TY - JOUR AB - Elevated cyclooxygenase-2 (COX-2) expression in breast tumors is associated with a lower survival rate in patients with estrogen receptor α (ERα)-positive tumors. We hypothesized that COX-2 reduces the survival rate of breast cancer patients with ERα-positive tumors since COX-2 increases the invasiveness of ERα-positive breast tumors and decreases tumor sensitivity to tamoxifen. Previously, we demonstrated that COX-2 stimulates the activity of protein kinase C (PKC) to increase the invasiveness of ERα-positive MCF-7 breast cancer cells and to decrease the sensitivity of MCF-7 cells to tamoxifen. High levels of COX-2 are associated with the activation of the mitogen-activated protein kinase (MAPK) family and the Akt kinase. However, it is not known whether these kinases mediate COX-2-induced invasive activity and tamoxifen resistance. In the present study, we report that COX-2 utilizes PKC to enhance the phosphorylation of Jun N-terminal kinases (JNKs), but not that of other MAPK family members or Akt. Inhibition aimed at JNKs reduced COX-2-induced invasion but not COX-2-induced tamoxifen resistance. We conclude that JNKs are essential for induced cell invasion by COX-2, but not tamoxifen resistance, in ERα-positive breast cancer cells. AD - Department of Biochemistry, Faculty of Biological Sciences, University of Nuevo Leon, San Nicolas de los Garza, Nuevo León, Mexico Department of Neuroscience, University of Florida, Gainesville, FL, USA AU - Gonzalez-Villasana,Vianey AU - Gutiérrez-Puente,Yolanda AU - Tari,Ana ,M. DA - 2013/09/01 DO - 10.3892/or.2013.2549 EP - 1510 IS - 3 JO - Oncol Rep KW - tamoxifen breast cancer invasion cyclooxygenase-2 Jun N-terminal kinases PY - 2013 SN - 1021-335X 1791-2431 SP - 1506 ST - Cyclooxygenase-2 utilizes Jun N-terminal kinases to induce invasion, but not tamoxifen resistance, in MCF-7 breast cancer cells T2 - Oncology Reports TI - Cyclooxygenase-2 utilizes Jun N-terminal kinases to induce invasion, but not tamoxifen resistance, in MCF-7 breast cancer cells UR - https://doi.org/10.3892/or.2013.2549 VL - 30 ER -