title: Expression of myopodin induces suppression of tumor growth and metastasis.
abstract: Myopodin was previously reported as a gene that was frequently deleted in prostate cancer. This gene shares significant homology with a cell shape-regulating gene, synaptopodin. Myopodin was shown to bind actin and to induce actin bundling when cells were stimulated. To clarify the functional role of myopodin in prostate cancer, several assays were performed to evaluate the tumor suppression activity of myopodin. Our results indicate that myopodin inhibits tumor growth and invasion both in vitro and in vivo. The activity of tumor suppression of myopodin is located at the C-terminus region. To further evaluate the role of myopodin in suppressing the invasiveness of prostate cancer, an expression analysis of myopodin protein was performed in prostate tissues. The results indicate that down-regulation of myopodin expression occurs mostly in invasive stages of prostate cancer, implying a potential invasion suppression role for myopodin in prostate cancer. In addition, hemizygous deletion and down-regulation of myopodin expression occur in three aggressive prostate cancer cell lines. All these results support the hypothesis that myopodin functions as a tumor suppressor gene to limit the growth and to inhibit the metastasis of cancer cells.
authors.affiliation: Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
authors.forename: Ling
authors.initials: L
authors.lastname: Jing
authors.forename: Lijun
authors.initials: L
authors.lastname: Liu
authors.forename: Yan Ping
authors.initials: YP
authors.lastname: Yu
authors.forename: Rajiv
authors.initials: R
authors.lastname: Dhir
authors.forename: Marie
authors.initials: M
authors.lastname: Acquafondada
authors.forename: Doug
authors.initials: D
authors.lastname: Landsittel
authors.forename: Kathleen
authors.initials: K
authors.lastname: Cieply
authors.forename: Alan
authors.initials: A
authors.lastname: Wells
authors.forename: Jian-Hua
authors.initials: JH
authors.lastname: Luo
mesh_terms: D000362:Agar / Q000494:pharmacology; D000818:Animals; D002455:Cell Division; D045744:Cell Line, Tumor; D003094:Collagen / Q000494:pharmacology; D018450:Disease Progression; D015536:Down-Regulation; D004338:Drug Combinations; D017353:Gene Deletion; D006801:Humans; D015151:Immunoblotting; D007150:Immunohistochemistry; D007797:Laminin / Q000494:pharmacology; D008297:Male; D051379:Mice; D016513:Mice, SCID; D008840:Microfilament Proteins / Q000737:chemistry / Q000502:physiology*; D009362:Neoplasm Metastasis; D009368:Neoplasm Transplantation; D011471:Prostatic Neoplasms / Q000378:metabolism / Q000473:pathology*; D017434:Protein Structure, Tertiary; D011509:Proteoglycans / Q000494:pharmacology; D013997:Time Factors
chemical_list: D004338:Drug Combinations; D007797:Laminin; D008840:Microfilament Proteins; D011509:Proteoglycans; C503979:SYNPO2 protein, human; C503980:Synpo2 protein, mouse; C059485:matrigel; D000362:Agar; D003094:Collagen