Ultra-pulsed fractional CO2 laser is an efficient, precise, and safe therapeutic intervention for skin refreshing, although accompanied with prolonged edema and erythema. In recent years, autologous platelet-rich plasma (PRP) has been proven to promote wound and soft tissue healing and collagen regeneration. To investigate whether the combination of PRP and ultra-pulsed fractional CO2 laser had a synergistic effect on therapy for facial rejuvenation. Totally, 13 facial aging females were treated with ultra-pulsed fractional CO2 laser. One side of the face was randomly selected as experimental group and injected with PRP, the other side acted as the control group and was injected with physiological saline at the same dose. Comprehensive assessment of clinical efficacy was performed by satisfaction scores, dermatologists' double-blind evaluation and the VISIA skin analysis system. After treatment for 3 months, subjective scores of facial wrinkles, skin texture, and skin elasticity were higher than that in the control group. Similarly, improvement of skin wrinkles, texture, and tightness in the experimental group was better compared with the control group. Additionally, the total duration of erythema, edema, and crusting was decreased, in the experimental group compared with the control group. PRP combined with ultra-pulsed fractional CO2 laser had a synergistic effect on facial rejuvenation, shortening duration of side effects, and promoting better therapeutic effect.

No abstract

Oxymatrine effectively suppressed the phosphorylation of EGFR (Tyr845), and EGFR was the target of oxymatrine.

Melanoma is the deadliest cutaneous neoplasm. To prevent metastasis, early diagnosis and surgical treatment is vital. Long non-coding RNAs (lncRNAs) may serve as biomarkers and therapeutic targets in tumors. We investigated the molecular mechanisms of lncRNA KCNQ1OT1 in melanoma. Real time PCR demonstrated that KCNQ1OT1 expression is up-regulated in melanoma tissues and cells. KCNQ1OT1 promoted cell proliferation and metastasis in melanoma. By directly bindin to miR-153, KCNQ1OT1 acted as a competing endogenous RNA (ceRNA) to de-repress MET expression. Our results may provide the basis for a novel strategy for early detection and/or treatment of melanoma.

The p21-activated kinase 5 (PAK5) is overexpressed in advanced cancer and the transcription factor E47 is a direct repressor of E-cadherin and inducer of epithelial-mesenchymal transition (EMT). However, the relationship between PAK5 and E47 has not been explored. In this study, we found that PAK5-mediated E47 phosphorylation promoted EMT in advanced colon cancer. PAK5 interacted with E47 and phosphorylated E47 on Ser39 under hepatocyte growth factor (HGF) stimulation, which decreased cell-cell cohesion, increased cell migration and invasion in vitro and promoted metastasis in a xenograft model. Furthermore, phosphorylation of E47 facilitated its accumulating in nucleus in an importin α-dependent manner, and enhanced E47 binding to E-cadherin promoter directly, leading to inhibition of E-cadherin transcription. In contrast, PAK5-knockdown resulted in blockage of HGF-induced E47 phosphorylation, attenuated association of E47 with importin α and decreased E47 binding to E-cadherin promoter. In addition, we demonstrated a close correlation between PAK5 and phospho-Ser39 E47 expression in colon cancer specimens. More importantly, high expression of phospho-E47 was associated with an aggressive phenotype of colon cancer and nuclear phospho-E47 staining was found in certain cases of colon cancer with metastasis. Collectively, E47 is a novel substrate of PAK5, and PAK5-mediated phosphorylation of E47 promotes EMT and metastasis of colon cancer, suggesting that phosphorylated E47 on Ser39 may be a potential therapeutic target in progressive colon cancer.

Stanniocalcin-1 (STC1) is a secreted glycoprotein hormone and highly expressed in various types of human malignancies. Although evidence points to the role of STC1 in human cancers, the clinical significance of STC1 expression in glioma has not been established. Here, we investigated the relationship between STC1 expression and clinicopathological significance in glioma. In our study, we selected 60 cases of different grades glioma tissues to detect the expression of STC1. Data showed that the mRNA and protein levels of STC1 in high-grade glioma tissues were significantly higher than that in low-grade tissues. The results of double immunofluorescent staining disclosed STC1 distribution in vascular endothelial cells and the cytoplasm in high-grade glioma, but almost distributed only in vascular endothelial cells in low-grade glioma. By immunohistochemistry, we got the same results and the expression of STC1 has significant difference in high-grade gliomas and low-grade gliomas. Furthermore, the results of Kaplan-Meier analysis indicated that cases with high STC1expression had significantly worse overall survival than those with low level of STC1. These results suggested that STC1 may be a valuable biomarker in diagnosing malignant degree of glioma and evaluating prognostic following surgery. Next, we would study the pathophysiological mechanism of STC1 in glioma.

No abstract

Fangchinoline could inhibit the phosphorylation of FAK(p-Tyr397), at least partially. Fangchinoline as a kinase inhibitor targets FAK and suppresses FAK-mediated signaling pathway and inhibits the growth and the invasion in tumor cells which highly expressed FAK such as A549 cell line.