<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>28(1_suppl)</volume><submitter>Zhang X</submitter><pubmed_abstract>Ovarian cancer is the leading cause of death among gynecological malignancies. Cyclooxygenase 2 is widely expressed in various cancer cells and participates in the occurrence and development of tumors by regulating a variety of downstream signaling pathways. However, the function and molecular mechanisms of cyclooxygenase 2 remain unclear in ovarian cancer. Here, we demonstrated that cyclooxygenase 2 was highly expressed in ovarian cancer and the expression level was highly correlated with ovarian tumor grades. Further, ovarian cancer cells with high expression of cyclooxygenase 2 exhibit enhanced proliferation and invasion abilities. Specifically, cyclooxygenase 2 promoted the release of prostaglandin E2 upregulated the phosphorylation levels of phospho-nuclear factor-kappa B p65. Celecoxib, AH6809, and BAY11-7082 all can inhibit the promoting effect of cyclooxygenase 2 on SKOV3 and OVCAR3 cell proliferation and invasion. Besides, celecoxib inhibited SKOV3 cell growth in the xenograft tumor model. These data suggest that high expression of cyclooxygenase 2 promotes the proliferation and invasion of ovarian cancer cells through the prostaglandin E2/nuclear factor-kappa B signaling pathway. Cyclooxygenase 2 may be a potential therapeutic target for the treatment of ovarian cancer.</pubmed_abstract><journal>Cell transplantation</journal><pagination>1S-13S</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7016469</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Cyclooxygenase 2 Promotes Proliferation and Invasion in Ovarian Cancer Cells via the PGE2/NF-?B Pathway.</pubmed_title><pmcid>PMC7016469</pmcid><pubmed_authors>Yan K</pubmed_authors><pubmed_authors>Ling B</pubmed_authors><pubmed_authors>Liang H</pubmed_authors><pubmed_authors>Zhang X</pubmed_authors><pubmed_authors>Liang J</pubmed_authors><pubmed_authors>Deng L</pubmed_authors><pubmed_authors>Feng D</pubmed_authors></additional><is_claimable>false</is_claimable><name>Cyclooxygenase 2 Promotes Proliferation and Invasion in Ovarian Cancer Cells via the PGE2/NF-?B Pathway.</name><description>Ovarian cancer is the leading cause of death among gynecological malignancies. Cyclooxygenase 2 is widely expressed in various cancer cells and participates in the occurrence and development of tumors by regulating a variety of downstream signaling pathways. However, the function and molecular mechanisms of cyclooxygenase 2 remain unclear in ovarian cancer. Here, we demonstrated that cyclooxygenase 2 was highly expressed in ovarian cancer and the expression level was highly correlated with ovarian tumor grades. Further, ovarian cancer cells with high expression of cyclooxygenase 2 exhibit enhanced proliferation and invasion abilities. Specifically, cyclooxygenase 2 promoted the release of prostaglandin E2 upregulated the phosphorylation levels of phospho-nuclear factor-kappa B p65. Celecoxib, AH6809, and BAY11-7082 all can inhibit the promoting effect of cyclooxygenase 2 on SKOV3 and OVCAR3 cell proliferation and invasion. Besides, celecoxib inhibited SKOV3 cell growth in the xenograft tumor model. These data suggest that high expression of cyclooxygenase 2 promotes the proliferation and invasion of ovarian cancer cells through the prostaglandin E2/nuclear factor-kappa B signaling pathway. Cyclooxygenase 2 may be a potential therapeutic target for the treatment of ovarian cancer.</description><dates><release>2019-01-01T00:00:00Z</release><publication>2019 Dec</publication><modification>2021-02-21T07:59:28Z</modification><creation>2020-05-22T11:10:59Z</creation></dates><accession>S-EPMC7016469</accession><cross_references><pubmed>31822119</pubmed><doi>10.1177/0963689719890597</doi></cross_references></HashMap>