title: Mitochondrial p32/C1QBP is highly expressed in prostate cancer and is associated with shorter prostate-specific antigen relapse time after radical prostatectomy.
abstract: Mitochondria are key organelles for ATP production and apoptosis. Therefore, impairment of mitochondria can modulate or accelerate cancer progression. p32, originally identified as a pre-mRNA splicing factor SF2/ASF-associated protein, is localized predominantly in the mitochondrial matrix and involved in mitochondria respiration. Recently, p32 was implicated in apoptosis and resultantly cancer progression. However, little is known about the expression and function of p32 in human tumors including prostate cancer. Here, we investigated the expression of p32 in 148 prostate carcinoma tissues by immunohistochemistry and found a positive correlation of p32 expression to clinicopathological parameters including follow-up data. p32 is highly expressed in prostate tumor samples and its expression is significantly associated with the Gleason score, pathological stage and relapse. For localized cancers, high p32 is a strong and independent predictor of clinical recurrence in multivariate analysis (P=0.01). In addition, p32 is overexpressed in the prostate cancer cell lines examined. The selective knockdown of p32 by RNA interference inhibits the growth of prostate cancer cell lines but not of a non-cancerous cell line. The p32 RNA interference decreases cyclin D1, increases p21 expression and causes a G1/S cell cycle arrest in prostate cancer cells. These data suggest that p32 is critical for prostate cancer cell proliferation and may be a novel marker of clinical progression in prostate cancer.
authors.affiliation: Department of Clinical Chemistry and Laboratory Medicine, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
authors.forename: Rie
authors.initials: R
authors.lastname: Amamoto
authors.forename: Mikako
authors.initials: M
authors.lastname: Yagi
authors.forename: YooHyun
authors.initials: Y
authors.lastname: Song
authors.forename: Yoshinao
authors.initials: Y
authors.lastname: Oda
authors.forename: Masazumi
authors.initials: M
authors.lastname: Tsuneyoshi
authors.forename: Seiji
authors.initials: S
authors.lastname: Naito
authors.forename: Akira
authors.initials: A
authors.lastname: Yokomizo
authors.forename: Kentaro
authors.initials: K
authors.lastname: Kuroiwa
authors.forename: Shoji
authors.initials: S
authors.lastname: Tokunaga
authors.forename: Seiji
authors.initials: S
authors.lastname: Kato
authors.forename: Hisahide
authors.initials: H
authors.lastname: Hiura
authors.forename: Tomohiro
authors.initials: T
authors.lastname: Samori
authors.forename: Dongchon
authors.initials: D
authors.lastname: Kang
authors.forename: Takeshi
authors.initials: T
authors.lastname: Uchiumi
mesh_terms: D000368:Aged; D014408:Biomarkers, Tumor / Q000032:analysis; D002352:Carrier Proteins / Q000032:analysis* / Q000502:physiology; D002453:Cell Cycle; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D019938:Cyclin D1 / Q000037:antagonists & inhibitors; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000096:biosynthesis; D006801:Humans; D008297:Male; D008875:Middle Aged; D008928:Mitochondria / Q000737:chemistry*; D024101:Mitochondrial Proteins / Q000032:analysis* / Q000502:physiology; D017430:Prostate-Specific Antigen / Q000097:blood*; D011468:Prostatectomy; D011471:Prostatic Neoplasms / Q000737:chemistry / Q000401:mortality / Q000473:pathology* / Q000601:surgery; D012008:Recurrence; D013997:Time Factors
chemical_list: D014408:Biomarkers, Tumor; C087299:C1QBP protein, human; C530104:CCND1 protein, human; C493956:CDKN1A protein, human; D002352:Carrier Proteins; D050759:Cyclin-Dependent Kinase Inhibitor p21; D024101:Mitochondrial Proteins; D019938:Cyclin D1; D017430:Prostate-Specific Antigen