resulted in down-regulation of MMP-9. Conclusion This study is the first to report the effectiveness of arsenic trioxide as an inhibitor of osteosarcoma migration and invasion and the mechanism may be down-regulation of MMP-9.

ObjectiveTo investigate the effect of arsenic trioxide (As2O3) on the metastasis capability of Ewing's sarcoma ceils. MethodsMTT assays were performed to choose appropriate concentrations of As2O3 (＜ 2 μmol/L) for the experiments.Migration and invasion assays were performed to assess the effect of As2O3 on the metastasis of Ewing's sarcoma cells. Changes in matrix metalloproteinase(MMP)-9 expressions were detected by gel zymography assay and the phosphoinositide 3-kinase/AKT(PI3K-AKT)pathway was investigated using Western blot. ResultsThe amount of Ewing's sarcoma cells across basal membrane of Transwell in migration and invasion assay decreased gradually with the increase in As2O3 concentration. The average quantities of A-673 across the membrane after treatment by gradual concentrations accounted for 54.3 ％,49.0 ％ and 17.0 ％ of that of untreated group respectively in migration assay (F=112.78,P ＜ 0.01), while 52.7 ％, 32.3 ％ and 10.3 ％ in invasion assay(F =183.76, P ＜ 0.01). Similarly, the percentage of RD-ES was 46.0 ％,39.0 ％ and 8.0 ％ in migration assay (F =408.25,P ＜ 0.01) and 58.7 ％,22.3 ％ and 9.0 ％ in invasion assay (F =373.25, P ＜ 0.01)respectively. The difference had statistics significance.The expression of MMP-9 was suppressed by As2O3 treatment according to gel zymography assay.Western blot assay showed that PI3K-AKT pathway was inhibited and nuclear factor kappa B(NF-κB)was inactivated.ConclusionLow-concentration As2O3 may inhibit metastasis capability of Ewing's sarcoma cells.

By summarizing and analyzing the research status of the influence of needling different acupoints on heart rate variability (HRV) and autonomic nervous function, it is found that Neiguan (PC 6), Zusanli (ST 36) and Shenmen (HT 7) are common acupoints for HRV analysis involving Tongli (HT 5), Hegu (LI 4), Taichong (LR 3), Zhongwan (RN 12), Danzhong (RN 17), Xinshu (BL 15), Shenshu (BL 23) and other acupoints. Different acupoints have different influences on HRV but followed by some rules, which are possibly related to the efficacy of acupoints, meridian tropism and acupoint distributions. Needling on the same acupoint also has different influences on HRV, which is possibly affected by sample size, intervention object, data processing method and other factors, so more standardized measurement process is required in further studies.

Lipophagy, the selective engulfment of lipid droplets (LDs) by autophagosomes for lysosomal degradation, is critical to lipid and energy homeostasis. Here we show that the lipid transfer protein ORP8 is located on LDs and mediates the encapsulation of LDs by autophagosomal membranes. This function of ORP8 is independent of its lipid transporter activity and is achieved through direct interaction with phagophore-anchored LC3/GABARAPs. Upon lipophagy induction, ORP8 has increased localization on LDs and is phosphorylated by AMPK, thereby enhancing its affinity for LC3/GABARAPs. Deletion of ORP8 or interruption of ORP8-LC3/GABARAP interaction results in accumulation of LDs and increased intracellular triglyceride. Overexpression of ORP8 alleviates LD and triglyceride deposition in the liver of ob/ob mice, and Osbpl8-/- mice exhibit liver lipid clearance defects. Our results suggest that ORP8 is a lipophagy receptor that plays a key role in cellular lipid metabolism.
Animals ; Mice ; Lipid Droplets ; Autophagy ; Autophagosomes ; Homeostasis ; Triglycerides