ROS enhances CXCR4-mediated functions through inactivation of PTEN in prostate cancer cells

Biochemical and Biophysical Research Communications

Volumn 410, Issue 2, 2011, Pages 195-200

  Chetram, Mahandranauth A ^a   Don Salu Hewage, Ayesha S ^a   Hinton, Cimona V ^a  

^a CLARK ATLANTA UNIVERSITY   (United States)

Author keywords

AKT; CXCR4; H2O2; Prostate cancer; PTEN; ROS

Indexed keywords

CHEMOKINE RECEPTOR CXCR4; PHOSPHATIDYLINOSITOL 3,4,5 TRISPHOSPHATE 3 PHOSPHATASE; PROTEIN KINASE B; REACTIVE OXYGEN METABOLITE;

ARTICLE; CANCER CELL; CANCER GROWTH; CARCINOGENESIS; CATALYSIS; CELL INVASION; CELL MIGRATION; CONTROLLED STUDY; ENZYME INACTIVATION; HUMAN; HUMAN CELL; PRIORITY JOURNAL; PROSTATE CANCER; PROTEIN EXPRESSION; PROTEIN FUNCTION; TUMOR MICROENVIRONMENT;

CELL LINE, TUMOR; HUMANS; HYDROGEN PEROXIDE; MALE; PROSTATIC NEOPLASMS; PTEN PHOSPHOHYDROLASE; REACTIVE OXYGEN SPECIES; RECEPTORS, CXCR4; TUMOR MICROENVIRONMENT;

EID: 79959745176     PISSN: 0006291X     EISSN: 10902104     Source Type: Journal    
DOI: 10.1016/j.bbrc.2011.05.074     Document Type: Article

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