Rottlerin induces Wnt co-receptor LRP6 degradation and suppresses both Wnt/β-catenin and mTORC1 signaling in prostate and breast cancer cells

Cellular Signalling

Volumn 26, Issue 6, 2014, Pages 1303-1309

  Lu, Wenyan ^a   Lin, Cuihong ^a,b   Li, Yonghe ^a  

^a SOUTHERN RESEARCH INSTITUTE   (United States)

^b FUJIAN MEDICAL UNIVERSITY   (China)

Author keywords

Cancer; Drug discovery; LRP6; MTORC1 signaling; Rottlerin; Wnt signaling

Indexed keywords

BETA CATENIN; CYCLIN D1; HYDROXYMETHYLGLUTARYL COENZYME A REDUCTASE KINASE; LOW DENSITY LIPOPROTEIN RECEPTOR RELATED PROTEIN 6; MAMMALIAN TARGET OF RAPAMYCIN COMPLEX 1; NICLOSAMIDE; ROTTLERIN; SURVIVIN; WNT PROTEIN; ACETOPHENONE DERIVATIVE; ANTINEOPLASTIC AGENT; BENZOPYRAN DERIVATIVE; BIRC5 PROTEIN, HUMAN; CCND1 PROTEIN, HUMAN; INHIBITOR OF APOPTOSIS PROTEIN; LRP6 PROTEIN, HUMAN; MECHANISTIC TARGET OF RAPAMYCIN COMPLEX 1; MULTIPROTEIN COMPLEX; TARGET OF RAPAMYCIN KINASE; WNT3A PROTEIN; WNT3A PROTEIN, HUMAN;

ANTINEOPLASTIC ACTIVITY; ARTICLE; BREAST CANCER; CANCER CELL CULTURE; CANCER INHIBITION; CONTROLLED STUDY; DOWN REGULATION; DRUG TARGETING; EMBRYO; ENZYME ACTIVATION; GENETIC TRANSCRIPTION; HUMAN; HUMAN CELL; IC 50; PRIORITY JOURNAL; PROSTATE CANCER; PROTEIN DEGRADATION; PROTEIN EXPRESSION; PROTEIN PHOSPHORYLATION; SIGNAL TRANSDUCTION; BREAST TUMOR; CELL PROLIFERATION; DRUG EFFECTS; DRUG SCREENING; FEMALE; GENETICS; HEK293 CELL LINE; IC50; MALE; METABOLISM; PROMOTER REGION; PROSTATE TUMOR; TUMOR CELL LINE; WNT SIGNALING PATHWAY;

ACETOPHENONES; ANTINEOPLASTIC AGENTS; BENZOPYRANS; BREAST NEOPLASMS; CELL LINE, TUMOR; CELL PROLIFERATION; CYCLIN D1; DRUG SCREENING ASSAYS, ANTITUMOR; FEMALE; HEK293 CELLS; HUMANS; INHIBITOR OF APOPTOSIS PROTEINS; INHIBITORY CONCENTRATION 50; LOW DENSITY LIPOPROTEIN RECEPTOR-RELATED PROTEIN-6; MALE; MULTIPROTEIN COMPLEXES; PROMOTER REGIONS, GENETIC; PROSTATIC NEOPLASMS; PROTEOLYSIS; TOR SERINE-THREONINE KINASES; TRANSCRIPTION, GENETIC; WNT SIGNALING PATHWAY; WNT3A PROTEIN;

EID: 84896514225     PISSN: 08986568     EISSN: 18733913     Source Type: Journal    
DOI: 10.1016/j.cellsig.2014.02.018     Document Type: Article

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