Pentraxin 3 (PTX3) as an inflammatory molecule has been shown to be involved in immune response, inflammation, and cancer. However, the effects of PTX3 on the biological features of cervical cancer cells in vitro and in vivo have not been delineated. Immunohistochemical staining showed that increased PTX3 expression was significantly associated with tumor grade (P < 0.011) and differentiation (P < 0.019). Knocking down PTX3 with lentivirus-mediated small hairpin RNA (shRNA) in cervical cancer cell lines resulted in inhibited cell viability, diminished colony-forming ability, and induced cell cycle arrest at the G2/M phase of the cell cycle, along with downregulated expression of cyclin B1, cdc2, and cdc25c, and upregulated expression of p-cdc2, p-cdc25c, p21, and p27. Furthermore, knockdown of PTX3 significantly decreased the potential of migration and invasion of cervical cancer cells by inhibiting matrix metalloproteidase-2 (MMP-2), MMP-9, and urokinase plasminogen activator (uPA). Moreover, in vivo functional studies showed PTX3-knockdown in mice suppressed tumorigenicity and lung metastatic potential. Conversely, overexpression of PTX3 enhanced proliferation and invasion both in vitro and in vivo. Our results demonstrated that PTX3 contributes to tumorigenesis and metastasis of human cervical cancer cells. Further studies are warranted to demonstrate PTX3 as a novel therapeutic biomarker for human cervical cancer.

Background/Aims: α-mangostin has anti-carcinogenic effects against several cancers. We investigated the molecular mechanism of this compound on the metastasis of human renal carcinoma cells. Methods: Cell viability was measured using the MTT assay, and cell cycle distribution using flow cytometry. A Matrigel-based assay was used to measure in vitro cell migration and invasion. MAPK-related proteins and matrix metalloproteinase (MMP)-9 and MMP-2 expression were measured by western blotting, and MMP2/-9 activities were determined by gelatin zymography. RT-qPCR and a luciferase assay were used to examine the transcriptional activity of MMP-9. Results: α-mangostin inhibited the migration and invasion of RCC cells in a dose-dependent manner, but had no evident cytotoxic effects. Treatment of 786-O cells with α-mangostin inhibited activation of MEK and ERK. Treatment with a specific MEK inhibitor (U0126) enhanced the inhibitory effects of α-mangostin on cell migration and invasion, and the phosphorylation of ERK and MEK. Moreover, α-mangostin inhibited the expression of the MMP-9 mRNA levels as well as the activity of MMP-9 promoter, and these suppressive effects were further enhanced by U0126. Conclusions: Our results suggest that α-mangostin suppresses cell migration and invasion via MEK/ERK/MMP9 pathway, and might be a promising anti-metastatic agent against human renal cell carcinoma.

Loss of endothelial cell-specific molecule 1 promotes the tumorigenicity and metastasis of prostate cancer cells through regulation of the TIMP-1/MMP-9 expression Loss of endothelial cell-specific molecule 1 promotes the tumorigenicity and metastasis of prostate cancer cells through regulation of the TIMP-1/MMP-9 expression

Adipocyte fatty acid binding protein (A-FABP) is a novel fat-derived circulating protein, which is independently and positively associated with atherosclerosis. The present study evaluated the relationship between fasting serum A-FABP and central arterial stiffness in geriatric adults. Fasting blood samples were obtained from 87 geriatric patients and the serum A-FABP levels were measured using an enzyme immunoassay. Carotid-femoral pulse wave velocity (cfPWV) was determined using the SphygmoCor system. cfPWV values of >10 m/s represented the high arterial stiffness group, while values ≤10 m/s defined the low arterial stiffness group. High arterial stiffness group comprised of 42 geriatric adults (48.3 %). When compared to those in the low arterial stiffness group, the high arterial stiffness group had a higher rate of diabetes mellitus (P = 0.044) and hypertension (P = 0.043). Body weight (P = 0.027), waist circumference (P = 0.035), body mass index (P = 0.001), systolic blood pressure (P = 0.005), diastolic blood pressure (P = 0.045), pulse pressure (P = 0.038), and serum A-FABP level (P < 0.001) were also higher in the high arterial stiffness group than in the low arterial stiffness group. Multivariate logistic regression analysis of the factors significantly associated with arterial stiffness revealed that A-FABP (odds ratio: 1.833, 95 % confidence interval 1.123–2.993, P = 0.015) was an independent predictor of arterial stiffness in geriatric adults. Serum A-FABP levels constitute a major risk factor in the development of central arterial stiffness in the geriatric population.