Rat MMP2 ELISA Kit

Cervical cancer is one of the most common women cancers. The tumor screening by nurse care is efficacy for cancer prevention. Serum amyloid A1 (SAA1) has shown to be associated with cervical cancer malignancy. The detail information for SAA1 in cervical cancer has not yet been investigated. IL-1 beta was performed to induce cervical cancer cell lines. Subsequently, SAA1 was silenced or overexpressed in c-33A respectively. The data showed that the expression levels of SAA1 were increased in IL-1 beta induced cervical cell lines. Downregulation of SAA1 reduced cell proliferation, migration and invasion in c-33A cells, whereas overexpression increased, indicating that SAA1 is a tumor promoter in cervical cancer. Also, SAA1 positively regulates the expression of MMP2, MMP7 and MMP9, which is associated with extracellular matrix reproduction. Furthermore, NF-kappa B inhibitor, SC75741, reversed the effects of SAA1 in cervical cancer, revealing that it might be a potential mechanism for SAA1 in cervical cancer. Therefore, SAA1 is a potential biomarker for cervical cancer in the inflammatory microenvironment.

Long non-coding RNAs (lncRNAs) play an essential role in multitudinous physiological and pathological processes, including vascular disease. We previously showed that lncRNA GUSBP5-AS (enst00000511042) is upregulated in endothelial progenitor cells (EPCs) of deep vein thrombosis (DVT) patients. Here, we investigate the role and mechanism of GUSBP5-AS in EPCs and DVT. Using the DVT model, we found that GUSBP5-AS significantly reduced the thrombus size and weight and enhanced the homing ability of EPC to DVT sites to promote resolution and recanalization of thrombus. GUSBP5-AS promoted cell cycle progression, proliferation, migration and invasion in EPCs, enhanced EPC angiogenesis in vitro and in vivo, and inhibited apoptosis. Strikingly, this study showed that GUSBP5-AS was unbalanced and modulated Forkhead Box Protein O1 (FOXO1) in EPCs in patients with DVT by interacting with miR-223-3p. Mechanistically, GUSBP5-AS functions as a sponge of miR-223-3p, which targets FOXO1. Both GUSBP5-AS knockdown and miR-223-3p overexpression remarkably inhibited angiogenesis, migration and invasion in EPCs. Additionally, our data suggested that GUSBP-AS activated the Akt pathway and enhanced fibroblast growth factor 2 (FGF2), matrix metalloproteinase-2/9 (MMP2/9) and F-actin expression. Taken together, this study indicates that GUSBP5-AS modulates angiogenesis, proliferation and homing ability of EPCs via regulating FGF2 and MMP2/9 expression through the miR-223-3p/FOXO1/Akt pathway, which may provide a new direction for the development of DVT therapeutics.