The aim of the present study was to investigate the significance of the phosphorylation of mitogen-activated protein kinase (MAPK) and the protein expression of cyclin D1 in human osteosarcoma tissues. Human osteosarcoma tissue samples were collected from 30 patients, benign bone tumor samples were collected from 30 patients, and normal bone tissues were collected from 10 individuals as controls. Immunohistochemistry was performed to measure the levels of phosphorylated (p)-MAPK and cyclin D1 protein in cases of human osteosarcoma. The results showed that the positive rates of MAPK and cyclin D1 in osteosarcoma were 86.67% (26/30) and 73.00% (22/30), respectively. The positive staining rates of MAPK and cyclin D1 in benign bone tumor tissues were 10.00% (3/30) and 3.30% (1/30), respectively. The positive rate in the normal bone tissues was 0% (0/30), which was significantly lower, compared with that of the cancerous bone tissue. The positive rates of MAPK and cyclin D1 in osteosarcoma were increased (P<0.05), and the expression of cyclin D1 and p‑MAPK were positively correlated. The phosphorylation of MAPK may be important in the development of osteosarcoma, and the overactivation of MAPK may induce high expression of cyclin D1 and induce tumor cells to proliferate continuously.

Objective: To investigate the regulatory effect of curcumin on expression of signal transducer and activator of transcription 3 (STAT3) in skin squamous cell carcinoma tissues as well as possible mechanisms of curcumin in prevention and treatment of skin squamous cell carcinoma. Materials and Methods: Highly invasive A431 cells were treated with curcumin at various doses .The cytotoxic effects of treatment with 5, 10, 15, 20, 25, 30, 35, 40 and 50 umol/L curcumin for 24, 48 and 72 hours on A431 cells were measured by MTT assay. The invasion capacity of cells treated with 5, 10 and 15 umol/L curcumin was measured by Transwell test, while adhesive ability was assessed by cell adhesion assay. The effects of 5,10 and 15 umol/L curcumin on expression levels of STAT3 were determined by Western blotting and on transcription levels of STAT3 mRNA by RT-PCR. Results: Treatment with curcumin at a doses of more than 15 umol/L for more than 24 hour inhibited the growth of A431 cells in a time-and dose-dependent fashion (p<0.001). The doses of 15 umol/L and less for 24 hours showed no significant cytotoxic effects on the cells, survival rates being more than 85%.The invasion and adhesive abilities decreased gradually with the increasing curcumin concentration, 15 umol/L exerting the strongest inhibitory effects (p<0.05). Curcumin showed significant dose-dependent inhibitory effects on the transcription level of STAT3 mRNA (p<0.05). Conclusions: Curcumin may reduce the invasive ability of A431 cells by inhibiting the activation of STAT3 signal pathway and expression of STAT3 as a target gene in the pathway.

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The present study aimed to investigate the significance of the phosphorylation of signal transducer and activator of transcription 3 (STAT3) and mitogen‑activated protein kinase (MAPK), and the protein expression of cyclin D1, in skin squamous cell carcinoma (SCC) tissues. SCC specimens from the skin were collected from 30 patients, and normal skin tissues were collected from 10 individuals as a control. Immunohistochemistry was used to assess the protein expression levels of phosphorylated (p‑)STAT3, p‑MAPK and cyclin D1 in the SCC tissues. The levels of p‑STAT3 protein were abnormally increased in SCC (P<0.05); however, no significant differences in the protein expression of p‑MAPK were identified between the normal skin and the SCC specimens. The extent of the upregulation of the expression of p‑STAT3 and cyclin D1 correlated with the depth of tumor invasion (P<0.05). A positive correlation existed between the expression of p‑STAT3 and cyclin D1 in SCC. However, no association between the expression intensity of p‑MAPK and cyclin D1 was identified in SCC. It is postulated that the activation of STAT3 may induce the overexpression of cyclin D1, which results in the persistent proliferation of these tumor cells in SCC.