Aspirin ameliorates the long-term adverse effects of doxorubicin through suppression of cellular senescence.

A number of childhood cancer survivors develop adverse, late onset side effects of earlier cancer treatments, known as the late effects of cancer therapy. As the number of survivors continues to increase, this growing population is at increased risk for a number of health-related problems. In the present study, we have examined the effect of aspirin on the late effects of chemotherapy by treating juvenile mice with doxorubicin (DOX).

Jagged-2 (JAG2) enhances tumorigenicity and chemoresistance of colorectal cancer cells.

Colorectal cancer (CRC) is one of the leading causes of cancer-related mortality. Recent studies have stated that NOTCH signaling plays an important role in the development and progression of CRC. However, the role of Jagged-2 (JAG2), one of the NOTCH ligands, has not been delineated in colorectal tumorigenesis and drug resistance.

Transgenic expression of cyclooxygenase-2 (COX2) causes premature aging phenotypes in mice.

Cyclooxygenase (COX) is a key enzyme in the biosynthesis of prostanoids, lipid signaling molecules that regulate various physiological processes. COX2, one of the isoforms of COX, is highly inducible in response to a wide variety of cellular and environmental stresses. Increased COX2 expression is thought to play a role in the pathogenesis of many age-related diseases.

Lentivirus-mediated somatic recombination and development of a novel mouse model for sporadic colorectal cancer.

In this study, we have developed a novel mouse model for sporadic colorectal cancer (CRC) by utilizing APC conditional knockout (Apc(CKO) ) mouse and lentivirus encoding Cre recombinase and a reporter gene (EGFP or LacZ). Lentiviral transduction of colonic crypt stem cells allowed for the long-term expression of reporter gene as well as excision of floxed Apc alleles, which resulted in tumor development. Tumors represented adenoma stages along with the nuclear accumulation of β-catenin.

COX-2 inhibitor NS-398 suppresses doxorubicin-induced p53 accumulation through inhibition of ROS-mediated Jnk activation.

Cyclooxygenase-2 (COX-2) is one of the isoforms of cyclooxygenase, a rate-limiting enzyme in the arachidonic acid cascade. COX-2 protein expression is highly induced by numerous factors and it has been reportedly overexpressed in various human malignancies. Although anti-tumorigenic effects of COX-2 inhibitors have been shown, several lines of evidence suggest that COX-2 inhibitors antagonize the cytotoxicity of chemotherapeutic agents.

Prostaglandin F2α receptor (FP) signaling regulates Bmp signaling and promotes chondrocyte differentiation.

Prostaglandins are a group of lipid signaling molecules involved in various physiological processes. In addition, prostaglandins have been implicated in the development and progression of diseases including cancer, cardiovascular disease, and arthritis. Prostaglandins exert their effects through the activation of specific G protein-coupled receptors (GPCRs).