{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Kandala PK"],"funding":["NCI NIH HHS"],"pagination":["297-309"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC2917853"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["78(2)"],"pubmed_abstract":["We evaluated the effect of 3,3'-diindolylmethane (DIM) in ovarian cancer cells. DIM treatment inhibited the growth of SKOV-3, TOV-21G, and OVCAR-3 ovarian cancer cells in both a dose- and time-dependent manner with effective concentrations ranging from 40 to 100 muM. Growth-inhibitory effects of DIM were mediated by cell cycle arrest in G(2)/M phase in all the three cell lines. G(2)/M arrest was associated with DNA damage as indicated by phosphorylation of H(2)A.X at Ser139 and activation of checkpoint kinase 2 (Chk2) in all the three cell lines. Other G(2)/M regulatory molecules such as Cdc25C, Cdk1, cyclin B1 were down-regulated by DIM. Cycloheximide or Chk2 inhibitor pretreatment abrogated not only activation of Chk2 but also G(2)/M arrest and apoptosis mediated by DIM. To further estab"],"journal":["Molecular pharmacology"],"pubmed_title":["Activation of checkpoint kinase 2 by 3,3'-diindolylmethane is required for causing G2/M cell cycle arrest in human ovarian cancer cells."],"pmcid":["PMC2917853"],"funding_grant_id":["R01-CA106953","R01 CA129038","R01-CA129038","R01 CA106953"],"pubmed_authors":["Srivastava SK","Kandala PK"],"additional_accession":[]},"is_claimable":false,"name":"Activation of checkpoint kinase 2 by 3,3'-diindolylmethane is required for causing G2/M cell cycle arrest in human ovarian cancer cells.","description":"We evaluated the effect of 3,3'-diindolylmethane (DIM) in ovarian cancer cells. DIM treatment inhibited the growth of SKOV-3, TOV-21G, and OVCAR-3 ovarian cancer cells in both a dose- and time-dependent manner with effective concentrations ranging from 40 to 100 muM. Growth-inhibitory effects of DIM were mediated by cell cycle arrest in G(2)/M phase in all the three cell lines. G(2)/M arrest was associated with DNA damage as indicated by phosphorylation of H(2)A.X at Ser139 and activation of checkpoint kinase 2 (Chk2) in all the three cell lines. Other G(2)/M regulatory molecules such as Cdc25C, Cdk1, cyclin B1 were down-regulated by DIM. Cycloheximide or Chk2 inhibitor pretreatment abrogated not only activation of Chk2 but also G(2)/M arrest and apoptosis mediated by DIM. To further estab","dates":{"release":"2010-01-01T00:00:00Z","publication":"2010 Aug","modification":"2025-04-18T15:50:26.221Z","creation":"2019-03-27T00:33:05Z"},"accession":"S-EPMC2917853","cross_references":{"pubmed":["20444961"],"doi":["10.1124/mol.110.063750"]}}