Aim of the studyPlatelet-derived growth factor B (PDGF-B), a vital growth factor which can induce angiogenesis and epithelial-mesenchymal transition (EMT), is important in the metastasis of many tumors. However, the roles of PDGF-B in gastric carcinoma are largely unknown. We investigated the correlation between PDGF-B, PDGFR-β and E-cadherin expression with the clinical features of gastric carcinoma patients to evaluate the relationship between PDGF-B signaling, E-cadherin and metastasis of gastric carcinoma, the correlation between PDGF-B and E-cadherin expression to assess the roles of PDGF-B signaling in metastasis of gastric carcinoma..Material and methodsWe detected expressions of PDGF-B, PDGFR-β and E-cadherin in gastric carcinoma tissues and normal gastric mucosa tissues of 64 patients with gastric carcinoma who had undergone surgical resection, and investigated their relationships with clinical features and the relationships between PDGF-B and E-cadherin expression in gastric carcinoma.ResultsIn surgical specimens, tumor cells expressed PDGF-B, and PDGFR-β was expressed by tumor stromal cells. E-cadherin was expressed by both tumor cells and normal gastric mucosa cells. Expressions of PDGF-B and PDGFR-β were increased in gastric carcinoma tissues (p < 0.05) and were positively correlated with the depth of cancer invasion, lymph node metastasis and TNM stage (p < 0.05). The expression of E-cadherin was reduced in gastric carcinoma tissues (p < 0.05) and was negatively correlated with the depth of cancer invasion, lymph node metastasis and TNM stage (p < 0.05). The correlation between PDGF-B and E-cadherin expression was negative (p < 0.05).ConclusionOur data indicate that either the overexpression of PDGF-B and PDGFR-β or the underexpression of E-cadherin is correlated with cancer progression and lymphogenous metastasis of gastric carcinoma. The PDGF-B signal pathway might induce EMT by down-regulating expression of E-cadherin to promote metastasis of gastric carcinoma.
Purpose
The homeobox (HOX) family plays an important role in multi‐biological processes, such as morphogenesis and tumors. However, the function of HOXD13 in colon cancer remains unclear.
Materials and Methods
The Cancer Genome Atlas database was used to analyze the expression of HOXD13 and its effect on the survival rate of colon cancer patients. Wound healing, Transwell, and clone formation were used to evaluate the effects of changes in HOXD13 expression on the function of colon cancer cells. A nude mouse xenograft tumor model was used to test the effects of HOXD13 on tumor growth in vivo.
Results
Our results showed that HOXD13 was highly expressed in colon cancer and predicted a poor prognosis for patients. In in vitro experiments, the knockdown of HOXD13 can inhibit the proliferation and invasion of colon cancer cells. In vivo experiments showed the inhibited tumor growth after the knockdown of HODX13. In addition, HOXD13 bound to the protein tyrosine phosphatase receptor type N2 (PTPRN2) promoter and promoted the transcription of PTPRN2.
Conclusion
We revealed the function and mechanism of HOXD13 in colon cancer and suggest that HOXD13 may be a candidate marker for the diagnosis and treatment of colon cancer.
Introduction: Present investigation determines the beneficial effect of picroliv against lipopolysaccharide (LPS)-induced neuronal inflammation and injury. Material and methods: Neuronal injury was induced by LPS 250 µg/kg, i.p. for the period of one week, and picroliv 12.5 and 25 mg/kg was given i.p. 30 min prior to the administration of LPS for the duration of 12 days. The effect of picroliv was determined on the cognitive function by Morris water maze (MWM). Mediators of inflammation were estimated by using enzyme-linked immunosorbent assay (ELISA) and western blot, reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemical analysis was done to determine the expressions of several proteins. Results: Data of the study reveal that picroliv ameliorates the reduced memory impairment and cognitive dysfunction in LPS-induced mice. Moreover, expressions of inflammatory protein and β-amyloid protein and level of inflammatory mediators were found to be reduced in the picroliv-treated group as compared to the negative control group. Data of RT-PCR reveal that the gene of Toll-like receptor 4 (TLR-4), α-synuclein, neurotrophic factor (BDNF) and interleukin-1β (IL-1β) protein were also decreased in the picroliv-treated group as compared to the negative control group. In addition picroliv attenuates the altered level of nuclear factor-kB (p-NF-kB), amyloid-β (Aβ), α-synuclein and glial fibrillary acidic protein (GFAP) positive cells in the brain of LPS-induced mice. Conclusions: The report concludes that picroliv protects the neuroinflammation and injury in LPS-induced mice by regulating the inflammatory pathway.
Endothelial inflammation caused by tobacco smoking is widely considered as a pathogenic factor in many vascular diseases. Drugs such as atorvastatin were found to be an effective treatment in smoking-dependent vascular diseases, but the underlying mechanism is still unclear. Here, we investigated the mechanism of atorvastatin resisting endothelial inflammation caused by tobacco smoking. Firstly, isolated human umbilical vein endothelial cells (HUVECs) were divided into normal control group, cigarette smoking extract (CSE) group, and atorvastatin (AS)+CSE group. Then the expressions of inflammatory factors (vascular cell adhesion molecule-1 (VCAM-1) and E-selectin) and nuclear transcription factor kappa (NF-κB) in HUVECs were detected by western blot after separate treatments. The results showed that the expressions of VCAM-1, E-selectin, and NF-κB in CSE group were significantly higher than the other two groups (P< 0.05). We also found that the expressions of VCAM-1, E-selectin, and NF-κB in CSE + atorvastatin group were a little higher than the normal control group (P< 0.05). Our results showed that atorvastatin might partly resist tobacco smoking-induced endothelial inflammation through the inhibition of NF-κB signal pathway.
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