Cdca7-Regulated Inflammatory Mechanism Through Tlr4/Nf-Kappa B Signaling Pathway In Stomach Adenocarcinoma

To investigate the role of cell division cycle associated 7 (CDCA7) in stomach carcinoma, detect whether CDCA7 knockdown could regulate the development of stomach carcinoma, and further observe the relationship between CDCA7 and inflammation through TLR4/NF-kappa B signaling pathway in stomach adenocarcinoma (STAD) in vitro and in vivo. TIMER2.0, Kaplan-Meier plotter, Target Gene, and GEPIA systems were used to predict the potential function of CDCA7. Western blot and immunohistochemistry was used to analyze the expression of CDCA7 at different tissue or cell lines. The proliferation, development, inflammation, and apoptosis of STAD in vitro and in vivo were observed by using CDCA7 knockdown lentivirus through TLR4 suppression by its inhibitor. Bioinformatics analysis of CDCA7 with inflammation and western blot of CDCA7 with target protein of immune-associated cells were observed by using CDCA7 knockdown lentivirus in vivo. Finally, the prognosis and associated of CDCA7 in some gene mutations of STAD was observed by Target Gene system. CDCA7 expression in STAD tumor tissue was higher than the normal. The CDCA7 expression in tumor or MGC803 cells was increased. Furthermore, CDCA7 knockdown lentivirus could inhibit STAD development in vitro and in vivo through weakening tumor cells proliferation, reducing tumor volume and biomarker levels, and then increasing apoptotic level. CDCA7 is possibly able to regulate inflammation in STAD through TLR4/NF-kappa B signaling pathway. Furthermore, CDCA7 may be related with mast cells and the upstream target factor of TLR4/NF-kappa B signaling pathway in inflammation. These results may provide a new strategy to stomach carcinoma development by regulating inflammation.